Sample records for maternal obesity up-regulates

  1. Maternal androgen excess and obesity induce sexually dimorphic anxiety-like behavior in the offspring.

    PubMed

    Manti, Maria; Fornes, Romina; Qi, Xiaojuan; Folmerz, Elin; Lindén Hirschberg, Angelica; de Castro Barbosa, Thais; Maliqueo, Manuel; Benrick, Anna; Stener-Victorin, Elisabet

    2018-03-22

    Maternal polycystic ovary syndrome (PCOS), a condition associated with hyperandrogenism, is suggested to increase anxiety-like behavior in the offspring. Because PCOS is closely linked to obesity, we investigated the impact of an adverse hormonal or metabolic maternal environment and offspring obesity on anxiety in the offspring. The obese PCOS phenotype was induced by chronic high-fat-high-sucrose (HFHS) consumption together with prenatal dihydrotestosterone exposure in mouse dams. Anxiety-like behavior was assessed in adult offspring with the elevated-plus maze and open-field tests. The influence of maternal androgens and maternal and offspring diet on genes implicated in anxiety were analyzed in the amygdala and hypothalamus with real-time PCR ( n = 47). Independent of diet, female offspring exposed to maternal androgens were more anxious and displayed up-regulation of adrenoceptor α 1B in the amygdala and up-regulation of hypothalamic corticotropin-releasing hormone ( Crh). By contrast, male offspring exposed to a HFHS maternal diet had increased anxiety-like behavior and showed up-regulation of epigenetic markers in the amygdala and up-regulation of hypothalamic Crh. Overall, there were substantial sex differences in gene expression in the brain. These findings provide novel insight into how maternal androgens and obesity exert sex-specific effects on behavior and gene expression in the offspring of a PCOS mouse model.-Manti, M., Fornes, R., Qi, X., Folmerz, E., Lindén Hirschberg, A., de Castro Barbosa, T., Maliqueo, M., Benrick, A., Stener-Victorin, E. Maternal androgen excess and obesity induce sexually dimorphic anxiety-like behavior in the offspring.

  2. Maternal obesity is associated with ovarian inflammation and up-regulation of early growth response factor 1

    USDA-ARS?s Scientific Manuscript database

    Obesity impairs reproductive functions through multiple mechanisms, possibly through disruption of ovarian function. We hypothesized that increased adiposity will lead to a pro-inflammatory gene signature and up-regulation of Egr-1 protein in ovaries from obese (OB, n=7) compared to lean (LN, n=10) ...

  3. Increased placental nutrient transport in a novel mouse model of maternal obesity with fetal overgrowth.

    PubMed

    Rosario, Fredrick J; Kanai, Yoshikatsu; Powell, Theresa L; Jansson, Thomas

    2015-08-01

    To identify possible mechanisms linking obesity in pregnancy to increased fetal adiposity and growth, a unique mouse model of maternal obesity associated with fetal overgrowth was developed, and the hypothesis that maternal obesity causes up-regulation of placental nutrient transporter expression and activity was tested. C57BL/6J female mice were fed a control (C) or a high-fat/high-sugar (HF/HS) pelleted diet supplemented by ad libitum access to sucrose (20%) solution, mated, and studied at embryonic day 18.5. HF/HS diet increased maternal fat mass by 2.2-fold (P < 0.01) and resulted in glucose intolerance with normal fasting glucose. Maternal circulating insulin, leptin, and cholesterol were increased (P < 0.05) whereas total and high-molecular-weight adiponectin was decreased (P < 0.05). HF/HS diet increased fetal weight (+18%, P = 0.0005). In trophoblast plasma membranes (TPM) isolated from placentas of HF/HS-fed animals, protein expression of glucose transporter (GLUT) 1 and 3, sodium-coupled neutral amino acid transporter (SNAT) 2, and large neutral amino acid transporter 1 (LAT1) was increased. TPM System A and L amino acid transporter activity was increased in the HF/HS group. Up-regulation of specific placental nutrient transporter isoforms may constitute a mechanism underlying fetal overgrowth in maternal obesity. © 2015 The Obesity Society.

  4. Prenatal Exposure to Maternal Obesity Alters Anxiety and Stress Coping Behaviors in Aged Mice.

    PubMed

    Balsevich, Georgia; Baumann, Valentin; Uribe, Andres; Chen, Alon; Schmidt, Mathias V

    2016-01-01

    There is growing evidence that maternal obesity and prenatal exposure to a high-fat diet program fetal development to regulate the physiology and behavior of the offspring in adulthood. Yet the extent to which the maternal dietary environment contributes to adult disease vulnerability remains unclear. In the current study we tested whether prenatal exposure to maternal obesity increases the offspring's vulnerability to stress-related psychiatric disorders. We used a mouse model of maternal diet-induced obesity to investigate whether maternal obesity affects the response to adult chronic stress exposure in young adult (3-month-old) and aged adult (12-month-old) offspring. Long-lasting, delayed impairments to anxiety-like behaviors and stress coping strategies resulted on account of prenatal exposure to maternal obesity. Although maternal obesity did not change the offspring's behavioral response to chronic stress per se, we demonstrate that the behavioral outcomes induced by prenatal exposure to maternal obesity parallel the deleterious effects of adult chronic stress exposure in aged male mice. We found that the glucocorticoid receptor (GR, Nr3c1) is upregulated in various hypothalamic nuclei on account of maternal obesity. In addition, gene expression of a known regulator of the GR, FKBP51, is increased specifically within the paraventricular nucleus. These findings indicate that maternal obesity parallels the deleterious effects of adult chronic stress exposure, and furthermore identifies GR/FKBP51 signaling as a novel candidate pathway regulated by maternal obesity. © 2015 S. Karger AG, Basel.

  5. Maternal obesity in Africa: a systematic review and meta-analysis

    PubMed Central

    Onubi, Ojochenemi J.; Marais, Debbi; Aucott, Lorna; Okonofua, Friday; Poobalan, Amudha S.

    2016-01-01

    Background Maternal obesity is emerging as a public health problem, recently highlighted together with maternal under-nutrition as a ‘double burden’, especially in African countries undergoing social and economic transition. This systematic review was conducted to investigate the current evidence on maternal obesity in Africa. Methods MEDLINE, EMBASE, Scopus, CINAHL and PsycINFO were searched (up to August 2014) and identified 29 studies. Prevalence, associations with socio-demographic factors, labour, child and maternal consequences of maternal obesity were assessed. Pooled risk ratios comparing obese and non-obese groups were calculated. Results Prevalence of maternal obesity across Africa ranged from 6.5 to 50.7%, with older and multiparous mothers more likely to be obese. Obese mothers had increased risks of adverse labour, child and maternal outcomes. However, non-obese mothers were more likely to have low-birthweight babies. The differences in measurement and timing of assessment of maternal obesity were found across studies. No studies were identified either on the knowledge or attitudes of pregnant women towards maternal obesity; or on interventions for obese pregnant women. Conclusions These results show that Africa's levels of maternal obesity are already having significant adverse effects. Culturally adaptable/sensitive interventions should be developed while monitoring to avoid undesired side effects. PMID:26487702

  6. Maternal obesity in Africa: a systematic review and meta-analysis.

    PubMed

    Onubi, Ojochenemi J; Marais, Debbi; Aucott, Lorna; Okonofua, Friday; Poobalan, Amudha S

    2016-09-01

    Maternal obesity is emerging as a public health problem, recently highlighted together with maternal under-nutrition as a 'double burden', especially in African countries undergoing social and economic transition. This systematic review was conducted to investigate the current evidence on maternal obesity in Africa. MEDLINE, EMBASE, Scopus, CINAHL and PsycINFO were searched (up to August 2014) and identified 29 studies. Prevalence, associations with socio-demographic factors, labour, child and maternal consequences of maternal obesity were assessed. Pooled risk ratios comparing obese and non-obese groups were calculated. Prevalence of maternal obesity across Africa ranged from 6.5 to 50.7%, with older and multiparous mothers more likely to be obese. Obese mothers had increased risks of adverse labour, child and maternal outcomes. However, non-obese mothers were more likely to have low-birthweight babies. The differences in measurement and timing of assessment of maternal obesity were found across studies. No studies were identified either on the knowledge or attitudes of pregnant women towards maternal obesity; or on interventions for obese pregnant women. These results show that Africa's levels of maternal obesity are already having significant adverse effects. Culturally adaptable/sensitive interventions should be developed while monitoring to avoid undesired side effects. © The Author 2015. Published by Oxford University Press on behalf of Faculty of Public Health.

  7. A Primary Human Trophoblast Model to Study the Effect of Inflammation Associated with Maternal Obesity on Regulation of Autophagy in the Placenta.

    PubMed

    Simon, Bailey; Bucher, Matthew; Maloyan, Alina

    2017-09-27

    Maternal obesity is associated with an increased risk of adverse perinatal outcomes that are likely mediated by compromised placental function that can be attributed to, in part, the dysregulation of autophagy. Aberrant changes in the expression of autophagy regulators in the placentas from obese pregnancies may be regulated by inflammatory processes associated with both obesity and pregnancy. Described here is a protocol for sampling of villous tissue and isolation of villous cytotrophoblasts from the term human placenta for primary cell culture. This is followed by a method for simulating the inflammatory milieu in the obese intrauterine environment by treating primary trophoblasts from lean pregnancies with tumor necrosis factor alpha (TNFα), a proinflammatory cytokine that is elevated in obesity and in pregnancy. Through the implementation of the protocol described here, it is found that exposure to exogenous TNFα regulates the expression of Rubicon, a negative regulator of autophagy, in trophoblasts from lean pregnancies with female fetuses. While a variety of biological factors in the obese intrauterine environment maintain the potential to modulate critical pathways in trophoblasts, this ex vivo system is especially useful for determining if expression patterns observed in vivo in human placentas with maternal obesity are a direct result of TNFα signaling. Ultimately, this approach affords the opportunity to parse out the regulatory and molecular implications of inflammation associated with maternal obesity on autophagy and other critical cellular pathways in trophoblasts that have the potential to impact placental function.

  8. Maternal pre-pregnancy obesity and risk for inattention and negative emotionality in children.

    PubMed

    Rodriguez, Alina

    2010-02-01

    This study aimed to replicate and extend previous work showing an association between maternal pre-pregnancy adiposity and risk for attention deficit hyperactivity disorder (ADHD) symptoms in children. A Swedish population-based prospective pregnancy-offspring cohort was followed up when children were 5 years old (N = 1,714). Mothers and kindergarten teachers rated children's ADHD symptoms, presence and duration of problems, and emotionality. Dichotomized outcomes examined difficulties of clinical relevance (top 15% of the distribution). Analyses adjusted for pregnancy (maternal smoking, depressive symptoms, life events, education, age, family structure), birth outcomes (birth weight, gestational age, infant sex) and concurrent variables (family structure, maternal depressive symptoms, parental ADHD symptoms, and child overweight) in an attempt to rule out confounding. Maternal pre-pregnancy overweight and obesity predicted high inattention symptom scores and obesity was associated with a two-fold increase in risk of difficulties with emotion intensity and emotion regulation according to teacher reports. Means of maternal ratings were unrelated to pre-pregnancy body mass index (BMI). Presence and duration of problems were associated with both maternal over and underweight according to teachers. Despite discrepancies between maternal and teacher reports, these results provide further evidence that maternal pre-pregnancy overweight and obesity are associated with child inattention symptoms and extend previous work by establishing a link between obesity and emotional difficulties. Maternal adiposity at the time of conception may be instrumental in programming child mental health, as prenatal brain development depends on maternal energy supply. Possible mechanisms include disturbed maternal metabolic function. If maternal pre-pregnancy obesity is a causal risk factor, the potential for prevention is great.

  9. Placental fatty acid transport in maternal obesity.

    PubMed

    Cetin, I; Parisi, F; Berti, C; Mandò, C; Desoye, G

    2012-12-01

    Pregestational obesity is a significant risk factor for adverse pregnancy outcomes. Maternal obesity is associated with a specific proinflammatory, endocrine and metabolic phenotype that may lead to higher supply of nutrients to the feto-placental unit and to excessive fetal fat accumulation. In particular, obesity may influence placental fatty acid (FA) transport in several ways, leading to increased diffusion driving force across the placenta, and to altered placental development, size and exchange surface area. Animal models show that maternal obesity is associated with increased expression of specific FA carriers and inflammatory signaling molecules in placental cotyledonary tissue, resulting in enhanced lipid transfer across the placenta, dislipidemia, fat accumulation and possibly altered development in fetuses. Cell culture experiments confirmed that inflammatory molecules, adipokines and FA, all significantly altered in obesity, are important regulators of placental lipid exchange. Expression studies in placentas of obese-diabetic women found a significant increase in FA binding protein-4 expression and in cellular triglyceride content, resulting in increased triglyceride cord blood concentrations. The expression and activity of carriers involved in placental lipid transport are influenced by the endocrine, inflammatory and metabolic milieu of obesity, and further studies are needed to elucidate the strong association between maternal obesity and fetal overgrowth.

  10. Maternal Pre-Pregnancy Obesity Is Associated with Altered Placental Transcriptome.

    PubMed

    Altmäe, Signe; Segura, Maria Teresa; Esteban, Francisco J; Bartel, Sabine; Brandi, Pilar; Irmler, Martin; Beckers, Johannes; Demmelmair, Hans; López-Sabater, Carmen; Koletzko, Berthold; Krauss-Etschmann, Susanne; Campoy, Cristina

    2017-01-01

    Maternal obesity has a major impact on pregnancy outcomes. There is growing evidence that maternal obesity has a negative influence on placental development and function, thereby adversely influencing offspring programming and health outcomes. However, the molecular mechanisms underlying these processes are poorly understood. We analysed ten term placenta's whole transcriptomes in obese (n = 5) and normal weight women (n = 5), using the Affymetrix microarray platform. Analyses of expression data were carried out using non-parametric methods. Hierarchical clustering and principal component analysis showed a clear distinction in placental transcriptome between obese and normal weight women. We identified 72 differentially regulated genes, with most being down-regulated in obesity (n = 61). Functional analyses of the targets using DAVID and IPA confirm the dysregulation of previously identified processes and pathways in the placenta from obese women, including inflammation and immune responses, lipid metabolism, cancer pathways, and angiogenesis. In addition, we detected new molecular aspects of obesity-derived effects on the placenta, involving the glucocorticoid receptor signalling pathway and dysregulation of several genes including CCL2, FSTL3, IGFBP1, MMP12, PRG2, PRL, QSOX1, SERPINE2 and TAC3. Our global gene expression profiling approach demonstrates that maternal obesity creates a unique in utero environment that impairs the placental transcriptome.

  11. Sirtuins-mediators of maternal obesity-induced complications in offspring?

    PubMed

    Nguyen, Long T; Chen, Hui; Pollock, Carol A; Saad, Sonia

    2016-04-01

    Obesity is a complex metabolic disease, attributed to diverse and interactive genetic and environmental factors. The associated health consequences of obesity are pleiotropic, with individuals being more susceptible to chronic diseases such as type 2 diabetes mellitus, hypertension, and lipotoxicity-related chronic diseases. The contribution of maternal obesity to the offspring's predisposition to both obesity and its complications is increasingly recognized. Understanding the mechanisms underlying these "transmissible" effects is critical to develop therapeutic interventions to reduce the risk for "programmed" obesity. Sirtuins (SIRTs), particularly SIRT1 and SIRT3, are NAD(+)-dependent deacetylases that regulate metabolic balance and stress responses in both central and peripheral tissues, of which dysregulation is a well-established mediator for the development and effects of obesity. Nevertheless, their implication in the transmissible effects of maternal obesity across generations remains largely elusive. In this review, we examine multiple pathways and systems that are likely to mediate such effects, with particular emphasis on the role of SIRTs.-Nguyen, L. T., Chen, H., Pollock, C. A., Saad, S. Sirtuins-mediators of maternal obesity-induced complications in offspring? © FASEB.

  12. The role of maternal obesity in the risk of neuropsychiatric disorders

    PubMed Central

    Rivera, Heidi M.; Christiansen, Kelly J.; Sullivan, Elinor L.

    2015-01-01

    Recent evidence indicates that perinatal exposure to maternal obesity, metabolic disease, including diabetes and hypertension, and unhealthy maternal diet has a long-term impact on offspring behavior and physiology. During the past three decades, the prevalence of both obesity and neuropsychiatric disorders has rapidly increased. Epidemiologic studies provide evidence that maternal obesity and metabolic complications increase the risk of attention deficit hyperactivity disorder (ADHD), autism spectrum disorders, anxiety, depression, schizophrenia, eating disorders (food addiction, anorexia nervosa, and bulimia nervosa), and impairments in cognition in offspring. Animal models of maternal high-fat diet (HFD) induced obesity also document persistent changes in offspring behavior and impairments in critical neural circuitry. Animals exposed to maternal obesity and HFD consumption display hyperactivity, impairments in social behavior, increased anxiety-like and depressive-like behaviors, substance addiction, food addiction, and diminished cognition. During development, these offspring are exposed to elevated levels of nutrients (fatty acids, glucose), hormones (leptin, insulin), and inflammatory factors (C-reactive protein, interleukin, and tumor necrosis factor). Such factors appear to permanently change neuroendocrine regulation and brain development in offspring. In addition, inflammation of the offspring brain during gestation impairs the development of neural pathways critical in the regulation of behavior, such as serotoninergic, dopaminergic, and melanocortinergic systems. Dysregulation of these circuits increases the risk of mental health disorders. Given the high rates of obesity in most developed nations, it is critical that the mechanisms by which maternal obesity programs offspring behavior are thoroughly characterized. Such knowledge will be critical in the development of preventative strategies and therapeutic interventions. PMID:26150767

  13. Effects of maternal obesity on placental function and fetal development

    PubMed Central

    Howell, Kristy R.; Powell, Theresa L.

    2017-01-01

    Obesity has reached epidemic proportions and pregnancies in obese mothers have increased risk for complications including gestational diabetes, hypertensive disorders, preterm birth and caesarian section. Children born to obese mothers are at increased risk of obesity and metabolic disease and are susceptible to develop neuropsychiatric and cognitive disorders. Changes in placental function not only play a critical role in the development of pregnancy complications but may also be involved in linking maternal obesity to long-term health risks in the infant. Maternal adipokines i.e., interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α), leptin and adiponectin link maternal nutritional status and adipose tissue metabolism to placental function. Adipokines and metabolic hormones have direct impact on placental function by modulating placental nutrient transport. Nutrient delivery to the fetus is regulated by a complex interaction between insulin signaling, cytokine profile and insulin responsiveness, which is modulated by adiponectin and IL-1β. In addition, obese pregnant women are at risk for hypertension and preeclampsia with reduced placental vascularity and blood flow, which would restrict placental nutrient delivery to the developing fetus. These sometimes opposing signals regulating placental function may contribute to the diversity of short and long-term outcomes observed in pregnant obese women. This review focuses on the changes in adipokines and obesity-related metabolic hormones, how these factors influence placental function and fetal development to contribute to long-term metabolic and behavioral consequences of children born to obese mothers. PMID:27864335

  14. Maternal Obesity: Lifelong Metabolic Outcomes for Offspring from Poor Developmental Trajectories During the Perinatal Period.

    PubMed

    Zambrano, Elena; Ibáñez, Carlos; Martínez-Samayoa, Paola M; Lomas-Soria, Consuelo; Durand-Carbajal, Marta; Rodríguez-González, Guadalupe L

    2016-01-01

    The prevalence of obesity in women of reproductive age is increasing in developed and developing countries around the world. Human and animal studies indicate that maternal obesity adversely impacts both maternal health and offspring phenotype, predisposing them to chronic diseases later in life including obesity, dyslipidemia, type 2 diabetes mellitus, and hypertension. Several mechanisms act together to produce these adverse health effects including programming of hypothalamic appetite-regulating centers, increasing maternal, fetal and offspring glucocorticoid production, changes in maternal metabolism and increasing maternal oxidative stress. Effective interventions during human pregnancy are needed to prevent both maternal and offspring metabolic dysfunction due to maternal obesity. This review addresses the relationship between maternal obesity and its negative impact on offspring development and presents some maternal intervention studies that propose strategies to prevent adverse offspring metabolic outcomes. Copyright © 2016 IMSS. Published by Elsevier Inc. All rights reserved.

  15. High-fat diet and maternal obesity-associated epigenetic regulation of bone development

    USDA-ARS?s Scientific Manuscript database

    Due to the worldwide epidemic in obesity, maternal obesity has recently seen an explosion in investigations in both animal models and humans on its effects on offspring phenotype and pathologies including diabetes, hyperlipidemia, cardiovascular disease, and cancer. Epigenetic mechanisms presumably ...

  16. Quality of early maternal-child relationship and risk of adolescent obesity.

    PubMed

    Anderson, Sarah E; Gooze, Rachel A; Lemeshow, Stanley; Whitaker, Robert C

    2012-01-01

    The goal of this study was to determine whether obesity in adolescence is related to the quality of the early maternal-child relationship. We analyzed data from 977 of 1364 participants in the Study of Early Child Care and Youth Development. Child attachment security and maternal sensitivity were assessed by observing mother-child interaction at 15, 24, and 36 months of age. A maternal-child relationship quality score was constructed as the number of times across the 3 ages that the child was either insecurely attached or experienced low maternal sensitivity. Adolescent obesity was defined as a measured BMI ≥95th percentile at age 15 years. Poor-quality maternal-child relationships (score: ≥3) were experienced by 24.7% of children compared with 22.0% who, at all 3 ages, were neither insecurely attached nor exposed to low maternal sensitivity (score: 0). The prevalence of adolescent obesity was 26.1%, 15.5%, 12.1%, and 13.0% for those with risk scores of ≥3, 2, 1, and 0, respectively. After adjustment for gender and birth weight, the odds (95% confidence interval) of adolescent obesity was 2.45 (1.49-4.04) times higher in those with the poorest quality early maternal-child relationships (score: ≥3) compared with those with the highest quality (score: 0). Low maternal sensitivity was more strongly associated with obesity than insecure attachment. Poor quality of the early maternal-child relationship was associated with a higher prevalence of adolescent obesity. Interventions aimed at improving the quality of maternal-child interactions should consider assessing effects on children's weight and examining potential mechanisms involving stress response and emotion regulation.

  17. Inflammation in maternal obesity and gestational diabetes mellitus.

    PubMed

    Pantham, P; Aye, I L M H; Powell, T L

    2015-07-01

    The prevalence of maternal obesity is rising rapidly worldwide and constitutes a major obstetric problem, increasing mortality and morbidity in both mother and offspring. Obese women are predisposed to pregnancy complications such as gestational diabetes mellitus (GDM), and children of obese mothers are more likely to develop cardiovascular and metabolic disease in later life. Maternal obesity and GDM may be associated with a state of chronic, low-grade inflammation termed "metainflammation", as opposed to an acute inflammatory response. This inflammatory environment may be one mechanism by which offspring of obese women are programmed to develop adult disorders. Herein we review the evidence that maternal obesity and GDM are associated with changes in the maternal, fetal and placental inflammatory profile. Maternal inflammation in obesity and GDM may not always be associated with fetal inflammation. We propose that the placenta 'senses' and adapts to the maternal inflammatory environment, and plays a central role as both a target and producer of inflammatory mediators. In this manner, maternal obesity and GDM may indirectly program the fetus for later disease by influencing placental function. Published by Elsevier Ltd.

  18. Obesity Disrupts the Rhythmic Profiles of Maternal and Fetal Progesterone in Rat Pregnancy.

    PubMed

    Crew, Rachael C; Mark, Peter J; Clarke, Michael W; Waddell, Brendan J

    2016-09-01

    Maternal obesity increases the risk of abnormal fetal growth, but the underlying mechanisms remain unclear. Because steroid hormones regulate fetal growth, and both pregnancy and obesity markedly alter circadian biology, we hypothesized that maternal obesity disrupts the normal rhythmic profiles of steroid hormones in rat pregnancy. Obesity was established by cafeteria (CAF) feeding for 8 wk prior to mating and throughout pregnancy. Control (CON) animals had ad libitum access to chow. Daily profiles of plasma corticosterone, 11-dehydrocorticosterone, progesterone, and testosterone were measured at Days 15 and 21 of gestation (term = 23 days) in maternal (both days) and fetal (Day 21) plasma. CAF mothers exhibited increased adiposity relative to CON and showed fetal and placental growth restriction. There was no change, however, in total fetal or placental mass due to slightly larger litter sizes in CAF. Nocturnal declines in progesterone were observed in maternal (39% lower) and fetal (45% lower) plasma in CON animals, but these were absent in CAF animals. CAF mothers were hyperlipidemic at both days of gestation, but this effect was isolated to the dark period at Day 21. CAF maternal testosterone was slightly lower at Day 15 (8%) but increased above CON by Day 21 (16%). Despite elevated maternal testosterone, male fetal testosterone was suppressed by obesity on Day 21. Neither maternal nor fetal glucocorticoid profiles were affected by obesity. In conclusion, obesity disrupts rhythmic profiles of maternal and fetal progesterone, preventing the normal nocturnal decline. Obesity subtly changed testosterone profiles but did not alter maternal and fetal glucocorticoids. © 2016 by the Society for the Study of Reproduction, Inc.

  19. Comprehending emotional eating in obese youngsters: the role of parental rejection and emotion regulation.

    PubMed

    Vandewalle, J; Moens, E; Braet, C

    2014-04-01

    The present study examined the role of emotion regulation in the relation between parental rejection and emotional eating of obese youngsters. Participants were 110 obese youngsters between the ages of 10 and 16 years who were referred to a Belgian treatment centre for obesity. Participants completed questionnaires assessing maternal and paternal rejection, emotion regulation strategies and emotional eating during their intake at the treatment centre. Bootstrapping procedure was used to test if emotion regulation mediated the relationship between maternal and paternal rejection on the one hand and emotional eating of the youngster on the other hand. Results revealed that the use of maladaptive emotion regulation strategies mediated the relation between maternal rejection and emotional eating. Paternal rejection was neither associated with the emotion regulation nor with the emotional eating of the youngster. The findings highlight the importance of assessing the emotional bond between mother and child and the emotion regulation of the youngster in the treatment of pediatric obesity.

  20. Increasing maternal obesity is associated with alterations in both maternal and neonatal thyroid hormone levels.

    PubMed

    Kahr, Maike K; Antony, Kathleen M; DelBeccaro, Melanie; Hu, Min; Aagaard, Kjersti M; Suter, Melissa A

    2016-04-01

    Obesity is associated with alterations in thyroid hormone (TH) levels in obese, pregnant individuals. The maintenance of TH levels throughout gestation is important for proper foetal development. The aim of this study was to measure levels of fT3, fT4 and TSH in maternal and matched cord blood serum from normal weight, overweight and obese gravidae to determine alterations in maternal and neonatal TH levels by virtue of maternal obesity. ELISA was utilized to measure fT3, fT4 and TSH levels from banked, matched maternal and neonatal (cord blood) serum (N = 205 matched pairs). Data were stratified according to prepregnancy or first trimester BMI. Both maternal and neonatal fT3 levels consistently increased with increasing maternal obesity, and maternal and neonatal fT3 were significantly correlated (r = 0·422, P < 0·001). Maternal and neonatal fT3 were also significantly associated with birthweight (β = 0·155, P = 0·027 and β = 0·171, P = 0·018, respectively). Both the maternal and neonatal fT3 to fT4 ratio significantly increased with increasing maternal obesity. We further found that excess gestational weight gain was associated with a decrease in maternal fT4 compared with gravidae who had insufficient gestational weight gain (0·86 ± 0·17 vs 0·95 ± 0·22, P < 0·01). Maternal obesity is not only associated with maternal alterations in TH, but with accompanying neonatal changes. Because both maternal obesity and alterations in TH levels are associated with childhood obesity, based on these findings and our prior analyses in a nonhuman primate model, we propose that changes in fT3 levels in the offspring of obese mothers may be a potential molecular mediator of foetal overgrowth and childhood obesity. © 2015 The Authors. Clinical Endocrinology Published by John Wiley & Sons Ltd.

  1. Interrupting Intergenerational Cycles of Maternal Obesity

    PubMed Central

    Gillman, Matthew W.

    2016-01-01

    Factors operating in the preconception and prenatal periods, such as maternal obesity, excessive gestational weight gain, and gestational diabetes, predict a substantial fraction of childhood obesity as well as lifelong adverse health consequences in the mother. These periods may lend themselves to successful intervention to reduce such risk factors because parents may be especially willing to change behavior if it confers health advantages to their children. If effective interventions started before or during pregnancy can be maintained after birth, they have the potential to lower the risk of both maternal obesity in the next pregnancy and obesity in the growing child, thus helping to interrupt maternal and child inter-generational vicious cycles of obesity, diabetes, and related cardiometabolic health consequences. While this paradigm is appealing, challenges include determining the magnitude, causality, and modifiability of these risk factors, and quantifying any adverse consequences of intervention. PMID:27088333

  2. Maternal Obesity, Inflammation, and Developmental Programming

    PubMed Central

    Segovia, Stephanie A.; Vickers, Mark H.; Reynolds, Clare M.

    2014-01-01

    The prevalence of obesity, especially in women of child-bearing age, is a global health concern. In addition to increasing the immediate risk of gestational complications, there is accumulating evidence that maternal obesity also has long-term consequences for the offspring. The concept of developmental programming describes the process in which an environmental stimulus, including altered nutrition, during critical periods of development can program alterations in organogenesis, tissue development, and metabolism, predisposing offspring to obesity and metabolic and cardiovascular disorders in later life. Although the mechanisms underpinning programming of metabolic disorders remain poorly defined, it has become increasingly clear that low-grade inflammation is associated with obesity and its comorbidities. This review will discuss maternal metainflammation as a mediator of programming in insulin sensitive tissues in offspring. Use of nutritional anti-inflammatories in pregnancy including omega 3 fatty acids, resveratrol, curcumin, and taurine may provide beneficial intervention strategies to ameliorate maternal obesity-induced programming. PMID:24967364

  3. Maternal obesity and prenatal programming.

    PubMed

    Elshenawy, Summer; Simmons, Rebecca

    2016-11-05

    Obesity is a significant and increasing public health concern in the United States and worldwide. Clinical and epidemiological evidence clearly shows that genetic and environmental factors contribute to the increased susceptibility of humans to obesity and its associated comorbidities; the interplay of these factors is explained by the concept of epigenetics. The impact of maternal obesity goes beyond the newborn period; fetal programming during the critical window of pregnancy, can have long term detrimental effects on the offspring as well as future generations. Emerging evidence is uncovering a link between the clinical and molecular findings in the offspring with epigenetic changes in the setting of maternal obesity. Research targeted towards reducing the transgenerational propagation and developmental programming of obesity is vital in reducing the increasing rates of disease. Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.

  4. Impact of maternal obesity on perinatal and childhood outcomes.

    PubMed

    Santangeli, Louise; Sattar, Naveed; Huda, Shahzya S

    2015-04-01

    Maternal obesity is of major consequence, affecting every aspect of maternity care including both short- and long-term effects on the health of the offspring. Obese mothers are at a higher risk of developing gestational diabetes and pre-eclampsia, potentially exposing the foetus to an adverse intrauterine environment. Maternal obesity is linked to foetal macrosomia, resulting in increased neonatal and maternal morbidity. Foetal macrosomia is a result of a change in body composition in the neonate with an increase in both percentage fat and fat mass. Maternal obesity and gestational weight gain are associated with childhood obesity, and this effect extends into adulthood. Childhood obesity in turn increases chances of later life obesity, thus type 2 diabetes, and cardiovascular disease in the offspring. Further clinical trials of lifestyle and, potentially, pharmacological interventions in obese pregnant women are required to determine whether short- and long-term adverse effects for the mother and child can be reduced. Copyright © 2014. Published by Elsevier Ltd.

  5. Oxidative stress and maternal obesity: feto-placental unit interaction.

    PubMed

    Malti, N; Merzouk, H; Merzouk, S A; Loukidi, B; Karaouzene, N; Malti, A; Narce, M

    2014-06-01

    To determine oxidative stress markers in maternal obesity during pregnancy and to evaluate feto-placental unit interaction, especially predictors of fetal metabolic alterations. 40 obese pregnant women (prepregnancy BMI > 30 kg/m²) were compared to 50 control pregnant women. Maternal, cord blood and placenta samples were collected at delivery. Biochemical parameters (total cholesterol and triglycerides) and oxidative stress markers (malondialdehyde, carbonyl proteins, superoxide anion expressed as reduced Nitroblue Tetrazolium, nitric oxide expressed as nitrite, reduced glutathione, catalase, superoxide dismutase) were assayed by biochemical methods. Maternal, fetal and placental triglyceride levels were increased in obese group compared to control. Maternal malondialdehyde, carbonyl proteins, nitric oxide and superoxide anion levels were high while reduced glutathione concentrations and superoxide dismutase activity were low in obesity. In the placenta and in newborns of these obese mothers, variations of redox balance were also observed indicating high oxidative stress. Maternal and placental interaction constituted a strong predictor of fetal redox variations in obese pregnancies. Maternal obesity compromised placental metabolism and antioxidant status which strongly impacted fetal redox balance. Oxidative stress may be one of the key downstream mediators that initiate programming of the offspring. Maternal obesity is associated with metabolic alterations and dysregulation of redox balance in the mother-placenta - fetus unit. These perturbations could lead to maternal and fetal complications and should be carefully considered. Copyright © 2014 Elsevier Ltd. All rights reserved.

  6. Maternal high-fat diet and obesity compromise fetal hematopoiesis

    PubMed Central

    Kamimae-Lanning, Ashley N.; Krasnow, Stephanie M.; Goloviznina, Natalya A.; Zhu, Xinxia; Roth-Carter, Quinn R.; Levasseur, Peter R.; Jeng, Sophia; McWeeney, Shannon K.; Kurre, Peter; Marks, Daniel L.

    2014-01-01

    Objective Recent evidence indicates that the adult hematopoietic system is susceptible to diet-induced lineage skewing. It is not known whether the developing hematopoietic system is subject to metabolic programming via in utero high-fat diet (HFD) exposure, an established mechanism of adult disease in several organ systems. We previously reported substantial losses in offspring liver size with prenatal HFD. As the liver is the main hematopoietic organ in the fetus, we asked whether the developmental expansion of the hematopoietic stem and progenitor cell (HSPC) pool is compromised by prenatal HFD and/or maternal obesity. Methods We used quantitative assays, progenitor colony formation, flow cytometry, transplantation, and gene expression assays with a series of dietary manipulations to test the effects of gestational high-fat diet and maternal obesity on the day 14.5 fetal liver hematopoietic system. Results Maternal obesity, particularly when paired with gestational HFD, restricts physiological expansion of fetal HSPCs while promoting the opposing cell fate of differentiation. Importantly, these effects are only partially ameliorated by gestational dietary adjustments for obese dams. Competitive transplantation reveals compromised repopulation and myeloid-biased differentiation of HFD-programmed HSPCs to be a niche-dependent defect, apparent in HFD-conditioned male recipients. Fetal HSPC deficiencies coincide with perturbations in genes regulating metabolism, immune and inflammatory processes, and stress response, along with downregulation of genes critical for hematopoietic stem cell self-renewal and activation of pathways regulating cell migration. Conclusions Our data reveal a previously unrecognized susceptibility to nutritional and metabolic developmental programming in the fetal HSPC compartment, which is a partially reversible and microenvironment-dependent defect perturbing stem and progenitor cell expansion and hematopoietic lineage commitment. PMID

  7. Maternal high-fat diet and obesity impact palatable food intake and dopamine signaling in nonhuman primate offspring.

    PubMed

    Rivera, Heidi M; Kievit, Paul; Kirigiti, Melissa A; Bauman, Leigh Ann; Baquero, Karalee; Blundell, Peter; Dean, Tyler A; Valleau, Jeanette C; Takahashi, Diana L; Frazee, Tim; Douville, Luke; Majer, Jordan; Smith, M Susan; Grove, Kevin L; Sullivan, Elinor L

    2015-11-01

    To utilize a nonhuman primate model to examine the impact of maternal high-fat diet (HFD) consumption and pre-pregnancy obesity on offspring intake of palatable food and to examine whether maternal HFD consumption impaired development of the dopamine system, critical for the regulation of hedonic feeding. The impact of exposure to maternal HFD and obesity on offspring consumption of diets of varying composition was assessed after weaning. The influence of maternal HFD consumption on the development of the prefrontal cortex-dopaminergic system at 13 months of age was also examined. During a preference test, offspring exposed to maternal HFD consumption and obesity displayed increased intake of food high in fat and sugar content relative to offspring from lean control mothers. Maternal HFD consumption suppressed offspring dopamine signaling (as assessed by immunohistochemistry) relative to control offspring. Specifically, there was decreased abundance of dopamine fibers and of dopamine receptor 1 and 2 proteins. This study reveals that offspring exposed to both maternal HFD consumption and maternal obesity during early development are at increased risk for obesity due to overconsumption of palatable energy-dense food, a behavior that may be related to reduced central dopamine signaling. © 2015 The Obesity Society.

  8. Childhood consequences of maternal obesity and excessive weight gain during pregnancy.

    PubMed

    Gaillard, Romy; Felix, Janine F; Duijts, Liesbeth; Jaddoe, Vincent W V

    2014-11-01

    Obesity is a major public health concern. In western countries, the prevalence of obesity in pregnant women has strongly increased, with reported prevalence rates reaching 30%. Also, up to 40% of women gain an excessive amount of weight during pregnancy. Recent observational studies and meta-analyses strongly suggest long-term impact of maternal obesity and excessive weight gain during pregnancy on adiposity, cardiovascular and respiratory related health outcomes in their children. These observations suggest that maternal adiposity during pregnancy may program common health problems in the offspring. Currently, it remains unclear whether the observed associations are causal, or just reflect confounding by family-based sociodemographic or lifestyle-related factors. Parent-offspring studies, sibling comparison studies, Mendelian randomization studies and randomized trials can help to explore the causality and underlying mechanisms. Also, the potential for prevention of common diseases in future generations by reducing maternal obesity and excessive weight gain during pregnancy needs to be explored. © 2014 Nordic Federation of Societies of Obstetrics and Gynecology.

  9. Does maternal obesity have an influence on feeding behavior of obese children?

    PubMed

    Cebeci, A N; Guven, A

    2015-12-01

    Although the pathogenesis of childhood obesity is multi factorial, maternal obesity and parenting have major roles. The aim of this study was to evaluate the influence of maternal obesity on feeding practices toward their obese school children. Obese children and adolescents referred to the pediatric endocrinology department were enrolled consecutively. Height and weight of all children and their mothers were measured. Maternal feeding practices were measured using an adapted version of the Child Feeding Questionnaire (CFQ). Answers were compared between obese (Body Mass Index [BMI] ≥ 30 kg/m2) and non-obese mothers. A total of 491 obese subjects (292 girls, mean age 12.0 ± 2.8 years) and their mothers participated in this study. A direct correlation between children's BMI and their mothers' BMI was found (P<0.001) both in girls (r = 0.372) and boys (r = 0.337). While 64.4% of mothers were found obese in the study, only half of them consider themselves as obese. No difference were found in the scores of the subscales "perceived responsibility", "restriction", "concern for child's weight" and "monitoring" between obese and non-obese mothers. Child's BMI-SDS positively correlated with mothers' personal weight perception, concern for child's weight and restriction after adjustment for child's age (P < 0.001, P = 0.012 and P = 0.002, respectively). Mothers' BMI highly correlate with children's BMI-z-scores. The degree of child's obesity increases mothers' concern and food restriction behavior. While mothers of obese children have a high prevalence of obesity, maternal obesity was found to have no significant influence on feeding behavior of obese school children.

  10. Maternal obesity and infant mortality: a meta-analysis.

    PubMed

    Meehan, Sean; Beck, Charles R; Mair-Jenkins, John; Leonardi-Bee, Jo; Puleston, Richard

    2014-05-01

    Despite numerous studies reporting an elevated risk of infant mortality among women who are obese, the magnitude of the association is unclear. A systematic review and meta-analysis was undertaken to assess the association between maternal overweight or obesity and infant mortality. Four health care databases and gray literature sources were searched and screened against the protocol eligibility criteria. Observational studies reporting on the relationship between maternal overweight and obesity and infant mortality were included. Data extraction and risk of bias assessments were performed. Twenty-four records were included from 783 screened. Obese mothers (BMI ≥30) had greater odds of having an infant death (odds ratio 1.42; 95% confidence interval, 1.24-1.63; P < .001; 11 studies); these odds were greatest for the most obese (BMI >35) (odds ratio 2.03; 95% confidence interval, 1.61-2.56; P < .001; 3 studies). Our results suggest that the odds of having an infant death are greater for obese mothers and that this risk may increase with greater maternal BMI or weight; however, residual confounding may explain these findings. Given the rising prevalence of maternal obesity, additional high-quality epidemiologic studies to elucidate the actual influence of elevated maternal mass or weight on infant mortality are needed. If a causal link is determined and the biological basis explained, public health strategies to address the issue of maternal obesity will be needed. Copyright © 2014 by the American Academy of Pediatrics.

  11. Accelerated recovery from acute hypoxia in obese mice is due to obesity-associated up-regulation of interleukin-1 receptor antagonist.

    PubMed

    Sherry, Christina L; Kim, Stephanie S; Freund, Gregory G

    2009-06-01

    The proinflammatory consequences of obesity are thought to be due, in part, to macrophage infiltration into adipose tissue. There are, however, potential antiinflammatory consequences of obesity that include obesity-associated up-regulation of IL-1 receptor antagonist (IL-1RA). Here we show that obesity-associated up-regulation of IL-1RA speeds recovery from hypoxia. We found that high-fat diet-fed (HFD) mice recovered from acute hypoxia 5 times faster than normal-diet-fed (ND) mice. HFD mice had a 10-fold increase in serum IL-1RA when compared with ND mice. White adipose tissue (WAT) was a significant source of IL-RA, generating 330 +/- 77 pg/mg protein in HFD mice as compared with 15 +/- 5 pg/mg protein in ND mice. Peritoneal macrophages isolated from HFD mice showed little difference in IL-1RA production when compared with ND mice, but WAT macrophages from HFD mice generated 11-fold more IL-1RA than those from ND mice. When ND mice were given an ip transfer of the stromal vascular fraction portion of WAT from HFD mice, serum IL-1RA increased 836% and recovery from acute hypoxia was faster than in mice that did not receive a stromal vascular fraction transfer. To determine whether IL-1RA was important to this accelerated recovery, ND mice were administered exogenous IL-1RA prior to hypoxia, and their recovery matched that of HFD mice. Inversely, when IL-1RA was immunoabsorbed in HFD mice with IL-1RA antiserum, recovery from acute hypoxia was attenuated. Taken together these data demonstrate that HFD-induced obesity speeds recovery from hypoxia due to obesity-associated up-regulation of IL-1RA.

  12. Accelerated Recovery from Acute Hypoxia in Obese Mice Is Due to Obesity-Associated Up-Regulation of Interleukin-1 Receptor Antagonist

    PubMed Central

    Sherry, Christina L.; Kim, Stephanie S.; Freund, Gregory G.

    2009-01-01

    The proinflammatory consequences of obesity are thought to be due, in part, to macrophage infiltration into adipose tissue. There are, however, potential antiinflammatory consequences of obesity that include obesity-associated up-regulation of IL-1 receptor antagonist (IL-1RA). Here we show that obesity-associated up-regulation of IL-1RA speeds recovery from hypoxia. We found that high-fat diet-fed (HFD) mice recovered from acute hypoxia 5 times faster than normal-diet-fed (ND) mice. HFD mice had a 10-fold increase in serum IL-1RA when compared with ND mice. White adipose tissue (WAT) was a significant source of IL-RA, generating 330 ± 77 pg/mg protein in HFD mice as compared with 15 ± 5 pg/mg protein in ND mice. Peritoneal macrophages isolated from HFD mice showed little difference in IL-1RA production when compared with ND mice, but WAT macrophages from HFD mice generated 11-fold more IL-1RA than those from ND mice. When ND mice were given an ip transfer of the stromal vascular fraction portion of WAT from HFD mice, serum IL-1RA increased 836% and recovery from acute hypoxia was faster than in mice that did not receive a stromal vascular fraction transfer. To determine whether IL-1RA was important to this accelerated recovery, ND mice were administered exogenous IL-1RA prior to hypoxia, and their recovery matched that of HFD mice. Inversely, when IL-1RA was immunoabsorbed in HFD mice with IL-1RA antiserum, recovery from acute hypoxia was attenuated. Taken together these data demonstrate that HFD-induced obesity speeds recovery from hypoxia due to obesity-associated up-regulation of IL-1RA. PMID:19213834

  13. Maternal Obesity and its Short- and Long-Term Maternal and Infantile Effects

    PubMed Central

    Korkmaz, Levent; Baştuğ, Osman; Kurtoğlu, Selim

    2016-01-01

    Obesity, in childhood or in adulthood, remains to be a global health problem. The worldwide prevalence of obesity has increased in the last few decades, and consequently, the women of our time suffer more gestational problems than women in the past. The prevalence of obesity is greater in older women than in younger ones and in women with low educational level than in their counterparts with a higher level of education. Maternal obesity during pregnancy may increase congenital malformations and neonatal morbidity and mortality. Maternal obesity is associated with a decreased intention to breastfeed, decreased initiation of breastfeeding, and decreased duration of breastfeeding. We discuss the current epidemiological evidence for the association of maternal obesity with congenital structural neural tube and cardiac defects, fetal macrosomia that predisposes infants to birth injuries and to problems with physiological and metabolic transition, as well as potential for long-term complications secondary to prenatal and neonatal programming effects compounded by a reduction in sustained breastfeeding. PMID:26758575

  14. Maternal Obesity and its Short- and Long-Term Maternal and Infantile Effects.

    PubMed

    Korkmaz, Levent; Baştuğ, Osman; Kurtoğlu, Selim

    2016-06-05

    Obesity, in childhood or in adulthood, remains to be a global health problem. The worldwide prevalence of obesity has increased in the last few decades, and consequently, the women of our time suffer more gestational problems than women in the past. The prevalence of obesity is greater in older women than in younger ones and in women with low educational level than in their counterparts with a higher level of education. Maternal obesity during pregnancy may increase congenital malformations and neonatal morbidity and mortality. Maternal obesity is associated with a decreased intention to breastfeed, decreased initiation of breastfeeding, and decreased duration of breastfeeding. We discuss the current epidemiological evidence for the association of maternal obesity with congenital structural neural tube and cardiac defects, fetal macrosomia that predisposes infants to birth injuries and to problems with physiological and metabolic transition, as well as potential for long-term complications secondary to prenatal and neonatal programming effects compounded by a reduction in sustained breastfeeding.

  15. Maternal High-Fat Diet and Obesity Impact Palatable Food Intake and Dopamine Signaling in Nonhuman Primate Offspring

    PubMed Central

    Rivera, Heidi M.; Kievit, Paul; Kirigiti, Melissa A.; Bauman, Leigh Ann; Baquero, Karalee; Blundell, Peter; Dean, Tyler A.; Valleau, Jeanette C.; Takahashi, Diana L.; Frazee, Tim; Douville, Luke; Majer, Jordan; Smith, M. Susan; Grove, Kevin L.; Sullivan, Elinor L.

    2015-01-01

    Objective To utilize a nonhuman primate model to examine the impact of maternal high-fat diet (HFD) consumption and pre-pregnancy obesity on offspring intake of palatable food. We will also examine whether maternal HFD consumption impaired development of the dopamine system, critical for the regulation of hedonic feeding. Methods The impact of exposure to maternal HFD and obesity on offspring consumption of diets of varying composition was assessed after weaning. We also examined the influence of maternal HFD consumption on the development of the prefrontal cortex-dopamine system at 13 months of age. Results During a preference test, offspring exposed to maternal obesity and HFD consumption displayed increased intake of food high in fat and sugar content relative to offspring from lean control mothers. Maternal HFD consumption suppressed offspring dopamine signaling (as assessed by immunohistochemistry) relative to control offspring. Specifically, there was decreased abundance of dopamine fibers and of dopamine receptor 1 and 2 protein. Conclusion Our findings reveal that offspring exposed to both maternal HFD consumption and maternal obesity during early development are at increased risk for obesity due to overconsumption of palatable energy-dense food, a behavior that may be related to reduced central dopamine signaling. PMID:26530932

  16. Effects of Maternal Obesity on Fetal Programming: Molecular Approaches

    PubMed Central

    Neri, Caterina; Edlow, Andrea G.

    2016-01-01

    Maternal obesity has become a worldwide epidemic. Obesity and a high-fat diet have been shown to have deleterious effects on fetal programming, predisposing offspring to adverse cardiometabolic and neurodevelopmental outcomes. Although large epidemiological studies have shown an association between maternal obesity and adverse outcomes for offspring, the underlying mechanisms remain unclear. Molecular approaches have played a key role in elucidating the mechanistic underpinnings of fetal malprogramming in the setting of maternal obesity. These approaches include, among others, characterization of epigenetic modifications, microRNA expression, the gut microbiome, the transcriptome, and evaluation of specific mRNA expression via quantitative reverse transcription polmerase chain reaction (RT-qPCR) in fetuses and offspring of obese females. This work will review the data from animal models and human fluids/cells regarding the effects of maternal obesity on fetal and offspring neurodevelopment and cardiometabolic outcomes, with a particular focus on molecular approaches. PMID:26337113

  17. Maternal obesity alters brain derived neurotrophic factor (BDNF) signaling in the placenta in a sexually dimorphic manner.

    PubMed

    Prince, Calais S; Maloyan, Alina; Myatt, Leslie

    2017-01-01

    Obesity is a major clinical problem in obstetrics being associated with adverse pregnancy outcomes and fetal programming. Brain derived neurotrophic factor (BDNF), a validated miR-210 target, is necessary for placental development, fetal growth, glucose metabolism, and energy homeostasis. Plasma BDNF levels are reduced in obese individuals; however, placental BDNF has yet to be studied in the context of maternal obesity. In this study, we investigated the effect of maternal obesity and sexual dimorphism on placental BDNF signaling. BDNF signaling was measured in placentas from lean (pre-pregnancy BMI < 25) and obese (pre-pregnancy BMI>30) women at term without medical complications that delivered via cesarean section without labor. MiRNA-210, BDNF mRNA, proBDNF, and mature BDNF were measured by RT - PCR, ELISA, and Western blot. Downstream signaling via TRKB (BDNF receptor) was measured using Western blot. Maternal obesity was associated with increased miRNA-210 and decreased BDNF mRNA in placentas from female fetuses, and decreased proBDNF in placentas from male fetuses. We also identified decreased mature BDNF in placentas from male fetuses when compared to female fetuses. Mir-210 expression was negatively correlated with mature BDNF protein. TRKB phosphorylated at tyrosine 817, not tyrosine 515, was increased in placentas from obese women. Maternal obesity was associated with increased phosphorylation of MAPK p38 in placentas from male fetuses, but not phosphorylation of ERK p42/44. BDNF regulation is complex and highly regulated. Pre-pregnancy/early maternal obesity adversely affects BDNF/TRKB signaling in the placenta in a sexually dimorphic manner. These data collectively suggest that induction of placental TRKB signaling could ameliorate the placental OB phenotype, thus improving perinatal outcome. Copyright © 2016 Elsevier Ltd. All rights reserved.

  18. Epigenetic regulation in obesity.

    PubMed

    Drummond, Elaine M; Gibney, Eileen R

    2013-07-01

    Research suggests that 65% of variation in obesity is genetic. However, much of the known genetic associations have little known function and their effect size small, thus the gene-environment interaction, including epigenetic influences on gene expression, is suggested to be an important factor in the susceptibilty to obesity. This review will explore the potential of epigenetic markers to influence expression of genes associated with obesity. Epigenetic changes in utero are known to have direct implications on the phenotype of the offspring. More recently work has focused on how such epigenetic changes continue to regulate risk of obesity from infancy through to adulthood. Work has shown that, for example, hypomethylation of the MC4 gene causes an increase in expression, and has a direct impact on appetite and intake, and thus influences risk of obesity. Similar influences are also seen in other aspects of obesity including inflammation and adiposity. Maternal diet during foetal development has many epigenetic implications, which affect the offspring's risk factors for obesity during childhood and adulthood, and even in subsequent generations. Genes associated with risk of obesity, are susceptible to epigenetic mutations, which have subsequent effects on disease mechanisms, such as appetite and impaired glucose and insulin tolerance.

  19. The effect of maternal undernutrition on the rat placental transcriptome: protein restriction up-regulates cholesterol transport.

    PubMed

    Daniel, Zoe; Swali, Angelina; Emes, Richard; Langley-Evans, Simon C

    2016-01-01

    Fetal exposure to a maternal low protein diet during rat pregnancy is associated with hypertension, renal dysfunction and metabolic disturbance in adult life. These effects are present when dietary manipulations target only the first half of pregnancy. It was hypothesised that early gestation protein restriction would impact upon placental gene expression and that this may give clues to the mechanism which links maternal diet to later consequences. Pregnant rats were fed control or a low protein diet from conception to day 13 gestation. Placentas were collected and RNA sequencing performed using the Illumina platform. Protein restriction down-regulated 67 genes and up-regulated 24 genes in the placenta. Ingenuity pathway analysis showed significant enrichment in pathways related to cholesterol and lipoprotein transport and metabolism, including atherosclerosis signalling, clathrin-mediated endocytosis, LXR/RXR and FXR/RXR activation. Genes at the centre of these processes included the apolipoproteins ApoB, ApoA2 and ApoC2, microsomal triglyceride transfer protein (Mttp), the clathrin-endocytosis receptor cubilin, the transcription factor retinol binding protein 4 (Rbp4) and transerythrin (Ttr; a retinol and thyroid hormone transporter). Real-time PCR measurements largely confirmed the findings of RNASeq and indicated that the impact of protein restriction was often striking (cubilin up-regulated 32-fold, apoC2 up-regulated 17.6-fold). The findings show that gene expression in specific pathways is modulated by maternal protein restriction in the day-13 rat placenta. Changes in cholesterol transport may contribute to altered tissue development in the fetus and hence programme risk of disease in later life.

  20. Maternal employment and childhood obesity--a European perspective.

    PubMed

    Gwozdz, Wencke; Sousa-Poza, Alfonso; Reisch, Lucia A; Ahrens, Wolfgang; Eiben, Gabriele; M Fernandéz-Alvira, Juan; Hadjigeorgiou, Charalampos; De Henauw, Stefaan; Kovács, Eva; Lauria, Fabio; Veidebaum, Toomas; Williams, Garrath; Bammann, Karin

    2013-07-01

    The substantial increase in female employment rates in Europe over the past two decades has often been linked in political and public rhetoric to negative effects on child development, including obesity. We analyse this association between maternal employment and childhood obesity using rich objective reports of various anthropometric and other measures of fatness from the IDEFICS study of children aged 2-9 in 16 regions of eight European countries. Based on such data as accelerometer measures and information from nutritional diaries, we also investigate the effects of maternal employment on obesity's main drivers: calorie intake and physical activity. Our analysis provides little evidence for any association between maternal employment and childhood obesity, diet or physical activity. Copyright © 2013 Elsevier B.V. All rights reserved.

  1. Up-regulation of Toll-like receptor 4/nuclear factor-kappaB signaling is associated with enhanced adipogenesis and insulin resistance in fetal skeletal muscle of obese sheep at late gestation.

    PubMed

    Yan, Xu; Zhu, Mei J; Xu, Wei; Tong, Jun F; Ford, Stephen P; Nathanielsz, Peter W; Du, Min

    2010-01-01

    Maternal obesity is increasing at an alarming rate. We previously showed that maternal obesity induces an inflammatory response and enhances adipogenesis in fetal skeletal muscle at midgestation. The objective of this study was to evaluate effects of maternal obesity on adipogenesis, inflammatory signaling, and insulin pathways at late gestation when ovine fetal skeletal muscle matures. Nonpregnant ewes were assigned to a control diet (Con, fed 100% of National Research Council nutrient recommendations, n = 6) or obesogenic diet (OB, fed 150% of National Research Council recommendations, n = 6) from 60 d before to 135 d after conception (term 148 d) when the fetal semitendenosus skeletal muscle was sampled. Expression of the adipogenic marker, peroxisome proliferator-activated receptor-gamma, was increased in OB compared with Con fetal semitendenosus muscle, indicating up-regulation of adipogenesis. More intramuscular adipocytes were observed in OB muscle. Phosphorylation of inhibitor-kappaB kinase-alpha/beta and nuclear factor-kappaB RelA/p65 were both increased in OB fetal muscle, indicating activation of nuclear factor-kappaB pathway. Phosphorylation of c-Jun N-terminal kinase and c-Jun (at Ser 63 and Ser 73) was also elevated. Toll-like receptor 4 expression was higher in OB than Con fetal muscle. Moreover, despite higher insulin concentrations in OB vs. Con fetal plasma (2.89 +/- 0.53 vs. 1.06 +/- 0.52 ng/ml; P < 0.05), phosphorylation of protein kinase B at Ser 473 was reduced, indicating insulin resistance. In conclusion, our data show maternal obesity-induced inflammatory signaling in late gestation fetal muscle, which correlates with increased im adipogenesis and insulin resistance, which may predispose offspring to later-life obesity and diabetes.

  2. Maternal obesity and neurodevelopmental and psychiatric disorders in offspring

    PubMed Central

    Edlow, Andrea G.

    2017-01-01

    There is a growing body of evidence from both human epidemiologic and animal studies that prenatal and lactational exposure to maternal obesity and high-fat diet are associated with neurodevelopmental and psychiatric disorders in offspring. These disorders include cognitive impairment, autism spectrum disorders, attention deficit hyperactivity disorder, cerebral palsy, anxiety and depression, schizophrenia, and eating disorders. This review synthesizes human and animal data linking maternal obesity and high-fat diet consumption to abnormal fetal brain development and neurodevelopmental and psychiatric morbidity in offspring. In addition, it highlights key mechanisms by which maternal obesity and maternal diet might impact fetal and offspring neurodevelopment, including neuroinflammation; increased oxidative stress, dysregulated insulin, glucose, and leptin signaling; dysregulated serotonergic and dopaminergic signaling; and perturbations in synaptic plasticity. Finally, the review summarizes available evidence regarding investigational therapeutic approaches to mitigate the harmful effects of maternal obesity on fetal and offspring neurodevelopment. PMID:27684946

  3. Influence of maternal obesity on the long-term health of offspring

    PubMed Central

    Godfrey, Keith M.; Reynolds, Rebecca M.; Prescott, Susan L.; Nyirenda, Moffat; Jaddoe, Vincent W.V.; Eriksson, Johan G.; Broekman, Birit F.P

    2017-01-01

    Alongside its immediate implications for pregnancy complications, increasing evidence implicates maternal obesity as a major determinant of health in the offspring during childhood and later adult life. Observational studies provide evidence for effects of maternal obesity on the offspring’s risks of obesity, coronary heart disease, stroke, type 2 diabetes and asthma. Maternal obesity may also lead to poorer cognitive performance in the offspring and an increased risk of neurodevelopmental disorders including cerebral palsy. Preliminary evidence suggests potential implications for immune and infectious disease related outcomes. Insights from experimental studies support causal effects of maternal obesity on offspring outcomes, mediated at least in part through changes in epigenetic processes including alternations in DNA methylation, and perhaps through alterations in the gut microbiome. Although the offspring of obese women who lose weight prior to pregnancy have a reduced risk of obesity, to date few controlled intervention studies have reversed maternal obesity and examined the consequences for the offspring. The long term effects of maternal obesity may have profound public health implications and indicate the urgency of studies on causality, underlying mechanisms and effective interventions to reverse the epidemic of obesity in women of child-bearing age and to mitigate its consequences for the offspring. PMID:27743978

  4. Maternal obesity and childhood wheezing and asthma.

    PubMed

    Rusconi, Franca; Popovic, Maja

    2017-03-01

    Obesity represents one of the major public health problems worldwide, with an increased prevalence also among women of reproductive age. Maternal pre-pregnancy overweight and obesity are important risk factors for a number of maternal and foetal/neonatal complications. The objective of this review is to provide an overview of the most recent evidence regarding the associations between pre-pregnancy overweight/obesity and wheezing and asthma in childhood. Potential mechanisms, mediators and confounding factors involved in these associations are also discussed. Despite the relatively large body of studies examining these associations and taking into account main confounders and potential mediators, the causal relationship between maternal obesity and wheezing and asthma in childhood is still uncertain. This uncertainty is not trivial, as any prevention strategy aimed at reducing the burden of these conditions would necessarily imply better understanding of the factors that are in the causal chain. Copyright © 2016. Published by Elsevier Ltd.

  5. Maternal prepregnancy obesity and child neurodevelopment in the Collaborative Perinatal Project.

    PubMed

    Huang, Lisu; Yu, Xiaodan; Keim, Sarah; Li, Ling; Zhang, Lin; Zhang, Jun

    2014-06-01

    To examine the association between maternal prepregnancy weight and child neurodevelopment, and the effect of gestational weight gain. Using the U.S. Collaborative Perinatal Project data, 1959-76, a total of 30,212 women with a calculable prepregnancy body mass index (BMI) and gestational weight gain, and term singleton children followed up for more than 7 years were included in this study. Intelligence quotient (IQ) was measured at 7 years of age by Wechsler Intelligence Scales. Maternal prepregnancy BMI displayed inverted U-shaped associations with child IQ after adjustment for maternal age, maternal education levels, maternal race, marital status, socioeconomic status, smoking during pregnancy, parity and study center. Women with BMI at around 20 kg/m2 appeared to have the highest offspring IQ scores. After controlling for familial factors in the siblings' sample, maternal obesity (BMI≥30.0 kg/m2) was associated with lower Full-scale IQ (adjusted ß=-2.0, 95% confidence interval -3.5 to -0.5), and Verbal scale IQ (adjusted ß=-2.5, 95% confidence interval -4.0 to -1.0), using BMI of 18.5-24.9 kg/m2 as the reference category. Compared with children born to normal-weight women who gained 21-25 lb. during pregnancy, those born to obese women who gained more than 40 lb. had 6.5 points deficit in IQ after adjustment for potential confounders. Maternal prepregnancy obesity was associated with lower child IQ, and excessive weight gain accelerated the association. With obesity rising steadily, these results appear to raise serious public health concerns. © The Author 2014; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.

  6. Adolescent obesity and maternal and paternal sensitivity and monitoring.

    PubMed

    Neal Davis, R; Ashba, Jacqueline; Appugliese, Danielle P; Kaciroti, Niko; Corwyn, Robert F; Bradley, Robert H; Lumeng, Julie C

    2011-06-01

    To determine if adolescent obesity is associated with parenting characterized by lower sensitivity and lower monitoring of adolescent activities. We used data from 744 adolescents in the National Institute of Child Health and Human Development Study of Early Child Care and Youth Development. Height and weight were measured at age 15½ years and obesity defined as body mass index ≥ 95th percentile for age and sex. Maternal and paternal sensitivity were assessed by direct observation of a parent-adolescent interaction task. Maternal and paternal monitoring were assessed by parent report. Lower sensitivity and lower monitoring were each defined as the lowest quartiles. Two separate multivariate logistic regression models were created to evaluate, individually for mothers and fathers, associations of sensitivity and monitoring with adolescent obesity, controlling for adolescent sex and race, family income-to-needs ratio, and parental obesity. Fourteen percent of the adolescents were obese. Lower sensitivity was associated with adolescent obesity in the maternal parenting model (adjusted odds ratio [AOR] 2.36, 95% confidence interval [CI] 1.44-3.86, n = 709), but not paternal parenting model (AOR = 0.79, 95% CI 0.38-1.63, n = 460). Neither maternal nor paternal monitoring was associated with adolescent obesity (AOR = 1.03, 95% CI 0.63-1.68; AOR = 1.07, 95% CI 0.52-2.22, respectively). Lower maternal sensitivity, measured by direct observation of parent-adolescent interactions, was associated with adolescent obesity. Efforts to prevent and treat childhood obesity, both at the practitioner level and the community level, may be enhanced by educating parents that their reactions to their children's behaviors may have consequences related to obesity.

  7. Adiponectin supplementation in pregnant mice prevents the adverse effects of maternal obesity on placental function and fetal growth.

    PubMed

    Aye, Irving L M H; Rosario, Fredrick J; Powell, Theresa L; Jansson, Thomas

    2015-10-13

    Mothers with obesity or gestational diabetes mellitus have low circulating levels of adiponectin (ADN) and frequently deliver large babies with increased fat mass, who are susceptible to perinatal complications and to development of metabolic syndrome later in life. It is currently unknown if the inverse correlation between maternal ADN and fetal growth reflects a cause-and-effect relationship. We tested the hypothesis that ADN supplementation in obese pregnant dams improves maternal insulin sensitivity, restores normal placental insulin/mechanistic target of rapamycin complex 1 (mTORC1) signaling and nutrient transport, and prevents fetal overgrowth. Compared with dams on a control diet, female C57BL/6J mice fed an obesogenic diet before mating and throughout gestation had increased fasting serum leptin, insulin, and C-peptide, and reduced high-molecular-weight ADN at embryonic day (E) 18.5. Placental insulin and mTORC1 signaling was activated, peroxisome proliferator-activated receptor-α (PPARα) phosphorylation was reduced, placental transport of glucose and amino acids in vivo was increased, and fetal weights were 29% higher in obese dams. Maternal ADN infusion in obese dams from E14.5 to E18.5 normalized maternal insulin sensitivity, placental insulin/mTORC1 and PPARα signaling, nutrient transport, and fetal growth without affecting maternal fat mass. Using a mouse model with striking similarities to obese pregnant women, we demonstrate that ADN functions as an endocrine link between maternal adipose tissue and fetal growth by regulating placental function. Importantly, maternal ADN supplementation reversed the adverse effects of maternal obesity on placental function and fetal growth. Improving maternal ADN levels may serve as an effective intervention strategy to prevent fetal overgrowth caused by maternal obesity.

  8. Maternal distress associates with placental genes regulating fetal glucocorticoid exposure and IGF2: Role of obesity and sex.

    PubMed

    Mina, Theresia H; Räikkönen, Katri; Riley, Simon C; Norman, Jane E; Reynolds, Rebecca M

    2015-09-01

    Maternal emotional distress symptoms, including life satisfaction, anxiety and depressed mood, are worse in Severely Obese (SO) than lean pregnancy and may alter placental genes regulating fetal glucocorticoid exposure and placental growth. We hypothesised that the associations between increased maternal distress symptoms and changes in placental gene expression including IGF2 and genes regulating fetal glucocorticoid exposure are more pronounced in SO pregnancy. We also considered whether there were sex-specific effects. Placental mRNA levels of 11β-HSDs, NR3C1-α, NR3C2, ABC transporters, mTOR and the IGF2 family were measured in term placental samples from 43 lean (BMI≤25kg/m(2)) and 50 SO (BMI≥40kg/m(2)) women, in whom distress symptoms were prospectively evaluated during pregnancy. The mRNA levels of genes with a similar role in regulating fetal glucocorticoid exposure were strongly inter-correlated. Increased maternal distress symptoms associated with increased NR3C2 and IGF2 isoform 1(IGF2-1) in both lean and SO group (p≤0.05). Increased distress was associated with higher ABCB1 and ABCG2 mRNA levels in SO but lower ABCB1 and higher 11β-HSD1 mRNA levels in lean (p≤0.05) suggesting a protective adaptive response in SO placentas. Increased maternal distress associated with reduced mRNA levels of ABCB1, ABCG2, 11β-HSD2, NR3C1-α and IGF2-1 in placentas of female but not male offspring. The observed sex differences in placental responses suggest greater vulnerability of female fetuses to maternal distress with potentially greater fetal glucocorticoid exposure and excess IGF2. Further studies are needed to replicate these findings and to test whether this translates to potentially greater negative outcomes of maternal distress in female offspring in early childhood. Copyright © 2015 Elsevier Ltd. All rights reserved.

  9. Depot- and sex-specific effects of maternal obesity in offspring's adipose tissue.

    PubMed

    Lecoutre, Simon; Deracinois, Barbara; Laborie, Christine; Eberlé, Delphine; Guinez, Céline; Panchenko, Polina E; Lesage, Jean; Vieau, Didier; Junien, Claudine; Gabory, Anne; Breton, Christophe

    2016-07-01

    According to the Developmental Origin of Health and Disease (DOHaD) concept, alterations of nutrient supply in the fetus or neonate result in long-term programming of individual body weight (BW) setpoint. In particular, maternal obesity, excessive nutrition, and accelerated growth in neonates have been shown to sensitize offspring to obesity. The white adipose tissue may represent a prime target of metabolic programming induced by maternal obesity. In order to unravel the underlying mechanisms, we have developed a rat model of maternal obesity using a high-fat (HF) diet (containing 60% lipids) before and during gestation and lactation. At birth, newborns from obese dams (called HF) were normotrophs. However, HF neonates exhibited a rapid weight gain during lactation, a key period of adipose tissue development in rodents. In males, increased BW at weaning (+30%) persists until 3months of age. Nine-month-old HF male offspring was normoglycemic but showed mild glucose intolerance, hyperinsulinemia, and hypercorticosteronemia. Despite no difference in BW and energy intake, HF adult male offspring was predisposed to fat accumulation showing increased visceral (gonadal and perirenal) depots weights and hyperleptinemia. However, only perirenal adipose tissue depot exhibited marked adipocyte hypertrophy and hyperplasia with elevated lipogenic (i.e. sterol-regulated element binding protein 1 (Srebp1), fatty acid synthase (Fas), and leptin) and diminished adipogenic (i.e. peroxisome proliferator-activated receptor gamma (Pparγ), 11β-hydroxysteroid dehydrogenase type 1 (11β-Hds1)) mRNA levels. By contrast, very few metabolic variations were observed in HF female offspring. Thus, maternal obesity and accelerated growth during lactation program offspring for higher adiposity via transcriptional alterations of visceral adipose tissue in a depot- and sex-specific manner. © 2016 Society for Endocrinology.

  10. Adiponectin supplementation in pregnant mice prevents the adverse effects of maternal obesity on placental function and fetal growth

    PubMed Central

    Aye, Irving L. M. H.; Rosario, Fredrick J.; Powell, Theresa L.; Jansson, Thomas

    2015-01-01

    Mothers with obesity or gestational diabetes mellitus have low circulating levels of adiponectin (ADN) and frequently deliver large babies with increased fat mass, who are susceptible to perinatal complications and to development of metabolic syndrome later in life. It is currently unknown if the inverse correlation between maternal ADN and fetal growth reflects a cause-and-effect relationship. We tested the hypothesis that ADN supplementation in obese pregnant dams improves maternal insulin sensitivity, restores normal placental insulin/mechanistic target of rapamycin complex 1 (mTORC1) signaling and nutrient transport, and prevents fetal overgrowth. Compared with dams on a control diet, female C57BL/6J mice fed an obesogenic diet before mating and throughout gestation had increased fasting serum leptin, insulin, and C-peptide, and reduced high-molecular-weight ADN at embryonic day (E) 18.5. Placental insulin and mTORC1 signaling was activated, peroxisome proliferator-activated receptor-α (PPARα) phosphorylation was reduced, placental transport of glucose and amino acids in vivo was increased, and fetal weights were 29% higher in obese dams. Maternal ADN infusion in obese dams from E14.5 to E18.5 normalized maternal insulin sensitivity, placental insulin/mTORC1 and PPARα signaling, nutrient transport, and fetal growth without affecting maternal fat mass. Using a mouse model with striking similarities to obese pregnant women, we demonstrate that ADN functions as an endocrine link between maternal adipose tissue and fetal growth by regulating placental function. Importantly, maternal ADN supplementation reversed the adverse effects of maternal obesity on placental function and fetal growth. Improving maternal ADN levels may serve as an effective intervention strategy to prevent fetal overgrowth caused by maternal obesity. PMID:26417088

  11. Association of Maternal Obesity with Child Cerebral Palsy or Death.

    PubMed

    McPherson, Jessica A; Smid, Marcela C; Smiley, Sarah; Stamilio, David M

    2017-05-01

    Objective  The primary aim of this study was to determine if there is an association between maternal obesity and cerebral palsy or death in children. Study Design  This is a retrospective cohort analysis of a randomized controlled clinical trial previously performed by the Maternal-Fetal Medicine Units Network. Women in the original trial were included if at high risk for preterm delivery. The present study included singletons enrolled in the original study with complete data. Obese and nonobese women were compared. A secondary analysis comparing class 3 obese or classes 1 to 2 obese women to nonobese women was performed. The primary outcome was a composite of cerebral palsy or perinatal death. Results  In this study, 1,261 nonobese, 339 obese, and 69 morbidly obese women were included. When adjusted for gestational age at delivery and magnesium exposure, there was no association between maternal obesity and child cerebral palsy or death. In the analysis using obesity severity categories, excess risk for adverse outcome appeared confined to the class 3 obese group. Conclusion  In women at high risk of delivering preterm, maternal obesity was not independently associated with child cerebral palsy or death. The association in unadjusted analysis appears to be mediated by preterm birth among obese patients. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

  12. Maternal obesity, environmental factors, cesarean delivery and breastfeeding as determinants of overweight and obesity in children: results from a cohort.

    PubMed

    Portela, Daniel S; Vieira, Tatiana O; Matos, Sheila Ma; de Oliveira, Nelson F; Vieira, Graciete O

    2015-04-15

    Overweight and obesity are a public health problem with a multifactorial aetiology. The objective of this study was to evaluate risk factors for overweight and obesity in children at 6 years of age, including type of delivery and breastfeeding. This study relates to a cohort of 672 mother-baby pairs who have been followed from birth up to 6 years of age. The sample included mothers and infants seen at all ten maternity units in a large Brazilian city. Genetic, socioeconomic, demographic variables and postnatal characteristics were analyzed. The outcome analyzed was overweight and/or obesity defined as a body mass index greater than or equal to +1 z-score. The sample was stratified by breastfeeding duration, and a descriptive analysis was performed using a hierarchical logistic regression. P-values of <0.05 were considered significant. Prevalence rates (PR) of overweight and obesity among the children were 15.6% and 12.9%, respectively. Among the subset of breastfed children, factors associated with the outcome were maternal overweight and/or obesity (PR 1.92; 95% confidence interval "95% CI" 1.15-3.24) and lower income (PR 0.50; 95% CI 0.29-0.85). Among children who had not been breastfed or had been breastfed for shorter periods (less than 12 months), predictors were mothers with lower levels of education (PR 0.39; 95% CI 0.19-0.78), working mothers (PR 1.83; 95% CI 1.05-3.21), caesarean delivery (PR 1.98; 95% CI 1.14 - 3.50) and maternal obesity (PR 3.05; 95% CI 1.81 - 5.25). Maternal obesity and caesarean delivery were strongly associated with childhood overweight and/or obesity. Lower family income and lower levels of education were identified as protective factors. Breastfeeding duration appeared to modify the association between overweight/obesity and the other predictors studied.

  13. Maternal obesity, caesarean delivery and caesarean delivery on maternal request: a cohort analysis from China.

    PubMed

    Zhou, Yubo; Blustein, Jan; Li, Hongtian; Ye, Rongwei; Zhu, Liping; Liu, Jianmeng

    2015-05-01

    To quantify the association between maternal obesity and caesarean delivery, particularly caesarean delivery on maternal request (CDMR), a fast-growing component of caesarean delivery in many nations. We followed 1,019,576 nulliparous women registered in the Perinatal Healthcare Surveillance System during 1993-2010. Maternal body mass index (BMI, kg/m(2) ), before pregnancy or during early pregnancy, was classified as underweight (<18.5), normal (18.5 to <23; reference), overweight (23 to <27.5), or obese (≥27.5), consistent with World Health Organization guidelines for Asian people. The association between maternal obesity and overall caesarean and its subtypes was modelled using log-binomial regression. During the 18-year period, 404,971 (39.7%) caesareans and 93,927 (9.2%) CDMRs were identified. Maternal obesity was positively associated with overall caesarean and CDMR. Adjusted risk ratios for overall caesarean in the four ascending BMI categories were 0.96 [95% confidence interval (CI) 0.94, 0.97], 1.00 (Reference), 1.16 [95% CI 1.14, 1.18], 1.39 [95% CI 1.43, 1.54], and for CDMR were 0.95 [95% CI 0.94, 0.96], 1.00 (Reference), 1.20 [95% CI 1.18, 1.22], 1.48 [95% CI 1.433, 1.54]. Positive associations were consistently found in women residing in southern and northern provinces and in subgroups stratified by year of delivery, urban or rural residence, maternal age, education, level of delivering hospital, and birthweight. In a large Chinese cohort study, maternal obesity was associated with an increased risk of caesarean delivery and its subtypes, including CDMR. Given the rising global prevalence of obesity, and in view of the growth of CDMR, it seems likely that caesarean births will increase, unless there are changes in obstetrical practice. © 2015 John Wiley & Sons Ltd.

  14. Exploring the contribution of maternal antibiotics and breastfeeding to development of the infant microbiome and pediatric obesity.

    PubMed

    Lemas, Dominick J; Yee, Shanique; Cacho, Nicole; Miller, Darci; Cardel, Michelle; Gurka, Matthew; Janicke, David; Shenkman, Elizabeth

    2016-12-01

    Pediatric obesity, a significant public health concern, has been associated with adult premature mortality and the development of type 2 diabetes and cardiovascular disease. Evidence has suggested that the gut microbiota is associated with pediatric obesity. Establishment of the infant gut microbiome is dependent on a dynamic maternal-infant microbiota exchange during early life. The objective of this review is to describe maternal factors such as feeding practices and antibiotic use that may influence the infant gut microbiome and risk for obesity. The complex components in human milk have many nutritional benefits to the infant; however, the microbiome in human milk may be an important factor to help regulate the infant's weight. We discuss maternal antibiotics and the effects on breast milk as critical exposures that alter the infant's gut microbiome and influence the risk of pediatric obesity. Copyright © 2016 Elsevier Ltd. All rights reserved.

  15. Maternal diagnosis of obesity and risk of cerebral palsy in the child.

    PubMed

    Crisham Janik, Mary D; Newman, Thomas B; Cheng, Yvonne W; Xing, Guibo; Gilbert, William M; Wu, Yvonne W

    2013-11-01

    To examine the association between maternal hospital diagnoses of obesity and risk of cerebral palsy (CP) in the child. For all California hospital births from 1991-2001, we linked infant and maternal hospitalization discharge abstracts to California Department of Developmental Services records of children receiving services for CP. We identified maternal hospital discharge diagnoses of obesity (International Classification of Diseases, 9th edition 646.1, 278.00, or 278.01) and morbid obesity (International Classification of Diseases, 9th edition 278.01), and performed logistic regression to explore the relationship between maternal obesity diagnoses and CP. Among 6.2 million births, 67 200 (1.1%) mothers were diagnosed with obesity, and 7878 (0.1%) with morbid obesity; 8798 (0.14%) children had CP. A maternal diagnosis of obesity (relative risk [RR] 1.30, 95% CI 1.09-1.55) or morbid obesity (RR 2.70, 95% CI 1.89-3.86) was associated with increased risk of CP. In multivariable analysis adjusting for maternal race, age, education, prenatal care, insurance status, and infant sex, both obesity (OR 1.27, 95% CI 1.06-1.52) and morbid obesity (OR 2.56, 95% CI 1.79-3.66) remained independently associated with CP. On stratified analyses, the association of obesity (RR 1.72, 95% CI 1.25-2.35) or morbid obesity (RR 3.79, 95% CI 2.35-6.10) with CP was only significant among women who were hospitalized prior to the birth admission. Adjusting for potential comorbidities and complications of obesity did not eliminate this association. Maternal obesity may confer an increased risk of CP in some cases. Further studies are needed to confirm this finding. Copyright © 2013 Mosby, Inc. All rights reserved.

  16. In utero exposure to prepregnancy maternal obesity and postweaning high-fat diet impair regulators of mitochondrial dynamics in rat placenta and offspring

    USDA-ARS?s Scientific Manuscript database

    The proportion of obese women who become pregnant continues to rise. Compelling evidence suggests the intrauterine environment is an important determinant of offspring health. Maternal obesity and unhealthy diets are shown to promote metabolic programming in the offspring. Mitochondria are matern...

  17. Impact of maternal obesity on very preterm infants.

    PubMed

    Khalak, Rubia; Rijhsinghani, Asha; McCallum, Sarah E

    2017-05-01

    Infants born at less than  34 weeks' gestational age are at higher risk for morbidity and mortality. Data are limited on the impact of maternal obesity on the very preterm infant. This study reviewed whether maternal obesity further increases the intensive care needs of very preterm infants of less than 34 weeks' gestation. Maternal and neonatal data for live-born singleton births of 23 0/7 to 33 6/7 weeks' gestation delivering in upstate New York were reviewed. BMI categorization followed the National Institutes of Health BMI classification that subdivides obesity into three ascending BMI groups. Records were obtained on 1,224 women, of whom 31.6% were classified with obesity. Despite similar mean gestational age (31 to 31.6 weeks, P = 0.57) and birth weight (1,488 to 1,569 g, P = 0.51) of the infants in the BMI categories, delivery room (DR) resuscitation was more common for infants of women with level III obesity (63.2%, P = 0.04) with a trend toward the continued need for assisted ventilation (54.7%, P = 0.06). Preterm infants of women with level III obesity were more likely to require DR resuscitation with a trend to continued need for ventilatory support beyond 6 hours of age. This could impact utilization of DR resources at delivering hospitals. © 2017 The Obesity Society.

  18. Obesity-induced down-regulation of the mitochondrial translocator protein (TSPO) impairs placental steroid production.

    PubMed

    Lassance, Luciana; Haghiac, Maricela; Minium, Judi; Catalano, Patrick; Hauguel-de Mouzon, Sylvie

    2015-01-01

    Low concentrations of estradiol and progesterone are hallmarks of adverse pregnancy outcomes as is maternal obesity. During pregnancy, placental cholesterol is the sole source of sex steroids. Cholesterol trafficking is the limiting step in sex steroid biosynthesis and is mainly mediated by the translocator protein (TSPO), present in the mitochondrial outer membrane. The objective of the study was to investigate the effects of maternal obesity in placental sex steroid biosynthesis and TSPO regulation. One hundred forty-four obese (body mass index 30-35 kg/m(2)) and 90 lean (body mass index 19-25 kg/m(2)) pregnant women (OP and LP, respectively) recruited at scheduled term cesarean delivery. Placenta and maternal blood were collected. This study was conducted at MetroHealth Medical Center (Cleveland, Ohio). Maternal metabolic components (fasting glucose, insulin, leptin, estradiol, progesterone, and total cholesterol) and placental weight were measured. Placenta (mitochondria and membranes separated) and cord blood cholesterol values were verified. The expression and regulation of TSPO and mitochondrial function were analyzed. Plasma estradiol and progesterone concentrations were significantly lower (P < .04) in OP as compared with LP women. Maternal and cord plasma cholesterol were not different between groups. Placental citrate synthase activity and mitochondrial DNA, markers of mitochondrial density, were unchanged, but the mitochondrial cholesterol concentrations were 40% lower in the placenta of OP. TSPO gene and protein expressions were decreased 2-fold in the placenta of OP. In vitro trophoblast activation of the innate immune pathways with lipopolysaccharide and long-chain saturated fatty acids reduced TSPO expression by 2- to 3-fold (P < .05). These data indicate that obesity in pregnancy impairs mitochondrial steroidogenic function through the negative regulation of mitochondrial TSPO.

  19. Emotion Regulation Strategies and Childhood Obesity in High Risk Preschoolers

    PubMed Central

    Power, Thomas G.; Olivera, Yadira A.; Hill, Rachael A.; Beck, Ashley D.; Hopwood, Veronica; Garcia, Karina Silva; Ramos, Guadalupe G.; Fisher, Jennifer Orlet; O’Connor, Teresia M.; Hughes, Sheryl O.

    2016-01-01

    The current study examined the relationships between the specific strategies that preschool children use to regulate their emotions and childhood weight status to see if emotion regulation strategies would predict childhood weight status over and above measures of eating self-regulation. 185 4- to 5-year-old Latino children were recruited through Head Start centers in a large city in the southeastern U.S. Children completed both a delay of gratification task (emotion regulation) and an eating in the absence of hunger task (eating regulation). Eating regulation also was assessed by maternal reports. Four emotion regulation strategies were examined in the delay of gratification task: shut out stimuli, prevent movement, distraction, and attention to reward. Hierarchical linear regressions predicting children’s weight status showed that both measures of eating regulation negatively predicted child obesity, and the use of prevent movement negatively predicted child obesity. Total wait time during the delay of gratification tasks was not a significant predictor. The current findings are consistent with studies showing that for preschool children, summary measures of emotion regulation (e.g., wait time) are not concurrently associated with child obesity. In contrast, the use of emotion regulation strategies was a significant predictor of lower child weight status. These findings help identify emotion regulation strategies that prevention programs can target for helping children regulate their emotions and decrease their obesity risk. PMID:27620645

  20. Maternal Obesity Is Associated with Alterations in the Gut Microbiome in Toddlers

    PubMed Central

    Galley, Jeffrey D.; Bailey, Michael; Kamp Dush, Claire; Schoppe-Sullivan, Sarah; Christian, Lisa M.

    2014-01-01

    Children born to obese mothers are at increased risk for obesity, but the mechanisms behind this association are not fully delineated. A novel possible pathway linking maternal and child weight is the transmission of obesogenic microbes from mother to child. The current study examined whether maternal obesity was associated with differences in the composition of the gut microbiome in children in early life. Fecal samples from children 18–27 months of age (n = 77) were analyzed by pyro-tag 16S sequencing. Significant effects of maternal obesity on the composition of the gut microbiome of offspring were observed among dyads of higher socioeconomic status (SES). In the higher SES group (n = 47), children of obese (BMI≥30) versus non-obese mothers clustered on a principle coordinate analysis (PCoA) and exhibited greater homogeneity in the composition of their gut microbiomes as well as greater alpha diversity as indicated by the Shannon Diversity Index, and measures of richness and evenness. Also in the higher SES group, children born to obese versus non-obese mothers had differences in abundances of Faecalibacterium spp., Eubacterium spp., Oscillibacter spp., and Blautia spp. Prior studies have linked some of these bacterial groups to differences in weight and diet. This study provides novel evidence that maternal obesity is associated with differences in the gut microbiome in children in early life, particularly among those of higher SES. Among obese adults, the relative contribution of genetic versus behavioral factors may differ based on SES. Consequently, the extent to which maternal obesity confers measureable changes to the gut microbiome of offspring may differ based on the etiology of maternal obesity. Continued research is needed to examine this question as well as the relevance of the observed differences in gut microbiome composition for weight trajectory over the life course. PMID:25409177

  1. Maternal obesity is associated with alterations in the gut microbiome in toddlers.

    PubMed

    Galley, Jeffrey D; Bailey, Michael; Kamp Dush, Claire; Schoppe-Sullivan, Sarah; Christian, Lisa M

    2014-01-01

    Children born to obese mothers are at increased risk for obesity, but the mechanisms behind this association are not fully delineated. A novel possible pathway linking maternal and child weight is the transmission of obesogenic microbes from mother to child. The current study examined whether maternal obesity was associated with differences in the composition of the gut microbiome in children in early life. Fecal samples from children 18-27 months of age (n = 77) were analyzed by pyro-tag 16S sequencing. Significant effects of maternal obesity on the composition of the gut microbiome of offspring were observed among dyads of higher socioeconomic status (SES). In the higher SES group (n = 47), children of obese (BMI≥30) versus non-obese mothers clustered on a principle coordinate analysis (PCoA) and exhibited greater homogeneity in the composition of their gut microbiomes as well as greater alpha diversity as indicated by the Shannon Diversity Index, and measures of richness and evenness. Also in the higher SES group, children born to obese versus non-obese mothers had differences in abundances of Faecalibacterium spp., Eubacterium spp., Oscillibacter spp., and Blautia spp. Prior studies have linked some of these bacterial groups to differences in weight and diet. This study provides novel evidence that maternal obesity is associated with differences in the gut microbiome in children in early life, particularly among those of higher SES. Among obese adults, the relative contribution of genetic versus behavioral factors may differ based on SES. Consequently, the extent to which maternal obesity confers measureable changes to the gut microbiome of offspring may differ based on the etiology of maternal obesity. Continued research is needed to examine this question as well as the relevance of the observed differences in gut microbiome composition for weight trajectory over the life course.

  2. Maternal pre-pregnancy obesity and gestational weight gain influence neonatal neurobehaviour.

    PubMed

    Aubuchon-Endsley, Nicki; Morales, Monique; Giudice, Christina; Bublitz, Margaret H; Lester, Barry M; Salisbury, Amy L; Stroud, Laura R

    2017-04-01

    Maternal weight before and during pregnancy is associated with offspring neurobehaviour in childhood. We investigated maternal weight prior to and during pregnancy in relation to neonatal neurobehaviour. We hypothesized that maternal obesity and excessive gestational weight gain would be associated with poor neonatal attention and affective functioning. Participants (n = 261) were recruited, weighed and interviewed during their third trimester of pregnancy. Pre-pregnancy weight was self-reported and validated for 210 participants, with robust agreement with medical chart review (r = 0.99). Neurobehaviour was measured with the NICU Network Neurobehavioural Scale (NNNS) administered on Days 2 and 32 postpartum. Maternal exclusion criteria included severe or persistent physical or mental health conditions (e.g. chronic disease or diagnoses of Bipolar Disorder or Psychotic Spectrum Disorders), excessive substance use, and social service/foster care involvement or difficulty understanding English. Infants were from singleton, full-term (37-42 weeks gestation) births with no major medical concerns. Outcome variables were summary scores on the NNNS (n = 75-86). For women obese prior to pregnancy, those gaining in excess of Institute of Medicine guidelines had infants with poorer regulation, lower arousal and higher lethargy. There were no main effects of maternal pre-pregnancy body mass index on neurobehaviour. Women gaining above Institute of Medicine recommendations had neonates with better quality of movement. Additional studies to replicate and extend results past the neonatal period are needed. Results could support underlying mechanisms explaining associations between maternal perinatal weight and offspring outcomes. These mechanisms may inform future prevention/intervention strategies. © 2016 Blackwell Publishing Ltd. © 2016 Blackwell Publishing Ltd.

  3. Maternal prepregnancy obesity is an independent risk factor for frequent wheezing in infants by age 14 months.

    PubMed

    Guerra, Stefano; Sartini, Claudio; Mendez, Michelle; Morales, Eva; Guxens, Mònica; Basterrechea, Mikel; Arranz, Leonor; Sunyer, Jordi

    2013-01-01

    Maternal prepregnancy obesity has been linked to the offspring's risk for subsequent asthma. We determined whether maternal obesity is associated with increased risk of wheezing phenotypes early in life. We used data on 1107 mother-child pairs from two birth cohorts from the INMA-INfancia y Medio Ambiente project. Maternal height was measured and prepregnancy weight self-reported at enrolment (on average at 13.7 ± 2 weeks of gestation). Maternal prepregnancy body mass index was categorised as underweight, normal, overweight and obese according to WHO recommendations. Information on child's wheezing was obtained through questionnaires up to the age of 14 (± 1) months. Wheezing was classified as infrequent (<4 reported wheezing episodes) or frequent (≥ 4 episodes). Weight and length of infants were measured by trained study staff at 14.6 (± 1) months of age and weight-for-length z-scores computed. Although maternal obesity did not increase the risk of the child to have any or infrequent wheezing, children of obese mothers were more likely to have frequent wheezing than children of normal-weight mothers (11.8% vs. 3.8%; P = 0.002). In fully adjusted multinomial logistic regression models, including infants' weight-for-length z-scores and other covariates, maternal prepregnancy obesity was associated with increased risk of frequent [adjusted relative risk (RR) 4.18, 95% confidence interval (CI) 1.55, 11.3] but not infrequent (RR 1.05 [95% CI 0.55, 2.01]) wheezing in their children. Maternal prepregnancy obesity is independently associated with an increased risk of frequent wheezing in the infant by the age of 14 months. These findings add evidence on the potential effects of in utero exposures on asthma-related phenotypes. © 2012 Blackwell Publishing Ltd.

  4. Decreased maternal hypothalamic-pituitary-adrenal axis activity in very severely obese pregnancy: Associations with birthweight and gestation at delivery.

    PubMed

    Stirrat, Laura I; O'Reilly, James R; Barr, Sarah M; Andrew, Ruth; Riley, Simon C; Howie, Alexander F; Bowman, Maria; Smith, Roger; Lewis, John G; Denison, Fiona C; Forbes, Shareen; Seckl, Jonathan R; Walker, Brian R; Norman, Jane E; Reynolds, Rebecca M

    2016-01-01

    The maternal hypothalamic-pituitary-adrenal-axis (HPAA) undergoes dramatic activation during pregnancy. Increased cortisol and corticotrophin-releasing-hormone (CRH) associate with low birthweight and preterm labor. In non-pregnant obesity, the HPAA is activated but circulating cortisol levels are normal or lower than in lean women. We hypothesized that maternal cortisol levels would be lower in obese pregnancy, and would associate with increased fetal size and length of gestation. Fasting serum cortisol was measured at 16, 28 and 36 weeks gestation and at 3-6 months postpartum in 276 severely obese and 135 lean women. In a subset of obese (n=20) and lean (n=20) we measured CRH, hormones that regulate bioavailable cortisol (corticosteroid-binding-globulin, estradiol, estriol, and progesterone). Urinary glucocorticoid metabolites were measured in pregnant (obese n=6, lean n=5) and non-pregnant (obese n=7, lean n=7) subjects. Maternal cortisol and HPAA hormones were lower in obese pregnancy. Total urinary glucocorticoid metabolites increased significantly in lean pregnancy, but not in obese. Lower maternal cortisol in obese tended to be associated with increased birthweight (r=-0.13, p=0.066). In obese, CRH at 28 weeks correlated inversely with gestational length (r=-0.49, p=0.04), and independently predicted gestational length after adjustment for confounding factors (mean decrease in CRH of -0.25 pmol/L (95% CI -0.45 to -0.043 pmol/L) per/day increase in gestation). In obese pregnancy, lower maternal cortisol without an increase in urinary glucocorticoid clearance may indicate a lesser activation of the HPAA than in lean pregnancy. This may offer a novel mechanism underlying increased birthweight and longer gestation in obese pregnancy. Copyright © 2015 Elsevier Ltd. All rights reserved.

  5. Maternal Obesity: Risks for Developmental Delays in Early Childhood.

    PubMed

    Duffany, Kathleen O'Connor; McVeigh, Katharine H; Kershaw, Trace S; Lipkind, Heather S; Ickovics, Jeannette R

    2016-02-01

    To assess the risk for neurodevelopmental delays for children of mothers who were obese (≥200 pounds) prior to pregnancy, and to characterize delays associated with maternal obesity among children referred to and found eligible to receive Early Intervention Program services. We conducted a retrospective cohort study (N = 541,816) using a population-based New York City data warehouse with linked birth and Early Intervention data. Risks for children suspected of a delay and 'significantly delayed', with two moderate or one severe delay, were calculated. Among the group of children eligible by delay for Early Intervention, analyses assessed risk for being identified with a moderate-to-severe delay across each of five functional domains as well as risks for multiple delays. Children of mothers who were obese were more likely to be suspected of a delay (adjusted RR 1.19 [CI 1.15-1.22]) and borderline association for 'significantly delayed' (adjusted RR 1.01 [CI 1.00-1.02). Among children eligible by delay, children of mothers who were obese evidenced an increased risk for moderate-to-severe cognitive (adjusted RR 1.04 [CI 1.02-1.07]) and physical (adjusted RR 1.04 [CI 1.01-1.08]) delays and for global developmental delay (adjusted RR 1.05 [CI 1.01-1.08]). Maternal obesity is associated with increased risk of developmental delay in offspring. Among children with moderate or severe delays, maternal obesity is associated with increased risk of cognitive and physical delays as well as with increased risk for global developmental delay. While causation remains uncertain, this adds to the growing body of research reporting an association between maternal obesity and neurodevelopmental delays in offspring.

  6. Voluntary exercise prevents colonic inflammation in high-fat diet-induced obese mice by up-regulating PPAR-γ activity

    DOE Office of Scientific and Technical Information (OSTI.GOV)

    Liu, Wei-Xin, E-mail: weixinliu@yahoo.com; Wang, Ting; Zhou, Feng

    Obesity is associated with increased colonic inflammation, which elevates the risk of colon cancer. Although exercise exerts anti-inflammatory actions in multiple chronic diseases associated with inflammation, it is unknown whether this strategy prevents colonic inflammation in obesity. We hypothesized that voluntary exercise would suppress colonic inflammation in high-fat diet (HFD)-induced obesity by modulation of peroxisome proliferator-activated receptor (PPAR)-γ. Male C57Bl/6J mice fed either a control diet (6.5% fat, CON) or a high-fat diet (24% fat, HFD) were divided into sedentary, voluntary exercise or voluntary exercise with PPAR-γ antagonist GW9662 (10 mg/kg/day). All interventions took place for 12 weeks. Compared with CON-sedentarymore » group, HFD-sedentary mice gained significantly more body weight and exhibited metabolic disorders. Molecular studies revealed that HFD-sedentary mice had increased expression of inflammatory mediators and activation of nuclear factor (NF)-κB in the colons, which were associated with decreased expression and activity of PPAR-γ. Voluntary exercise markedly attenuated body weight gain, improved metabolic disorders, and normalized the expression of inflammatory mediators and activation of NF-κB in the colons in HFD-mice while having no effects in CON-animals. Moreover, voluntary exercise significantly increased expression and activity of PPAR-γ in the colons in both HFD- and CON-animals. However, all of these beneficial effects induced by voluntary exercise were abolished by GW9662, which inhibited expression and activity of PPAR-γ. The results suggest that decreased PPAR-γ activity in the colon of HFD-induced obesity may facilitate the inflammatory response and colon carcinogenesis. Voluntary exercise prevents colonic inflammation in HFD-induced obesity by up-regulating PPAR-γ activity. - Highlights: • Obesity down-regulates PPAR-γ in the colon. • Down-regulated colonic PPAR-γ may facilitate inflammatory

  7. Intergenerational impact of maternal obesity and postnatal feeding practices on pediatric obesity

    PubMed Central

    Thompson, Amanda L.

    2014-01-01

    The postnatal feeding practices of obese and overweight mothers may place their children at particular risk for the development of obesity through shared biology and family environments. This paper reviews the feeding practices of obese mothers, describes potential mechanisms linking maternal feeding behaviors to child obesity risk, and highlights potential avenues for intervention. This review documents that supporting breastfeeding, improving the food choices of obese women, and encouraging the development of feeding styles that are responsive to hunger and satiety cues are important for improving the quality of the eating environment and preventing the intergenerational transmission of obesity. PMID:24147925

  8. Intergenerational impact of maternal obesity and postnatal feeding practices on pediatric obesity.

    PubMed

    Thompson, Amanda L

    2013-10-01

    The postnatal feeding practices of obese and overweight mothers may place their children at increased risk for the development of obesity through shared biology and family environments. This article reviews the feeding practices of obese mothers, describes the potential mechanisms linking maternal feeding behaviors to child obesity risk, and highlights the potential avenues of intervention. Strategies important for improving the quality of the eating environment and preventing the intergenerational transmission of obesity include supporting breastfeeding, improving the food choices of obese women, and encouraging the development of feeding styles that are responsive to hunger and satiety cues. © 2013 International Life Sciences Institute.

  9. Maternal obesity programs senescence signaling and glucose metabolism in osteo-progenitors from rat and human

    USDA-ARS?s Scientific Manuscript database

    Nutritional status during intrauterine and early postnatal life impacts the risk of chronic diseases, presumably via epigenetic mechanisms. However, evidence on the impact of gestational events on regulation of embryonic bone cell fate is sparse. We investigated the effects of maternal obesity on fe...

  10. Relationships between pediatric obesity and maternal emotional states and attitudes.

    PubMed

    Akay, Aynur Pekcanlar; Ozturk, Yesim; Avcil, Sibel Nur; Kavurma, Canem; Tufan, Evren

    2015-01-01

    The goal of this study was to investigate depression and anxiety levels of mothers whose child (7-11 years) and adolescent (12-18 years) offspring had obesity, as well as those mothers' attitudes toward their children and their family relationships. This is a cross-sectional, case-control study of 100 dyads. All mothers completed the Beck Depression Inventory, the State-Trait Anxiety Inventory, the Parental Attitude Research Instrument, and the Family Assessment Device. Maternal state anxiety in the group with obesity was significantly higher than controls (p = 0.03). As measured by Family Assessment Device, affective involvement (p = 0.05) and behavior control (p = 0.00) scores were significantly higher for those with obesity. Obesity and adolescence have independent effects on maternal state anxiety; affective involvement domain of family function is affected by both obesity and its interaction with adolescence, while behavior control domain is singularly affected by obesity. Our results may demonstrate that, for the mothers of children who have obesity, this condition may have an adverse effect on their lives and their family relationships. Pediatric obesity and developmental stage of offspring may have different effects on maternally reported psychometric variables. Cross-sectional design may hinder causal explanations. Further studies with longitudinal designs are needed. © The Author(s) 2015.

  11. Maternal depression and childhood obesity: a systematic review.

    PubMed

    Lampard, Amy M; Franckle, Rebecca L; Davison, Kirsten K

    2014-02-01

    Maternal depression is prevalent and has been associated with parenting practices that influence child weight. In this systematic review we aimed to examine the prospective association between maternal depression and child overweight. We searched four databases (PsycINFO, PubMed, Embase, and Academic Search Premier) to identify studies for inclusion. We included studies with a prospective design with at least one year follow-up, measuring maternal depression at any stage after childbirth, and examining child overweight or obesity status, body mass index z-score or percentile, or adiposity. Two authors extracted data independently and findings were qualitatively synthesized. We identified nine prospective studies for inclusion. Results were examined separately for episodic depression (depression at a single measurement occasion) and chronic depression (depression on multiple measurement occasions). Mixed results were observed for the relationship between episodic depression and indicators of child adiposity. Chronic depression, but not episodic depression, was associated with greater risk for child overweight. While chronic depression may be associated with child overweight, further research is needed. Research is also needed to determine whether maternal depression influences child weight outcomes in adolescence and to investigate elements of the family ecology that may moderate the effect of maternal depression on child overweight. Copyright © 2013 Elsevier Inc. All rights reserved.

  12. Does maternal psychopathology increase the risk of pre-schooler obesity? A systematic review.

    PubMed

    Benton, Pree M; Skouteris, Helen; Hayden, Melissa

    2015-04-01

    The preschool years may be a critical period for child obesity onset; however, literature examining obesity risk factors to date has largely focused on school-aged children. Several links have been made between maternal depression and childhood obesity risks; however, other types of maternal psychopathology have been widely neglected. The aim of the present review was to systematically identify articles that examined relationships between maternal psychopathology variables, including depressive and anxiety symptoms, self-esteem and body dissatisfaction, and risks for pre-schooler obesity, including weight outcomes, physical activity and sedentary behaviour levels, and nutrition/diet variables. Twenty articles meeting review criteria were identified. Results showed positive associations between maternal depressive symptoms and increased risks for pre-schooler obesity in the majority of studies. Results were inconsistent depending on the time at which depression was measured (i.e., antenatal, postnatal, in isolation or longitudinally). Anxiety and body dissatisfaction were only measured in single studies; however, both were linked to pre-schooler obesity risks; self-esteem was not measured by any studies. We concluded that maternal depressive symptoms are important to consider when assessing risks for obesity in preschool-aged children; however, more research is needed examining the impact of other facets of maternal psychopathology on obesity risk in pre-schoolers. Copyright © 2014 Elsevier Ltd. All rights reserved.

  13. Maternal Characteristics and Incidence of Overweight/Obesity in Children: A 13-Year Follow-up Study in an Eastern Mediterranean Population.

    PubMed

    Jalali-Farahani, Sara; Amiri, Parisa; Abbasi, Behnood; Karimi, Mehrdad; Cheraghi, Leila; Daneshpour, Maryam Sadat; Azizi, Fereidoun

    2017-05-01

    Objectives To investigate clustering of parental sociobehavioral factors and their relationship with the incidence of overweight and obesity in Iranian children. Methods Demographics, body weight, and certain medical characteristics of the parents of 2999 children were used to categorize parents by cluster; children's weights were assessed for each cluster. Specifically, survival analysis and Cox regression models were used to test the effect of parental clustering on the incidence of childhood overweight and obesity. Results Maternal metabolic syndrome, education level, age, body weight status, and paternal age had important roles in distinguishing clusters with low, moderate, and high risk. Crude incidence rates (per 10,000 person-years) of overweight and obesity were 416.8 (95% confidence interval (CI) 388.2-447.5) and 114.7 (95% CI 101.2-129.9), respectively. Children of parents with certain constellations of demographic and medical characteristics were 37.0 and 41.0% more likely to become overweight and obese, respectively. Conclusions for Practice The current study demonstrated the vital role of maternal characteristics in distinguishing familial clusters, which could be used to predict the incidence of overweight and obesity in children.

  14. Emotion regulation strategies and childhood obesity in high risk preschoolers.

    PubMed

    Power, Thomas G; Olivera, Yadira A; Hill, Rachael A; Beck, Ashley D; Hopwood, Veronica; Garcia, Karina Silva; Ramos, Guadalupe G; Fisher, Jennifer Orlet; O'Connor, Teresia M; Hughes, Sheryl O

    2016-12-01

    The current study examined the relationships between the specific strategies that preschool children use to regulate their emotions and childhood weight status to see if emotion regulation strategies would predict childhood weight status over and above measures of eating self-regulation. 185 4- to 5-year-old Latino children were recruited through Head Start centers in a large city in the southeastern U.S. Children completed both a delay of gratification task (emotion regulation) and an eating in the absence of hunger task (eating regulation). Eating regulation also was assessed by maternal reports. Four emotion regulation strategies were examined in the delay of gratification task: shut out stimuli, prevent movement, distraction, and attention to reward. Hierarchical linear regressions predicting children's weight status showed that both measures of eating regulation negatively predicted child obesity, and the use of prevent movement negatively predicted child obesity. Total wait time during the delay of gratification tasks was not a significant predictor. The current findings are consistent with studies showing that for preschool children, summary measures of emotion regulation (e.g., wait time) are not concurrently associated with child obesity. In contrast, the use of emotion regulation strategies was a significant predictor of lower child weight status. These findings help identify emotion regulation strategies that prevention programs can target for helping children regulate their emotions and decrease their obesity risk. Copyright © 2016 Elsevier Ltd. All rights reserved.

  15. Maternal obesity and high-fat diet program offspring metabolic syndrome.

    PubMed

    Desai, Mina; Jellyman, Juanita K; Han, Guang; Beall, Marie; Lane, Robert H; Ross, Michael G

    2014-09-01

    We determined the potential programming effects of maternal obesity and high-fat (HF) diet during pregnancy and/or lactation on offspring metabolic syndrome. A rat model of maternal obesity was created using an HF diet prior to and throughout pregnancy and lactation. At birth, pups were cross-fostered, thereby generating 4 paradigms of maternal diets during pregnancy/lactation: (1) control (Con) diet during pregnancy and lactation (Con/Con), (2) HF during pregnancy and lactation (HF/HF), (3) HF during pregnancy alone (HF/Con), and (4) HF during lactation alone (Con/HF). Maternal phenotype during pregnancy and the end of lactation evidenced markedly elevated body fat and plasma corticosterone levels in HF dams. In the offspring, the maternal HF diet during pregnancy alone programmed increased offspring adiposity, although with normal body weight, whereas the maternal HF diet during lactation increased both body weight and adiposity. Metabolic disturbances, particularly that of hyperglycemia, were apparent in all groups exposed to the maternal HF diet (during pregnancy and/or lactation), although differences were apparent in the manifestation of insulin resistant vs insulin-deficient phenotypes. Elevated systolic blood pressure was manifest in all groups, implying that exposure to an obese/HF environment is disadvantageous for offspring health, regardless of pregnancy or lactation periods. Nonetheless, the underlying mechanism may differ because offspring that experienced in utero HF exposure had increased corticosterone levels. Maternal obesity/HF diet has a marked impact on offspring body composition and the risk of metabolic syndrome was dependent on the period of exposure during pregnancy and/or lactation. Copyright © 2014 Mosby, Inc. All rights reserved.

  16. Identification and comparative analyses of myocardial miRNAs involved in the fetal response to maternal obesity.

    PubMed

    Maloyan, Alina; Muralimanoharan, Sribalasubashini; Huffman, Steven; Cox, Laura A; Nathanielsz, Peter W; Myatt, Leslie; Nijland, Mark J

    2013-10-01

    Human and animal studies show that suboptimal intrauterine environments lead to fetal programming, predisposing offspring to disease in later life. Maternal obesity has been shown to program offspring for cardiovascular disease (CVD), diabetes, and obesity. MicroRNAs (miRNAs) are small, noncoding RNA molecules that act as key regulators of numerous cellular processes. Compelling evidence links miRNAs to the control of cardiac development and etiology of cardiac pathology; however, little is known about their role in the fetal cardiac response to maternal obesity. Our aim was to sequence and profile the cardiac miRNAs that are dysregulated in the hearts of baboon fetuses born to high fat/high fructose-diet (HFD) fed mothers for comparison with fetal hearts from mothers eating a regular diet. Eighty miRNAs were differentially expressed. Of those, 55 miRNAs were upregulated and 25 downregulated with HFD. Twenty-two miRNAs were mapped to human; 14 of these miRNAs were previously reported to be dysregulated in experimental or human CVD. We used an Ingenuity Pathway Analysis to integrate miRNA profiling and bioinformatics predictions to determine miRNA-regulated processes and genes potentially involved in fetal programming. We found a correlation between miRNA expression and putative gene targets involved in developmental disorders and CVD. Cellular death, growth, and proliferation were the most affected cellular functions in response to maternal obesity. Thus, the current study reveals significant alterations in cardiac miRNA expression in the fetus of obese baboons. The epigenetic modifications caused by adverse prenatal environment may represent one of the mechanisms underlying fetal programming of CVD.

  17. The role of family and maternal factors in childhood obesity.

    PubMed

    Gibson, Lisa Y; Byrne, Susan M; Davis, Elizabeth A; Blair, Eve; Jacoby, Peter; Zubrick, Stephen R

    2007-06-04

    To investigate the relationship between a child's weight and a broad range of family and maternal factors. Cross-sectional data from a population-based prospective study, collected between January 2004 and December 2005, for 329 children aged 6-13 years (192 healthy weight, 97 overweight and 40 obese) and their mothers (n=265) recruited from a paediatric hospital endocrinology department and eight randomly selected primary schools in Perth, Western Australia. Height, weight and body mass index (BMI) of children and mothers; demographic information; maternal depression, anxiety, stress and self-esteem; general family functioning; parenting style; and negative life events. In a multilevel model, maternal BMI and family structure (single-parent v two-parent families) were the only significant predictors of child BMI z scores. Childhood obesity is not associated with adverse maternal or family characteristics such as maternal depression, negative life events, poor general family functioning or ineffective parenting style. However, having an overweight mother and a single-parent (single-mother) family increases the likelihood of a child being overweight or obese.

  18. Maternal Childhood Adversity, Prepregnancy Obesity, and Gestational Weight Gain.

    PubMed

    Ranchod, Yamini K; Headen, Irene E; Petito, Lucia C; Deardorff, Julianna K; Rehkopf, David H; Abrams, Barbara F

    2016-04-01

    Growing evidence suggests that exposure to childhood adversity may influence obesity across the life course. High maternal weight complicates pregnancy and increases the risk of child obesity. This study examined the association between maternal childhood adversity and pregnancy-related weight in a large U.S. Data on 6,199 pregnancies from 2,873 women followed from 1979 to 2012 by the National Longitudinal Survey of Youth 1979 were analyzed in 2014. Associations between three adversity exposures before age 18 years (history of physical abuse, alcohol problems, or mental illness in the household) and two maternal weight outcomes (prepregnancy obesity and excessive gestational weight gain) were modeled separately using survey-adjusted log-binomial models. After adjusting for race/ethnicity and early-life socioeconomic factors, childhood physical abuse was associated with a 60% increase in the risk of prepregnancy obesity (adjusted risk ratio=1.6, 95% CI=1.1, 2.2). Household alcohol abuse was associated with a 30% increase in prepregnancy obesity (adjusted risk ratio=1.3, 95% CI=1.0, 1.7), as was household mental illness (adjusted risk ratio=1.3, 95% CI=0.8, 1.9), but the mental illness exposure was not significant. Physical abuse and household alcohol abuse were associated with a significant 20% increase in the risk of excessive gestational weight gain; mental illness was not. Adversity in early life may affect maternal weight before and during pregnancy. Screening and treating women of reproductive age for childhood adversity and its negative effects could significantly reduce obesity-related health outcomes for women and their children. Copyright © 2016 American Journal of Preventive Medicine. Published by Elsevier Inc. All rights reserved.

  19. Higher Maternal Protectiveness Is Associated with Higher Odds of Child Overweight and Obesity: A Longitudinal Australian Study

    PubMed Central

    Hancock, Kirsten J.; Lawrence, David; Zubrick, Stephen R.

    2014-01-01

    In recent years there has been an increasing interest in overprotective parenting and the potential role it plays in child development. While some have argued that a trend towards increased parental fear and reduced opportunity for independent mobility may be linked to increasing rates of child overweight and obesity, there is limited empirical information available to support this claim. Using data from the Longitudinal Study of Australian Children, this study aimed to examine the longitudinal relationships between maternal protectiveness and child overweight and obesity. A cohort of 4–5 year old children was followed up at 6–7, 8–9 and 10–11 years of age (n  =  2596). Measures included a protective parenting scale administered when children were 6–7 and 8–9 years of age, child body mass index (BMI), family characteristics including household income, neighbourhood disadvantage, child's position amongst siblings, and maternal BMI, education, employment, mental health and age at first birth. International Obesity Taskforce age- and sex-specific BMI cut points were used to determine if children were in the normal, overweight or obese BMI range. There was no association between maternal protectiveness and the odds of children being overweight or obese at age 4–5, 6–7 or 8–9 years. However at age 10–11 years, a 1 standard deviation increase in maternal protectiveness was associated with a 13% increase in the odds of children being overweight or obese. The results provide evidence of a relationship between maternal protectiveness and child overweight and obesity, however further research is required to understand the mechanism(s) that links the two concepts. PMID:24955586

  20. Higher maternal protectiveness is associated with higher odds of child overweight and obesity: a longitudinal Australian study.

    PubMed

    Hancock, Kirsten J; Lawrence, David; Zubrick, Stephen R

    2014-01-01

    In recent years there has been an increasing interest in overprotective parenting and the potential role it plays in child development. While some have argued that a trend towards increased parental fear and reduced opportunity for independent mobility may be linked to increasing rates of child overweight and obesity, there is limited empirical information available to support this claim. Using data from the Longitudinal Study of Australian Children, this study aimed to examine the longitudinal relationships between maternal protectiveness and child overweight and obesity. A cohort of 4-5 year old children was followed up at 6-7, 8-9 and 10-11 years of age (n  =  2596). Measures included a protective parenting scale administered when children were 6-7 and 8-9 years of age, child body mass index (BMI), family characteristics including household income, neighbourhood disadvantage, child's position amongst siblings, and maternal BMI, education, employment, mental health and age at first birth. International Obesity Taskforce age- and sex-specific BMI cut points were used to determine if children were in the normal, overweight or obese BMI range. There was no association between maternal protectiveness and the odds of children being overweight or obese at age 4-5, 6-7 or 8-9 years. However at age 10-11 years, a 1 standard deviation increase in maternal protectiveness was associated with a 13% increase in the odds of children being overweight or obese. The results provide evidence of a relationship between maternal protectiveness and child overweight and obesity, however further research is required to understand the mechanism(s) that links the two concepts.

  1. Choline Supplementation Normalizes Fetal Adiposity and Reduces Lipogenic Gene Expression in a Mouse Model of Maternal Obesity

    PubMed Central

    Jack-Roberts, Chauntelle; Joselit, Yaelle; Nanobashvili, Khatia; Bretter, Rachel; Malysheva, Olga V.; Caudill, Marie A.; Saxena, Anjana; Axen, Kathleen; Gomaa, Ahmed

    2017-01-01

    Maternal obesity increases fetal adiposity which may adversely affect metabolic health of the offspring. Choline regulates lipid metabolism and thus may influence adiposity. This study investigates the effect of maternal choline supplementation on fetal adiposity in a mouse model of maternal obesity. C57BL/6J mice were fed either a high-fat (HF) diet or a control (NF) diet and received either 25 mM choline supplemented (CS) or control untreated (CO) drinking water for 6 weeks before timed-mating and throughout gestation. At embryonic day 17.5, HF feeding led to higher (p < 0.05) percent total body fat in fetuses from the HFCO group, while the choline supplemented HFCS group did not show significant difference versus the NFCO group. Similarly, HF feeding led to higher (p < 0.05) hepatic triglyceride accumulation in the HFCO but not the HFCS fetuses. mRNA levels of lipogenic genes such as Acc1, Fads1, and Elovl5, as well as the transcription factor Srebp1c that favors lipogenesis were downregulated (p < 0.05) by maternal choline supplementation in the HFCS group, which may serve as a mechanism to reduce fat accumulation in the fetal liver during maternal HF feeding. In summary, maternal choline supplementation improves indices of fetal adiposity in obese dams at late gestation. PMID:28820499

  2. Choline Supplementation Normalizes Fetal Adiposity and Reduces Lipogenic Gene Expression in a Mouse Model of Maternal Obesity.

    PubMed

    Jack-Roberts, Chauntelle; Joselit, Yaelle; Nanobashvili, Khatia; Bretter, Rachel; Malysheva, Olga V; Caudill, Marie A; Saxena, Anjana; Axen, Kathleen; Gomaa, Ahmed; Jiang, Xinyin

    2017-08-18

    Maternal obesity increases fetal adiposity which may adversely affect metabolic health of the offspring. Choline regulates lipid metabolism and thus may influence adiposity. This study investigates the effect of maternal choline supplementation on fetal adiposity in a mouse model of maternal obesity. C57BL/6J mice were fed either a high-fat (HF) diet or a control (NF) diet and received either 25 mM choline supplemented (CS) or control untreated (CO) drinking water for 6 weeks before timed-mating and throughout gestation. At embryonic day 17.5, HF feeding led to higher ( p < 0.05) percent total body fat in fetuses from the HFCO group, while the choline supplemented HFCS group did not show significant difference versus the NFCO group. Similarly, HF feeding led to higher ( p < 0.05) hepatic triglyceride accumulation in the HFCO but not the HFCS fetuses. mRNA levels of lipogenic genes such as Acc1 , Fads1 , and Elovl5 , as well as the transcription factor Srebp1c that favors lipogenesis were downregulated ( p < 0.05) by maternal choline supplementation in the HFCS group, which may serve as a mechanism to reduce fat accumulation in the fetal liver during maternal HF feeding. In summary, maternal choline supplementation improves indices of fetal adiposity in obese dams at late gestation.

  3. Maternal pre-pregnancy obesity and neuropsychological development in pre-school children: a prospective cohort study.

    PubMed

    Casas, Maribel; Forns, Joan; Martínez, David; Guxens, Mònica; Fernandez-Somoano, Ana; Ibarluzea, Jesus; Lertxundi, Nerea; Murcia, Mario; Rebagliato, Marisa; Tardon, Adonina; Sunyer, Jordi; Vrijheid, Martine

    2017-10-01

    BackgroundMaternal pre-pregnancy obesity may impair infant neuropsychological development, but it is unclear whether intrauterine or confounding factors drive this association.MethodsWe assessed whether maternal pre-pregnancy obesity was associated with neuropsychological development in 1,827 Spanish children. At 5 years, cognitive and psychomotor development was assessed using McCarthy Scales of Children's Abilities, attention deficit hyperactivity disorder (ADHD) symptoms using the Criteria of Diagnostic and Statistical Manual of Mental Disorders, and autism spectrum disorder symptoms using the Childhood Asperger Syndrome Test. Models were adjusted for sociodemographic factors and maternal intelligence quotient. We used paternal obesity as negative control exposure as it involves the same source of confounding than maternal obesity.ResultsThe percentage of obese mothers and fathers was 8% and 12%, respectively. In unadjusted models, children of obese mothers had lower scores than children of normal weight mothers in all McCarthy subscales. After adjustment, only the verbal subscale remained statistically significantly reduced (β: -2.8; 95% confidence interval: -5.3, -0.2). No associations were observed among obese fathers. Maternal and paternal obesity were associated with an increase in ADHD-related symptoms. Parental obesity was not associated with autism symptoms.ConclusionMaternal pre-pregnancy obesity was associated with a reduction in offspring verbal scores at pre-school age.

  4. Diet-induced changes in maternal gut microbiota and metabolomic profiles influence programming of offspring obesity risk in rats.

    PubMed

    Paul, Heather A; Bomhof, Marc R; Vogel, Hans J; Reimer, Raylene A

    2016-02-12

    Maternal obesity and overnutrition during pregnancy and lactation can program an increased risk of obesity in offspring. In this context, improving maternal metabolism may help reduce the intergenerational transmission of obesity. Here we show that, in Sprague-Dawley rats, selectively altering obese maternal gut microbial composition with prebiotic treatment reduces maternal energy intake, decreases gestational weight gain, and prevents increased adiposity in dams and their offspring. Maternal serum metabolomics analysis, along with satiety hormone and gut microbiota analysis, identified maternal metabolic signatures that could be implicated in programming offspring obesity risk and highlighted the potential influence of maternal gut microbiota on maternal and offspring metabolism. In particular, the metabolomic signature of insulin resistance in obese rats normalized when dams consumed the prebiotic. In summary, prebiotic intake during pregnancy and lactation improves maternal metabolism in diet-induced obese rats in a manner that attenuates the detrimental nutritional programming of offspring associated with maternal obesity. Overall, these findings contribute to our understanding of the maternal mechanisms influencing the developmental programming of offspring obesity and provide compelling pre-clinical evidence for a potential strategy to improve maternal and offspring metabolic outcomes in human pregnancy.

  5. Diet-induced changes in maternal gut microbiota and metabolomic profiles influence programming of offspring obesity risk in rats

    PubMed Central

    Paul, Heather A.; Bomhof, Marc R.; Vogel, Hans J.; Reimer, Raylene A.

    2016-01-01

    Maternal obesity and overnutrition during pregnancy and lactation can program an increased risk of obesity in offspring. In this context, improving maternal metabolism may help reduce the intergenerational transmission of obesity. Here we show that, in Sprague-Dawley rats, selectively altering obese maternal gut microbial composition with prebiotic treatment reduces maternal energy intake, decreases gestational weight gain, and prevents increased adiposity in dams and their offspring. Maternal serum metabolomics analysis, along with satiety hormone and gut microbiota analysis, identified maternal metabolic signatures that could be implicated in programming offspring obesity risk and highlighted the potential influence of maternal gut microbiota on maternal and offspring metabolism. In particular, the metabolomic signature of insulin resistance in obese rats normalized when dams consumed the prebiotic. In summary, prebiotic intake during pregnancy and lactation improves maternal metabolism in diet-induced obese rats in a manner that attenuates the detrimental nutritional programming of offspring associated with maternal obesity. Overall, these findings contribute to our understanding of the maternal mechanisms influencing the developmental programming of offspring obesity and provide compelling pre-clinical evidence for a potential strategy to improve maternal and offspring metabolic outcomes in human pregnancy. PMID:26868870

  6. Trajectories of maternal weight from before pregnancy through postpartum and associations with childhood obesity.

    PubMed

    Leonard, Stephanie A; Rasmussen, Kathleen M; King, Janet C; Abrams, Barbara

    2017-11-01

    Background: Prepregnancy body mass index [BMI (in kg/m 2 )], gestational weight gain, and postpartum weight retention may have distinct effects on the development of child obesity, but their combined effect is currently unknown. Objective: We described longitudinal trajectories of maternal weight from before pregnancy through the postpartum period and assessed the relations between maternal weight trajectories and offspring obesity in childhood. Design: We analyzed data from 4436 pairs of mothers and their children in the National Longitudinal Survey of Youth 1979 (1981-2014). We used latent-class growth modeling in addition to national recommendations for prepregnancy BMI, gestational weight gain, and postpartum weight retention to create maternal weight trajectory groups. We used modified Poisson regression models to assess the associations between maternal weight trajectory group and offspring obesity at 3 age periods (2-5, 6-11, and 12-19 y). Results: Our analysis using maternal weight trajectories based on either latent-class results or recommendations showed that the risk of child obesity was lowest in the lowest maternal weight trajectory group. The differences in obesity risk were largest after 5 y of age and persisted into adolescence. In the latent-class analysis, the highest-order maternal weight trajectory group consisted almost entirely of women who were obese before pregnancy and was associated with a >2-fold increase in the risk of offspring obesity at ages 6-11 y (adjusted RR: 2.39; 95% CI: 1.97, 2.89) and 12-19 y (adjusted RR: 2.74; 95% CI: 2.13, 3.52). In the analysis with maternal weight trajectory groups based on recommendations, the risk of child obesity was consistently highest for women who were overweight or obese at the beginning of pregnancy. Conclusion: These findings suggest that high maternal weight across the childbearing period increases the risk of obesity in offspring during childhood, but high prepregnancy BMI has a stronger

  7. Increased chemerin concentrations in fetuses of obese mothers and correlation with maternal insulin sensitivity.

    PubMed

    Barker, Gillian; Lim, Ratana; Rice, Gregory E; Lappas, Martha

    2012-11-01

    The aim of this study was to determine the effect of maternal obesity and gestational diabetes mellitus (GDM) on (i) the circulating concentrations of chemerin in cord and maternal plasma, and (ii) gene expression and release of chemerin from human placenta and adipose tissue. Chemerin concentrations were measured in maternal and cord plasma from 62 normal glucose tolerant women (NGT) and 69 women with GDM at the time of term elective Caesarean section. Placenta and adipose tissue expression and release of chemerin was measured from 22 NGT and 22 GDM women. There was no effect of maternal obesity or GDM on maternal chemerin concentrations. Chemerin concentrations were significantly higher in cord plasma from women with maternal obesity. Cord chemerin concentrations in NGT women negatively correlated with the concentrations of maternal insulin sensitivity. There was no effect of GDM on maternal and cord chemerin concentrations, and on the release of chemerin from placenta and adipose tissue. At the time of term Caesarean section, preexisting maternal obesity, and its associated insulin resistance, is associated with higher cord plasma chemerin concentrations.

  8. Early Maternal Employment and Childhood Obesity among Economically Disadvantaged Families in the USA

    ERIC Educational Resources Information Center

    Coley, Rebekah Levine; Lombardi, Caitlin McPherran

    2012-01-01

    Research indicates a link between maternal employment and children's risk of obesity, but little prior work has addressed maternal employment during children's infancy. This study examined the timing and intensity of early maternal employment and associations with children's later overweight and obesity in a sample of low-income families in…

  9. The renal consequences of maternal obesity in offspring are overwhelmed by postnatal high fat diet

    PubMed Central

    Glastras, Sarah J.; Chen, Hui; Tsang, Michael; Teh, Rachel; McGrath, Rachel T.; Zaky, Amgad; Chen, Jason; Wong, Muh Geot; Pollock, Carol A.; Saad, Sonia

    2017-01-01

    Aims/Hypothesis Developmental programming induced by maternal obesity influences the development of chronic disease in offspring. In the present study, we aimed to determine whether maternal obesity exaggerates obesity-related kidney disease. Methods Female C57BL/6 mice were fed high-fat diet (HFD) for six weeks prior to mating, during gestation and lactation. Male offspring were weaned to normal chow or HFD. At postnatal Week 8, HFD-fed offspring were administered one dose streptozotocin (STZ, 100 mg/kg i.p.) or vehicle control. Metabolic parameters and renal functional and structural changes were observed at postnatal Week 32. Results HFD-fed offspring had increased adiposity, glucose intolerance and hyperlipidaemia, associated with increased albuminuria and serum creatinine levels. Their kidneys displayed structural changes with increased levels of fibrotic, inflammatory and oxidative stress markers. STZ administration did not potentiate the renal effects of HFD. Though maternal obesity had a sustained effect on serum creatinine and oxidative stress markers in lean offspring, the renal consequences of maternal obesity were overwhelmed by the powerful effect of diet-induced obesity. Conclusion Maternal obesity portends significant risks for metabolic and renal health in adult offspring. However, diet-induced obesity is an overwhelming and potent stimulus for the development of CKD that is not potentiated by maternal obesity. PMID:28225809

  10. The renal consequences of maternal obesity in offspring are overwhelmed by postnatal high fat diet.

    PubMed

    Glastras, Sarah J; Chen, Hui; Tsang, Michael; Teh, Rachel; McGrath, Rachel T; Zaky, Amgad; Chen, Jason; Wong, Muh Geot; Pollock, Carol A; Saad, Sonia

    2017-01-01

    Developmental programming induced by maternal obesity influences the development of chronic disease in offspring. In the present study, we aimed to determine whether maternal obesity exaggerates obesity-related kidney disease. Female C57BL/6 mice were fed high-fat diet (HFD) for six weeks prior to mating, during gestation and lactation. Male offspring were weaned to normal chow or HFD. At postnatal Week 8, HFD-fed offspring were administered one dose streptozotocin (STZ, 100 mg/kg i.p.) or vehicle control. Metabolic parameters and renal functional and structural changes were observed at postnatal Week 32. HFD-fed offspring had increased adiposity, glucose intolerance and hyperlipidaemia, associated with increased albuminuria and serum creatinine levels. Their kidneys displayed structural changes with increased levels of fibrotic, inflammatory and oxidative stress markers. STZ administration did not potentiate the renal effects of HFD. Though maternal obesity had a sustained effect on serum creatinine and oxidative stress markers in lean offspring, the renal consequences of maternal obesity were overwhelmed by the powerful effect of diet-induced obesity. Maternal obesity portends significant risks for metabolic and renal health in adult offspring. However, diet-induced obesity is an overwhelming and potent stimulus for the development of CKD that is not potentiated by maternal obesity.

  11. Maternal Obesity and Developmental Programming of Metabolic Disorders in Offspring: Evidence from Animal Models

    PubMed Central

    Li, M.; Sloboda, D. M.; Vickers, M. H.

    2011-01-01

    The incidence of obesity and overweight has reached epidemic proportions in the developed world as well as in those countries transitioning to first world economies, and this represents a major global health problem. Concern is rising over the rapid increases in childhood obesity and metabolic disease that will translate into later adult obesity. Although an obesogenic nutritional environment and increasingly sedentary lifestyle contribute to our risk of developing obesity, a growing body of evidence links early life nutritional adversity to the development of long-term metabolic disorders. In particular, the increasing prevalence of maternal obesity and excess maternal weight gain has been associated with a heightened risk of obesity development in offspring in addition to an increased risk of pregnancy-related complications. The mechanisms that link maternal obesity to obesity in offspring and the level of gene-environment interactions are not well understood, but the early life environment may represent a critical window for which intervention strategies could be developed to curb the current obesity epidemic. This paper will discuss the various animal models of maternal overnutrition and their importance in our understanding of the mechanisms underlying altered obesity risk in offspring. PMID:21969822

  12. Childhood Health Consequences of Maternal Obesity during Pregnancy: A Narrative Review.

    PubMed

    Gaillard, Romy; Santos, Susana; Duijts, Liesbeth; Felix, Janine F

    2016-01-01

    Obesity is a major public health problem among women of reproductive age. In a narrative review, we examined the influence of maternal obesity during pregnancy on fetal outcomes and childhood adiposity, cardio-metabolic, respiratory and cognitive-related health outcomes. We discuss results from recent studies, the causality and potential underlying mechanisms of observed associations and challenges for future epidemiological studies. Evidence from observational studies strongly suggests that maternal pre-pregnancy obesity and excessive gestational weight gain are associated with increased risks of fetal pregnancy complications and adverse childhood cardio-metabolic, respiratory and cognitive-related health outcomes. It remains unclear whether these associations are due to intrauterine mechanisms or explained by confounding family-based sociodemographic, lifestyle and genetic factors. The underlying mechanisms have mainly been assessed in animal studies and small human studies, and are yet to be further explored in large human studies. Key Message: Maternal obesity is an important modifiable factor during pregnancy that is associated with a variety of adverse offspring health outcomes. Further studies are needed to explore the causality and underlying mechanisms of the observed associations. Ultimately, preventive strategies focused on reducing maternal obesity and excessive weight gain during pregnancy may reduce common diseases in future generations. © 2016 S. Karger AG, Basel.

  13. Obesity Disrupts Rhythmic Clock Gene Expression in Maternal Adipose Tissue during Rat Pregnancy.

    PubMed

    Crew, Rachael C; Mark, Peter J; Waddell, Brendan J

    2018-06-01

    Obesity during pregnancy causes numerous maternal and fetal health complications, but the underlying mechanisms remain unclear. Adipose tissue dysfunction in obesity has previously been linked to disruption of the intrinsic adipose clock gene network that is crucial for normal metabolic function. This adipose clock also undergoes major change as part of the maternal metabolic adaptation to pregnancy, but whether this is affected by maternal obesity is unknown. Consequently, in this study we tested the hypothesis that obesity disturbs rhythmic gene expression in maternal adipose tissue across pregnancy. A rat model of maternal obesity was established by cafeteria (CAF) feeding, and adipose expression of clock genes and associated nuclear receptors ( Ppars and Pgc1α) was measured across days 15-16 and 21-22 of gestation (term = 23 days). CAF feeding suppressed the mesor and/or amplitude of adipose tissue clock genes (most notably Bmal1, Per2, and Rev-erbα) relative to chow-fed controls (CON) across both days of gestation. On day 15, the CAF diet also induced adipose Pparα, Pparδ, and Pgc1α rhythmicity but repressed that of Pparγ, while expression of Pparα, Pparδ, and Pgc1α was reduced at select time points. CAF mothers were hyperleptinemic at both stages of gestation, and at day 21 this effect was time-of-day dependent. Fetal plasma leptin exhibited clear rhythmicity, albeit with low amplitude, but interestingly these levels were unaffected by CAF feeding. Our data show that maternal obesity disrupts rhythmic expression of clock and metabolic genes in maternal adipose tissue and leads to maternal but not fetal hyperleptinemia.

  14. Maternal pre-pregnancy obesity and childhood physical and cognitive development of children: a systematic review.

    PubMed

    Adane, A A; Mishra, G D; Tooth, L R

    2016-11-01

    Maternal obesity, usually associated with the adverse birth outcomes, has been a serious public health concern. Studies examining its effect on the physical and cognitive development of children have only recently emerged and the findings are inconsistent. This review aimed to systematically examine the role of maternal obesity on children's physical and cognitive development using the available evidence. The CINAHL, EMBASE, PSYCINFO, PUBMED and SCOPUS databases were searched. Studies addressing children's (⩽12 years) physical and cognitive development as outcome and maternal pre-pregnancy body mass index as an exposure were included. Data were extracted and evaluated for quality by two independent reviewers. A total of 17 articles were eligible for this systematic review; 10 of them were birth cohorts from the USA. Nine of the 14 studies supported an adverse association between maternal pre-pregnancy obesity and childhood cognitive development. A few studies also demonstrated a negative association between the maternal obesity and gross motor function in children (5 of 10), but not with fine motor function (none out of five studies). Whether the observed negative association between the maternal obesity and children's cognitive and gross motor abilities is casual or due to residual confounding effects is unclear. The current evidence is based on a limited number of studies with heterogeneous measurement scales and obesity definition. From the available evidence, it seems that exposure to maternal pre-pregnancy obesity in the intrauterine environment has a detrimental effect on children's cognitive development. However, evidence of the association between the maternal obesity and physical development of children is too scarce to offer a conclusion. More research work is required to delineate the intrauterine effect of the maternal obesity from the residual confounding effects.

  15. Maternal obesity and vitamin D sufficiency are associated with cord blood vitamin D insufficiency.

    PubMed

    Josefson, Jami L; Feinglass, Joseph; Rademaker, Alfred W; Metzger, Boyd E; Zeiss, Dinah M; Price, Heather E; Langman, Craig B

    2013-01-01

    An inverse relationship between total serum 25-hydroxyvitamin D (25-OH D) and increased adiposity has been established in children, adolescents, and adults. However, the relationship between neonatal adiposity and vitamin D status has not been reported. Both maternal obesity and vitamin D deficiency in pregnancy are common and are associated with adverse pregnancy outcomes. The aim of the study was to determine the relationship between vitamin D levels in mothers and newborns, as influenced by maternal obesity, and evaluate these associations with neonatal adiposity. Sixty-one maternal-neonatal pairs participated in this cross-sectional study at an academic medical center. Mothers had a prepregnancy body mass index that was normal or obese. Maternal and cord blood sera were assayed for 25-OH D, and neonatal body composition was measured by air displacement plethysmography. Mothers had similar and sufficient levels of 25-OH D when measured at 36-38 wk gestation, irrespective of body mass index category (normal weight, 46.05, vs. obese, 49.84 ng/ml; P = not significant). However, cord blood 25-OH D was higher in neonates of normal-weight mothers compared to neonates of obese mothers (27.45 vs. 20.81 ng/ml; P = 0.02). The variance in cord blood 25-OH D was explained by four factors: maternal 25-OH D level, the presence of maternal obesity, maternal age, and neonatal adiposity (r(2) = 0.66). Obese women transfer less 25-OH D to offspring than normal-weight women, despite similar serum levels. Cord blood 25-OH D levels directly correlate to neonatal percentage body fat. These novel findings underscore the evolving relationships between maternal obesity, vitamin D nutritional status, and adiposity in the neonatal period that may influence subsequent childhood and adulthood vitamin D-dependent processes.

  16. Lower levels of maternal capital in early life predict offspring obesity in adulthood.

    PubMed

    Gillette, Meghan T; Lohman, Brenda J; Neppl, Tricia K

    2017-05-01

    As of 2013, 65% of the world's population lived in countries where overweight/obesity kills more people than being underweight. Evolutionary perspectives provide a holistic understanding of both how and why obesity develops and its long-term implications. To test whether the maternal capital hypothesis, an evolutionary perspective, is viable for explaining the development of obesity in adulthood. Restricted-use data from the National Longitudinal Study of Adolescent Health (Add Health; n = 11 403) was analysed using logistic regressions. The sample included adolescents and their biological mothers. The odds of obesity in adulthood increased by 22% for every standard deviation increase in lack of maternal capital (Exp (B) = 1.22, p < .001). That is, individuals whose mothers were young, of an ethnic minority and had short breastfeeding durations were more likely to be obese in adulthood, even after controlling for other factors in infancy, adolescence and adulthood. The results showed that those whose mothers had lower capital were more prone to later life disease (specifically, obesity). The maternal capital perspective is useful for explaining how and why early life characteristics (including maternal resources) predict obesity in adulthood. Implications of the findings are discussed.

  17. Do Maternal Caregiver Perceptions of Childhood Obesity Risk Factors and Obesity Complications Predict Support for Prevention Initiatives Among African Americans?

    PubMed

    Alexander, Dayna S; Alfonso, Moya L; Cao, Chunhua; Wright, Alesha R

    2017-07-01

    Objectives African American maternal caregiver support for prevention of childhood obesity may be a factor in implementing, monitoring, and sustaining children's positive health behaviors. However, little is known about how perceptions of childhood obesity risk factors and health complications influence caregivers' support of childhood obesity prevention strategies. The objective of this study was to determine if childhood obesity risk factors and health complications were associated with maternal caregivers' support for prevention initiatives. Methods A convenience sample of maternal caregivers (N = 129, ages 22-65 years) completed the childhood obesity perceptions (COP) survey. A linear regression was conducted to determine whether perceptions about childhood obesity risk factors and subsequent health complications influenced caregivers' support for prevention strategies. Results Caregivers' perceptions of childhood obesity risk factors were moderate (M = 3.4; SD = 0.64), as were their perceptions of obesity-related health complications (M = 3.3; SD = 0.75); however, they perceived a high level of support for prevention strategies (M = 4.2; SD = 0.74). In the regression model, only health complications were significantly associated with caregiver support (β = 0.348; p < 0.004). Conclusions Childhood obesity prevention efforts should emphasize health complications by providing education and strategies that promote self-efficacy and outcome expectations among maternal caregivers.

  18. Maternal Pre-Gravid Obesity Changes Gene Expression Profiles Towards Greater Inflammation and Reduced Insulin Sensitivity in Umbilical Cord

    PubMed Central

    Thakali, Keshari M.; Saben, Jessica; Faske, Jennifer B.; Lindsey, Forrest; Gomez-Acevedo, Horacio; Lowery, Curtis L.; Badger, Thomas M.; Andres, Aline; Shankar, Kartik

    2014-01-01

    Background Maternal obesity is associated with unfavorable outcomes, which may be reflected in the as yet undiscovered gene expression profiles of the umbilical cord (UC). Methods UCs from 12 lean (pre-gravid BMI < 24.9) and 10 overweight/obese (OW/OB, pre-gravid BMI ≥25) women without gestational diabetes were collected for gene expression analysis using Human Primeview microarrays (Affymetrix). Metabolic parameters were assayed in mother’s plasma and cord blood. Results Although offspring birth weight and adiposity (at 2-wk) did not differ between groups, expression of 232 transcripts was affected in UC from OW/OB compared to those of lean mothers. GSEA analysis revealed an up-regulation of genes related to metabolism, stimulus and defense response and inhibitory to insulin signaling in the OW/OB group. We confirmed that EGR1, periostin, and FOSB mRNA expression was induced in UCs from OW/OB moms, while endothelin receptor B, KFL10, PEG3 and EGLN3 expression was decreased. Messenger RNA expression of EGR1, FOSB, MEST and SOCS1 were positively correlated (p<0.05) with mother’s first trimester body fat mass (%). Conclusions Our data suggest a positive association between maternal obesity and changes in UC gene expression profiles favoring inflammation and insulin resistance, potentially predisposing infants to develop metabolic dysfunction later on in life. PMID:24819376

  19. Effect of Maternal Obesity on Fetal Growth and Expression of Placental Fatty Acid Transporters.

    PubMed

    Ye, Kui; Li, Li; Zhang, Dan; Li, Yi; Wang, Hai Qing; Lai, Han Lin; Hu, Chuan Lai

    2017-12-15

    To explore the effects of maternal high-fat (HF) diet-induced obesity on fetal growth and the expression of placental nutrient transporters. Maternal obesity was established in rats by 8 weeks of pre-pregnancy fed HF diet, while rats in the control group were fed normal (CON) diet. Diet-induced obesity (DIO) rats and diet-induced obesity-resistant (DIR) rats were selected according to body weight gain over this period. After copulation, the CON rats were divided into two groups: switched to HF diet (CON-HF group) or maintained on the CON diet (CON-CON group). The DIO rats and DIR rats were maintained on the HF diet throughout pregnancy. Pregnant rats were euthanized at day 21 gestation, fetal and placental weights were recorded, and placental tissue was collected. Reverse transcription-polymerase chain reaction was used to determine mRNA expression of placental nutrient transporters. Protein expression was determined by Western blot. Average fetal weight of DIO dams was reduced by 6.9%, and the placentas of CON-HF and DIO dams were significantly heavier than the placentas of CON-CON and DIR dams at day 21 of gestation (p<0.05). The fetal/placental weight ratio of DIO dams was significantly reduced compared with the fetal/placental weight ratio of CON-CON dams (p<0.05). The mRNA expression of GLUT-1 and SNAT-2 were not significantly different between groups. The mRNA and protein expression levels of CD36, FATP-1, and FATP-4 in DIO dams were decreased significantly (p<0.05). Maternal obesity induced by a HF diet led to intrauterine growth retardation and down-regulated the expression of placental fatty acid transporters.

  20. Maternal immigrant status and high birth weight: implications for childhood obesity.

    PubMed

    El-Sayed, Abdulrahman M; Galea, Sandro

    2011-01-01

    Childhood obesity, a growing epidemic, is associated with greater risk of several chronic diseases in adulthood. Children of immigrant mothers are at higher risk for obesity than children of non-immigrant mothers. High birth weight is the most important neonatal predictor of childhood obesity in the general population. To understand the etiology of obesity in children of immigrant mothers, we assessed the relation between maternal immigrant status and risk for high birth weight. Data about all births in Michigan (N = 786,868) between 2000-2005 were collected. We used bivariate chi-square tests and multivariate logistic regression models to assess the relation between maternal immigrant status and risk for neonatal high birth weight. The prevalence of high birth weight among non-immigrant mothers was 10.6%; the prevalence among immigrant mothers was 8.0% (P < .01). In multivariate regression models adjusted for maternal age, education, marital status, parity, and tobacco use, children of immigrant mothers had lower odds (odds ratio = 0.69, 95% confidence interval = 0.67-0.70) of high birth weight compared to those of non-immigrant mothers. Although maternal immigrant status has been shown to be associated with greater childhood obesity, surprisingly, children of immigrant mothers have lower risk of high birth weight than children of non-immigrant mothers. This suggests that factors in early childhood, potentially cultural or behavioral factors, may play a disproportionately important role in the etiology of childhood obesity in children of immigrant vs non-immigrant mothers.

  1. Neuroendocrine Regulation of Maternal Behavior

    PubMed Central

    Bridges, Robert S.

    2015-01-01

    The expression of maternal behavior in mammals is regulated by the developmental and experiential events over a female’s lifetime. In this review the relationships between the endocrine and neural systems that play key roles in these developmental and experiential that affect both the establishment and maintenance of maternal care are presented. The involvement of the hormones estrogen, progesterone, and lactogens are discussed in the context of ligand, receptor, and gene activity in rodents and to a lesser extent in higher mammals. The roles of neuroendocrine factors, including oxytocin, vasopressin, classical neurotransmitters, and other neural gene products that regulate aspects of maternal care are set forth, and the interactions of hormones with central nervous system mediators of maternal behavior are discussed. The impact of prior developmental factors, including epigenetic events, and maternal experience on subsequent maternal care are assessed over the course of the female’s lifespan. It is proposed that common neuroendocrine mechanisms underlie the regulation of maternal care in mammals. PMID:25500107

  2. Maternal obesity and perinatal oxidative stress: the strength of the association.

    PubMed

    Negro, S; Boutsikou, T; Briana, D D; Tataranno, M L; Longini, M; Proietti, F; Bazzini, F; Dani, C; Malamitsi-Puchner, A; Buonocore, G; Perrone, S

    2017-01-01

    Maternal obesity is a chronic inflammatory state, which has been shown to induce increased levels of free fatty acids, reactive oxygen species and inflammatory cells. Recent evidence reveals increased levels of lipid peroxidation products in the plasma of obese women during pregnancy. The aim of this study was to test the hypothesis that maternal overweight or obesity is associated with increased oxidative stress (OS) in offspring. Two hundred and forty-five pregnant women and their newborns were prospectively enrolled. Mothers were divided in two groups: lean control - LC (n=175, Group I); overweight or obese (n=70, Group II) according to BMI ≥ 25 before pregnancy. Cord blood F2-isoprostanes (F2-IsoPs), as reliable markers of OS, were measured in all newborns. Lower 1 minute APGAR score and higher weight at discharge were found in Group II neonates, compared to those of Group I (p less than 0.05). Small for gestational age (SGA) newborns of both groups showed increased levels of F2-IsoPs than appropriate (AGA) or large (LGA) for gestational age (GA) (p less than 0.01). SGA newborns of Group II had higher F2-IsoPs levels compared to SGA of Group I (p less than 0.01), which were significantly correlated to maternal BMI at the end of pregnancy (r=0.451, p less than 0.01). Multivariate regression analysis corrected for confounding factors, showed that maternal overweight or obesity was significantly associated with high F2-IsoPs levels in SGA offspring (p less than 0.01). Maternal overweight or obesity is associated with increased OS in their SGA newborns. Data suggest the need of antioxidant protection for both mothers during pregnancy and infants soon after birth.

  3. Maternal gestational diabetes and childhood obesity at age 9-11: results of a multinational study.

    PubMed

    Zhao, Pei; Liu, Enqing; Qiao, Yijuan; Katzmarzyk, Peter T; Chaput, Jean-Philippe; Fogelholm, Mikael; Johnson, William D; Kuriyan, Rebecca; Kurpad, Anura; Lambert, Estelle V; Maher, Carol; Maia, José A R; Matsudo, Victor; Olds, Timothy; Onywera, Vincent; Sarmiento, Olga L; Standage, Martyn; Tremblay, Mark S; Tudor-Locke, Catrine; Hu, Gang

    2016-11-01

    The aim of this study was to examine the association between maternal gestational diabetes mellitus (GDM) and childhood obesity at age 9-11 years in 12 countries around the world. A multinational cross-sectional study of 4740 children aged 9-11 years was conducted. Maternal GDM was diagnosed according to the ADA or WHO criteria. Height and waist circumference were measured using standardised methods. Weight and body fat were measured using a portable Tanita SC-240 Body Composition Analyzer. Multilevel modelling was used to account for the nested nature of the data. The prevalence of reported maternal GDM was 4.3%. The overall prevalence of childhood obesity, central obesity and high body fat were 12.3%, 9.9% and 8.1%, respectively. The multivariable-adjusted (maternal age at delivery, education, infant feeding mode, gestational age, number of younger siblings, child unhealthy diet pattern scores, moderate-to-vigorous physical activity, sleeping time, sedentary time, sex and birthweight) odds ratios among children of GDM mothers compared with children of non-GDM mothers were 1.53 (95% CI 1.03, 2.27) for obesity, 1.73 (95% CI 1.14, 2.62) for central obesity and 1.42 (95% CI 0.90, 2.26) for high body fat. The positive association was still statistically significant for central obesity after additional adjustment for current maternal BMI but was no longer significant for obesity and high body fat. Maternal GDM was associated with increased odds of childhood obesity at 9-11 years old but this association was not fully independent of maternal BMI.

  4. Prenatal exposure to very severe maternal obesity is associated with adverse neuropsychiatric outcomes in children.

    PubMed

    Mina, T H; Lahti, M; Drake, A J; Räikkönen, K; Minnis, H; Denison, F C; Norman, J E; Reynolds, R M

    2017-01-01

    Prenatal maternal obesity has been linked to adverse childhood neuropsychiatric outcomes, including increased symptoms of attention deficit hyperactivity disorder (ADHD), internalizing and externalizing problems, affective disorders and neurodevelopmental problems but few studies have studied neuropsychiatric outcomes among offspring born to very severely obese women or assessed potential familial confounding by maternal psychological distress. We evaluated neuropsychiatric symptoms in 112 children aged 3-5 years whose mothers had participated in a longitudinal study of obesity in pregnancy (50 very severe obesity, BMI ⩾40 kg/m2, obese class III and 62 lean, BMI 18.5-25 kg/m2). The mothers completed the Conners' Hyperactivity Scale, Early Symptomatic Syndrome Eliciting Neurodevelopmental Clinical Examination Questionnaire (ESSENCE-Q), Child's Sleep Habits Questionnaire (CSHQ), Strengths and Difficulties Questionnaire (SDQ), and Child Behavior Checklist (CBCL) to assess child neuropsychiatric symptoms. Covariates included child's sex, age, birthweight, gestational age, socioeconomic deprivation levels, maternal age, parity, smoking status during pregnancy, gestational diabetes and maternal concurrent symptoms of anxiety and depression assessed using State Anxiety of Spielberger State-Trait Anxiety Index (STAI) and General Health Questionnaire (GHQ), respectively. Children exposed to prenatal maternal very severe obesity had significantly higher scores in the Conners' Hyperactivity Scale; ESSENCE-Q; total sleep problems in CSHQ; hyperactivity, conduct problems and total difficulties scales of the SDQ; higher externalizing and total problems, anxious/depressed, aggressive behaviour and other problem syndrome scores and higher DSM-oriented affective, anxiety and ADHD problems in CBCL. Prenatal maternal very severe obesity remained a significant predictor of child neuropsychiatric problems across multiple scales independent of demographic factors, prenatal factors and

  5. Neuroendocrine regulation of maternal behavior.

    PubMed

    Bridges, Robert S

    2015-01-01

    The expression of maternal behavior in mammals is regulated by the developmental and experiential events over a female's lifetime. In this review the relationships between the endocrine and neural systems that play key roles in these developmental and experiential processes that affect both the establishment and maintenance of maternal care are presented. The involvement of the hormones estrogen, progesterone, and lactogens are discussed in the context of ligand, receptor, and gene activity in rodents and to a lesser extent in higher mammals. The roles of neuroendocrine factors, including oxytocin, vasopressin, classical neurotransmitters, and other neural gene products that regulate aspects of maternal care are set forth, and the interactions of hormones with central nervous system mediators of maternal behavior are discussed. The impact of prior developmental factors, including epigenetic events, and maternal experience on subsequent maternal care are assessed over the course of the female's lifespan. It is proposed that common neuroendocrine mechanisms underlie the regulation of maternal care in mammals. Copyright © 2014 Elsevier Inc. All rights reserved.

  6. Maternal inheritance of BDNF deletion, with phenotype of obesity and developmental delay in mother and child.

    PubMed

    Harcourt, Brooke E; Bullen, Denise V R; Kao, Kung-Ting; Tassoni, Daniella; Alexander, Erin J; Burgess, Trent; White, Susan M; Sabin, Matthew A

    2018-01-01

    Childhood obesity is a significant world health problem. Understanding the genetic and environmental factors contributing to the development of obesity in childhood is important for the rational design of strategies for obesity prevention and treatment. Brain-derived neurotrophic factor (BDNF) plays an important role in the growth and development of the central nervous system, there is also an evidence that BDNF plays a role in regulation of appetite. Disruption of the expression of this gene in a child has been previously reported to result in a phenotype of severe obesity, hyperphagia, impaired cognitive function, and hyperactivity. We report a mother and child, both with micro-deletions encompassing the BDNF gene locus, who both have obesity and developmental delay, although without hyperactivity. This report highlights the maternal inheritance of a rare genetic cause of childhood obesity. © 2017 Wiley Periodicals, Inc.

  7. Maternal depression and socio-economic status moderate the parenting style/child obesity association.

    PubMed

    Topham, Glade L; Page, Melanie C; Hubbs-Tait, Laura; Rutledge, Julie M; Kennedy, Tay S; Shriver, Lenka; Harrist, Amanda W

    2010-08-01

    The purpose of the study was to test the moderating influence of two risk factors, maternal depression and socio-economic status (SES), on the association between authoritarian and permissive parenting styles and child obesity. Correlational, cross-sectional study. Parenting style was measured with the Parenting Styles and Dimensions Questionnaire (PSDQ). Maternal depression was measured using the Center for Epidemiologic Studies Depression Scale (CES-D). BMI-for-age percentile was used to categorize children by weight status (children with BMI-for-age > or = 95th percentile were classified as obese). SES was computed from parent education and occupational status using the four-factor Hollingshead index. Rural public schools in a mid-western state in the USA. One hundred and seventy-six mothers of first-grade children (ninety-one boys, eighty-five girls) enrolled in rural public schools. Both maternal depression and SES were found to moderate the permissive parenting style/child obesity association, but not the authoritarian/child obesity association. For depressed mothers, but not for non-depressed mothers, more permissive parenting was predictive of child obesity. Similarly more permissive parenting was predictive of child obesity among higher SES mothers, but not for lower SES mothers. Maternal depression and SES interact with permissive parenting style to predict child obesity. Future research should examine the relationship among these variables using a longitudinal design.

  8. Maternal obesity and rate of cesarean delivery in Djibouti.

    PubMed

    Minsart, Anne-Frederique; N'guyen, Thai-Son; Dimtsu, Hirut; Ratsimanresy, Rachel; Dada, Fouad; Ali Hadji, Rachid

    2014-11-01

    To calculate the prevalence of maternal obesity and to determine the relation between obesity and cesarean delivery in an urban hospital in Djibouti. In an observational cohort study, all women who had a live birth or stillbirth between October 2012 and November 2013 were considered for inclusion. Body mass index (BMI, calculated as weight in kilograms divided by the square of height in meters) was calculated throughout pregnancy, and women with a BMI of at least 30.0 were deemed to be obese. Multivariate logistic regression analyses were used to evaluate the relation between cesarean and obesity. Overall, 100 (24.8%) of 404 women were obese before 14 weeks of pregnancy, as were 112 (25.2%) of 445 before 22 weeks, and 200 (43.2%) of 463 at delivery. Obesity before 22 weeks was associated with a 127% excess risk of cesarean delivery (adjusted odds ratio 2.27; 95% CI 1.07-4.82; P=0.032). Similar trends were found when the analyses were limited to the subgroup of women without a previous cesarean delivery or primiparae. Prevalence of maternal obesity is high in Djibouti City and is related to an excess risk of cesarean delivery, even after controlling for a range of medical and socioeconomic variables. Copyright © 2014 International Federation of Gynecology and Obstetrics. Published by Elsevier Ireland Ltd. All rights reserved.

  9. A review of national health policies and professional guidelines on maternal obesity and weight gain in pregnancy.

    PubMed

    Schumann, N L; Brinsden, H; Lobstein, T

    2014-08-01

    Maternal obesity creates an additional demand for health-care services, as the routine obstetric care pathway requires alterations to ensure the most optimal care for obese women of childbearing age. This review examines the extent to which relevant national health documents reflect and respond to the health implications of maternal obesity and excessive gestational weight gain. A targeted search of peer-reviewed publications and grey literature was conducted for each country to identify national health documents, which were subsequently content analyzed according to an adapted framework. A total of 37 documents were identified, including one policy, 10 strategies and 26 guidelines, published within the last 10 years. Out of the 31 countries investigated, only 13 countries address maternal obesity while none address excessive gestational weight gain. We found inconsistencies and gaps in the recommendations to health-care service providers for the management of maternal obesity and weight gain in pregnancy. The findings show that only limited guidance on maternal obesity and gestational weight gain exists. The authors recommend that international, evidence-based guidelines on the management of maternal obesity and excessive gestational weight gain should be developed to reduce the associated health-care and economic costs. © 2014 The Authors. Clinical Obesity © 2014 World Obesity.

  10. Association between Maternal Obesity and Autism Spectrum Disorder in Offspring: A Meta-Analysis

    ERIC Educational Resources Information Center

    Li, Ya-Min; Ou, Jian-Jun; Liu, Li; Zhang, Dan; Zhao, Jing-Ping; Tang, Si-Yuan

    2016-01-01

    As the link between maternal obesity and risk of autism among offspring is unclear, the present study assessed this association. A systematic search of an electronic database was performed to identify observational studies that examined the association between maternal obesity and autism. The outcome measures were odds ratios comparing offspring…

  11. Evaluation of the Association between Maternal Smoking, Childhood Obesity, and Metabolic Disorders: A National Toxicology Program Workshop Review

    PubMed Central

    Behl, Mamta; Rao, Deepa; Aagaard, Kjersti; Davidson, Terry L.; Levin, Edward D.; Slotkin, Theodore A.; Srinivasan, Supriya; Wallinga, David; White, Morris F.; Walker, Vickie R.; Thayer, Kristina A.

    2012-01-01

    Background: An emerging literature suggests that environmental chemicals may play a role in the development of childhood obesity and metabolic disorders, especially when exposure occurs early in life. Objective: Here we assess the association between these health outcomes and exposure to maternal smoking during pregnancy as part of a broader effort to develop a research agenda to better understand the role of environmental chemicals as potential risk factors for obesity and metabolic disorders. Methods: PubMed was searched up to 8 March 2012 for epidemiological and experimental animal studies related to maternal smoking or nicotine exposure during pregnancy and childhood obesity or metabolic disorders at any age. A total of 101 studies—83 in humans and 18 in animals—were identified as the primary literature. Discussion: Current epidemiological data support a positive association between maternal smoking and increased risk of obesity or overweight in offspring. The data strongly suggest a causal relation, although the possibility that the association is attributable to unmeasured residual confounding cannot be completely ruled out. This conclusion is supported by findings from laboratory animals exposed to nicotine during development. The existing literature on human exposures does not support an association between maternal smoking during pregnancy and type 1 diabetes in offspring. Too few human studies have assessed outcomes related to type 2 diabetes or metabolic syndrome to reach conclusions based on patterns of findings. There may be a number of mechanistic pathways important for the development of aberrant metabolic outcomes following perinatal exposure to cigarette smoke, which remain largely unexplored. Conclusions: From a toxicological perspective, the linkages between maternal smoking during pregnancy and childhood overweight/obesity provide proof-of-concept of how early-life exposure to an environmental toxicant can be a risk factor for childhood

  12. What is common becomes normal: the effect of obesity prevalence on maternal perception.

    PubMed

    Binkin, N; Spinelli, A; Baglio, G; Lamberti, A

    2013-05-01

    This analysis investigates the poorly-known effect of local prevalence of childhood obesity on mothers' perception of their children's weight status. In 2008, a national nutritional survey of children attending the third grade of elementary school was conducted in Italy. Children were measured and classified as underweight, normal weight, overweight and obese, using the International Obesity Task Force cut-offs for body mass index (BMI). A parental questionnaire included parental perception of their child's weight status (underweight, normal, a little overweight and a lot overweight). Regions were classified by childhood obesity prevalence (<8%, 8-12%, ≥13%). The association between incorrect maternal perception and regional obesity prevalence, and maternal and child characteristics were examined using bivariate and logistic regression analyses. Complete data were available for 37 590 children, of whom 24% were overweight and 12% obese. Mothers correctly identified the status of 84% of normal weight, 52% of overweight and 14% of obese children. Among overweight children, factors associated with underestimation of the child's weight included lower maternal education (adjusted odds ratio, aOR, 1.9; 95% confidence interval (CI) 1.6-2.4), residence in a high-obesity region (aOR 2.2; 95% CI 1.9-2.6), male gender (aOR 1.4; 95% CI 1.2-1.6) and child's BMI. Higher regional obesity prevalence is associated with lower maternal perception, suggesting that what is common has a greater likelihood of being perceived as normal. As perception is a first step to change, it may be harder to intervene in areas with high-obesity prevalence where intervention is most urgent. Copyright © 2011 Elsevier B.V. All rights reserved.

  13. Maternal obesity and gestational weight gain are modestly associated with umbilical cord DNA methylation

    USDA-ARS?s Scientific Manuscript database

    Maternal obesity (OB) and excessive gestational weight gain (GWG) are strong independent contributors that augment obesity risk in offspring. However, direct evidence of epigenetic changes associated with maternal habitus remains sparse. We utilized Bisulfite Amplicon Sequencing (BSAS) to conduct t...

  14. The impact of maternal obesity on inflammatory processes and consequences for later offspring health outcomes.

    PubMed

    Segovia, S A; Vickers, M H; Reynolds, C M

    2017-10-01

    Obesity is a global epidemic, affecting both developed and developing countries. The related metabolic consequences that arise from being overweight or obese are a paramount global health concern, and represent a significant burden on healthcare systems. Furthermore, being overweight or obese during pregnancy increases the risk of offspring developing obesity and other related metabolic complications in later life, which can therefore perpetuate a transgenerational cycle of obesity. Obesity is associated with a chronic state of low-grade metabolic inflammation. However, the role of maternal obesity-mediated alterations in inflammatory processes as a mechanism underpinning developmental programming in offspring is less understood. Further, the use of anti-inflammatory agents as an intervention strategy to ameliorate or reverse the impact of adverse developmental programming in the setting of maternal obesity has not been well studied. This review will discuss the impact of maternal obesity on key inflammatory pathways, impact on pregnancy and offspring outcomes, potential mechanisms and avenues for intervention.

  15. Maternal pre-pregnancy overweight and obesity, and child neuropsychological development: two Southern European birth cohort studies.

    PubMed

    Casas, Maribel; Chatzi, Leda; Carsin, Anne-Elie; Amiano, Pilar; Guxens, Mònica; Kogevinas, Manolis; Koutra, Katerina; Lertxundi, Nerea; Murcia, Mario; Rebagliato, Marisa; Riaño, Isolina; Rodríguez-Bernal, Clara L; Roumeliotaki, Theano; Sunyer, Jordi; Mendez, Michelle; Vrijheid, Martine

    2013-04-01

    Maternal pre-pregnancy obesity may be associated with impaired infant neuropsychological development; however, there are few studies and it is unclear if reported associations are due to intrauterine mechanisms. We assessed whether maternal pre-pregnancy overweight and obesity were associated with cognitive and psychomotor development scores (mean 100 ± 15) of children aged 11-22 months in two birth cohorts: Environment and Childhood (INMA, Spain; n = 1967) and Mother-Child (RHEA, Greece: n = 412). Paternal body mass index (BMI) was used as a negative control exposure. The percentage of overweight and obese mothers was 18% and 8%, respectively, in INMA and 20% and 11% in RHEA, respectively. Maternal pre-pregnancy obesity was associated with reduced infant cognitive development scores in both INMA (score reduction: -2.72; 95% CI: -5.35, -0.10) and RHEA (score reduction: -3.71; 95% CI: -8.45, 1.02), after adjusting for socioeconomic variables and paternal BMI. There was evidence in both cohorts of a dose-response relationship with continuous maternal BMI. Paternal overweight/obesity was not associated with infant cognitive development. Associations with psychomotor scores were not consistent between cohorts, and were stronger for paternal than maternal BMI in RHEA. This study in two birth cohorts with moderately high obesity prevalence suggests that maternal pre-pregnancy obesity is associated with reduced child cognitive development at early ages. This association appears more likely to be due to maternal than shared family and social mechanisms, but further research is needed to disentangle a direct intrauterine effect from other maternal confounding factors.

  16. Maternal obesity alters feto-placental Cytochrome P4501A1 activity

    PubMed Central

    DuBois, Barent N.; O’Tierney, Perrie; Pearson, Jacob; Friedman, Jacob E.; Thornburg, Kent; Cherala, Ganesh

    2012-01-01

    Cytochrome P4501A1 (CYP1A1), an important drug metabolizing enzyme, is expressed in human placenta throughout gestation as well as in fetal liver. Obesity, a chronic inflammatory condition, is known to alter CYP enzyme expression in non-placental tissues. In the present study, we test the hypothesis that maternal obesity alters the distribution of CYP1A1 activity in feto-placental unit. Placentas were collected from non-obese (BMI<30) and obese (BMI>30) women at term. Livers were collected from gestation day 130 fetuses of non-human primates fed either control diet or high-fat diet (HFD). Cytosol and microsomes were collected using differential centrifugation, and incubated with 7-Ethoxyresorufin. The CYP1A1 specific activity (pmoles of resorufin formed/min/mg of protein) was measured at excitation/emission wavelength of 530/590nm. Placentas of obese women had significantly reduced microsomal CYP1A1 activity compared to non-obese women (0.046 vs. 0.082; p<0.05); however no such effect was observed on cytosolic activity. Similarly, fetal liver from HFD fed mothers had significantly reduced microsomal CYP1A1 activity (0.44±0.04 vs. 0.20±0.10; p<0.05), with no significant difference in cytosolic CYP1A1 activity (control, 1.23±0.20; HFD, 0.80±0.40). Interestingly, multiple linear regression analyses of placental efficiency indicates cytosolic CYP1A1 activity is a main effect (5.67±2.32 (β±SEM); p=0.022) along with BMI (−0.57±0.26; p=0.037), fetal gender (1.07±0.26; p<0.001), and maternal age (0.07±0.03; p=0.011). In summary, while maternal obesity affects microsomal CYP1A1 activity alone, cytosolic activity along with maternal BMI is an important determinant of placental efficiency. Together, these data suggest that maternal lifestyle could have a significant impact on CYP1A1 activity, and hints at a possible role for CYP1A1 in feto-placental growth and thereby well-being of fetus. PMID:23046808

  17. Chorionic plate arterial function is altered in maternal obesity

    PubMed Central

    Hayward, C.E.; Higgins, L.; Cowley, E.J.; Greenwood, S.L.; Mills, T.A.; Sibley, C.P.; Wareing, M.

    2013-01-01

    Objectives To characterise Chorionic Plate Artery (CPA) function in maternal obesity, and investigate whether leptin exposure reproduces the obese CPA phenotype in normal-BMI women. Study design CPA responses to the thromboxane-A2 mimetic U46619 (pre/post leptin incubation), to the nitric oxide donor sodium nitroprusside (SNP) and the occurrence of tone oscillations (pre/post leptin incubation) were assessed in 46 term placentas from women of normal (18.5–24.9) or obese (>30) Body Mass Index (BMI). Outcome measures Area Under the dose response Curve (AUC), maximum response (Vmax), sensitivity (EC50) to U46619 (pre/post leptin) and SNP; average vessel tone, oscillation amplitude and frequency (pre/post leptin). Results U46619 vasoconstriction was similar between BMI categories (p > 0.05), however vasodilatation to SNP was reduced in obesity (AUC p = 0.02, Vmaxp = 0.04) compared to normal-BMI women. Leptin incubation altered responses to U46619 in both normal-BMI (EC50 at 100 ng/ml leptin; p < 0.05) and obese women (AUC at 50 ng/ml; p < 0.05) but vasomotion was unaffected (p > 0.05). Conclusions Maternal obesity is associated with altered placental vascular function which may adversely affect placental oxygen and nutrient transport, placing the fetus at risk. Leptin incubation altered CPA vascular function but did not reproduce the obese phenotype. PMID:23360794

  18. Obesity and the association with maternal mental health symptoms.

    PubMed

    Ruhstaller, Kelly E; Elovitz, Michal A; Stringer, Marilyn; Epperson, C Neill; Durnwald, Celeste P

    2017-08-01

    To evaluate the association between maternal obesity and mood disorders including depression, anxiety, stress, and pregnancy-specific stress during pregnancy. This was a planned secondary analysis of a prospective cohort study investigating factors associated with preterm delivery. The cohort included women who initiated prenatal care before 20 weeks with a singleton pregnancy. Maternal mental health was assessed using four standard psychosocial behavioral measures to screen for depression, pregnancy-specific stress, anxiety, and stress. Screen positive scores for each tool were established based on previously published "high" scores. Of the 1010 women included in the cohort, 355 (35.1%) were obese. There was no significant difference in the number of obese women with stress (64.2% versus 68.4%, p = 0.18), pregnancy-specific stress (26.2% versus 22.1%, p = 0.15), or anxiety (38.6% versus 41.2%, p = 0.42); however, a greater number of obese women did report symptoms consistent with major depression when compared to women with BMIs <30 (30.4% versus 21.2%, p < 0.01). Obese women had higher rates of depression in early pregnancy compared to nonobese women. As many of the health behavior interventions for obese women during pregnancy have proven ineffective, incorporating depression screening and treatment into prenatal care may improve perinatal outcomes.

  19. Maternal depressive symptoms and child obesity in low-income urban families.

    PubMed

    Gross, Rachel S; Velazco, Nerissa K; Briggs, Rahil D; Racine, Andrew D

    2013-01-01

    To characterize the relationship between maternal depressive symptoms and child weight status, obesity-promoting feeding practices, and activity-related behaviors in low-income urban families. We conducted a cross-sectional survey of mothers with 5-year-old children receiving pediatric care at a federally qualified community health center. We used regression analyses to examine the relationship between maternal depressive symptoms (trichotomized: none, mild, moderate to severe) and 1) child weight status; 2) obesity-promoting feeding practices, including mealtime practices and feeding styles; and 3) activity-related behaviors, including sleep time, screen time, and outdoor playtime. The sample included 401 mother-child pairs (78.3% response rate), with 23.4% of mothers reporting depressive symptoms (15.7% mild, 7.7% moderate to severe). Mothers with moderate to severe depressive symptoms were more likely to have overweight and obese children than mothers without depressive symptoms (adjusted odds ratio 2.62; 95% confidence interval 1.02-6.70). Children of mildly depressed mothers were more likely to consume sweetened drinks and to eat out at restaurants and were less likely to eat breakfast than children of nondepressed mothers. Mothers with depressive symptoms were less likely to set limits, to use food as a reward, to restrict their child's intake, and to model healthy eating than nondepressed mothers. Children with depressed mothers had less sleep and outdoor playtime per day than children of nondepressed mothers. Maternal depressive symptoms are associated with child overweight and obese status and with several obesity-promoting practices. These results support the need for maternal depression screening in pediatric obesity prevention programs. Further research should explore how to incorporate needed mental health support. Copyright © 2013 Academic Pediatric Association. Published by Elsevier Inc. All rights reserved.

  20. Maternal obesity, gestational diabetes, breastfeeding and childhood overweight at age 2 years.

    PubMed

    Bider-Canfield, Z; Martinez, M P; Wang, X; Yu, W; Bautista, M P; Brookey, J; Page, K A; Buchanan, T A; Xiang, A H

    2017-04-01

    Maternal obesity, excessive gestational weight gain (EGWG), gestational diabetes mellitus (GDM) and breastfeeding are four important factors associated with childhood obesity. The objective of the study was to assess the interplay among these four factors and their independent contributions to childhood overweight in a cohort with standard clinical care. The cohort included 15 710 mother-offspring pairs delivered in 2011. Logistic regression was used to assess associations between maternal exposures and childhood overweight (body mass index >85th percentile) at age 2 years. Mothers with pre-pregnancy obesity or overweight were more likely to have EGWG, GDM and less likely to breastfeed ≥6 months. Mothers with GDM had 40-49% lower EGWG rates and similar breastfeeding rates compared with mothers without GDM. Analysis adjusted for exposures and covariates revealed an adjusted odds ratio (95% confidence interval) associated with childhood overweight at age 2 years of 2.34 (2.09-2.62), 1.50 (1.34-1.68), 1.23 (1.12-1.35), 0.95 (0.83-1.10) and 0.76 (0.69-0.83) for maternal obesity, overweight, EGWG, GDM and breastfeeding ≥6 months vs. <6 months, respectively. In this large clinical cohort, GDM was not associated with, but maternal pre-pregnancy obesity or overweight and EGWG were independently associated with an increased risk, and breastfeeding ≥6 months was associated with a decreased risk of childhood overweight at age 2 years. © 2016 World Obesity Federation.

  1. Maternal gestational diabetes and childhood obesity at age 9–11: results of a multinational study

    PubMed Central

    Zhao, Pei; Liu, Enqing; Qiao, Yijuan; Katzmarzyk, Peter T.; Chaput, Jean-Philippe; Fogelholm, Mikael; Johnson, William D.; Kuriyan, Rebecca; Kurpad, Anura; Lambert, Estelle V.; Maher, Carol; Maia, José A.R.; Matsudo, Victor; Olds, Timothy; Onywera, Vincent; Sarmiento, Olga L.; Standage, Martyn; Tremblay, Mark S.; Tudor-Locke, Catrine; Hu, Gang

    2016-01-01

    Aims/hypothesis The aim of this study was to examine the association between maternal gestational diabetes mellitus (GDM) and childhood obesity at age 9–11 years in 12 countries around the world. Methods A multinational cross-sectional study of 4,740 children aged 9–11 years was conducted. Maternal GDM was diagnosed according to the ADA or WHO criteria. Height and waist circumference were measured using standardised methods. Weight and body fat were measured using a portable Tanita SC-240 Body Composition Analyzer. Multilevel modelling was used to account for the nested nature of the data. Results The prevalence of reported maternal GDM was 4.3%. The overall prevalence of childhood obesity, central obesity and high body fat were 12.3%, 9.9% and 8.1%, respectively. The multivariable-adjusted (maternal age at delivery, education, infant feeding mode, gestational age, number of younger siblings, child unhealthy diet pattern scores, moderate-to-vigorous physical activity, sleeping time, sedentary time, sex and birthweight) odds ratios among children of GDM mothers compared with children of non-GDM mothers were 1.53 (95% CI 1.03, 2.27) for obesity, 1.73 (95% CI 1.14, 2.62) for central obesity and 1.42 (95% CI 0.90, 2.26) for high body fat. The positive association was still statistically significant for central obesity after additional adjustment for current maternal BMI but was no longer significant for obesity and high body fat. Conclusions/interpretation Maternal GDM was associated with increased odds of childhood obesity at 9–11 years old but this association was not fully independent of maternal BMI. PMID:27510911

  2. Maternal obesity during pregnancy and cardiovascular development and disease in the offspring.

    PubMed

    Gaillard, Romy

    2015-11-01

    Maternal obesity during pregnancy is an important public health problem in Western countries. Currently, obesity prevalence rates in pregnant women are estimated to be as high as 30%. In addition, approximately 40% of women gain an excessive amount of weight during pregnancy in Western countries. An accumulating body of evidence suggests a long-term impact of maternal obesity and excessive weight gain during pregnancy on adiposity, cardiovascular and metabolic related health outcomes in the offspring in fetal life, childhood and adulthood. In this review, we discuss results from recent studies, potential underlying mechanisms and challenges for future epidemiological studies.

  3. Maternal obesity reduces oxidative capacity in fetal skeletal muscle of Japanese macaques

    PubMed Central

    McCurdy, Carrie E.; Hetrick, Byron; Houck, Julie; Drew, Brian G.; Kaye, Spencer; Lashbrook, Melanie; Bergman, Bryan C.; Takahashi, Diana L.; Dean, Tyler A.; Gertsman, Ilya; Hansen, Kirk C.; Philp, Andrew; Hevener, Andrea L.; Chicco, Adam J.; Aagaard, Kjersti M.; Grove, Kevin L.; Friedman, Jacob E.

    2016-01-01

    Maternal obesity is proposed to alter the programming of metabolic systems in the offspring, increasing the risk for developing metabolic diseases; however, the cellular mechanisms remain poorly understood. Here, we used a nonhuman primate model to examine the impact of a maternal Western-style diet (WSD) alone, or in combination with obesity (Ob/WSD), on fetal skeletal muscle metabolism studied in the early third trimester. We find that fetal muscle responds to Ob/WSD by upregulating fatty acid metabolism, mitochondrial complex activity, and metabolic switches (CPT-1, PDK4) that promote lipid utilization over glucose oxidation. Ob/WSD fetuses also had reduced mitochondrial content, diminished oxidative capacity, and lower mitochondrial efficiency in muscle. The decrease in oxidative capacity and glucose metabolism was persistent in primary myotubes from Ob/WSD fetuses despite no additional lipid-induced stress. Switching obese mothers to a healthy diet prior to pregnancy did not improve fetal muscle mitochondrial function. Lastly, while maternal WSD alone led only to intermediary changes in fetal muscle metabolism, it was sufficient to increase oxidative damage and cellular stress. Our findings suggest that maternal obesity or WSD, alone or in combination, leads to programmed decreases in oxidative metabolism in offspring muscle. These alterations may have important implications for future health. PMID:27734025

  4. Maternal obesity influences the relationship between location of neonate fat mass and total fat mass.

    PubMed

    Hull, H R; Thornton, J; Paley, C; Navder, K; Gallagher, D

    2015-08-01

    It is suggested that maternal obesity perpetuates offspring obesity to future generations. To determine whether location of neonate fat mass (FM: central vs. peripheral) is related to total neonate FM and whether maternal obesity influences this relationship. Neonate body composition and skin-fold thicknesses were assessed in healthy neonates (n = 371; 1-3 days old). Linear regression models examined the relationship between total FM and location of FM (central vs. peripheral). Location of FM was calculated by skin-folds: peripheral was the sum of (biceps and triceps)/2 and central was represented by the subscapular skin-fold. A significant interaction was found for location of FM and maternal obesity. Holding all predictors constant, in offspring born to non-obese mothers, a 0.5 mm increase in central FM predicted a 15 g greater total FM, whereas a 0.5 mm increase in peripheral FM predicted a 66 g greater total FM. However, in offspring born to obese mothers, a 0.5 mm increase in central FM predicted a 56 g total FM, whereas a 0.5 mm increase in peripheral FM predicted a 14 g greater total FM. The relationship between total FM and location of FM is influenced by maternal obesity. © 2014 The Authors. Pediatric Obesity © 2014 World Obesity.

  5. A pragmatic controlled trial to prevent childhood obesity within a risk group at maternity and child health-care clinics: results up to six years of age (the VACOPP study).

    PubMed

    Mustila, Taina; Raitanen, Jani; Keskinen, Päivi; Luoto, Riitta

    2018-02-27

    Obesity in childhood appears often during the toddler years. The prenatal environment influences obesity risk. Maternal gestational diabetes, the child's diet, and physical activity in the first few years have an important role in subsequent weight gain. A study was conducted to evaluate effectiveness of a primary health-care lifestyle counselling intervention in prevention of childhood obesity up to 6 years of age. The study was a controlled pragmatic trial to prevent childhood obesity and was implemented at maternity and child health-care clinics. The participants (n = 185) were mothers at risk of gestational diabetes mellitus with their offspring born between 2008 and 2010. The prenatal intervention, started at the end of the first trimester of pregnancy, consisted of counselling on diet and physical activity by municipal health-care staff. The intervention continued at yearly appointments with a public health-nurse at child health-care clinics. The paper reports the offspring weight gain results for 2-6 years of age. Weight gain up to 6 years of age was assessed as BMI standard deviation scores (SDS) via a mixed-effect linear regression model. The proportion of children at 6 years with overweight/obesity was assessed as weight-for-height percentage and ISO-BMI. Priority was not given to power calculations, because of the study's pragmatic nature. One hundred forty seven children's (control n = 76/85% and intervention n = 71/56%) weight and height scores were available for analysis at 6 years of age. There was no significant difference in weight gain or overweight/obesity proportions between the groups at 6 years of age, but the proportion of children with obesity in both groups was high (assessed as ISO-BMI 9.9% and 11.8%) relative to prevalence in this age group in Finland. As the authors previously reported, the intervention-group mothers had lower prevalence of gestational diabetes mellitus, but a decrease in obesity incidence before school age

  6. Maternal obesity influences the relationship between location of neonate fat mass and total fat mass

    PubMed Central

    Hull, Holly R.; Thornton, John; Paley, Charles; Navder, Khursheed; Gallagher, Dympna

    2014-01-01

    Background It is suggested that maternal obesity perpetuates offspring obesity to future generations. Objective To determine whether location of neonate fat mass (FM: central vs. peripheral) is related to total neonate FM and whether maternal obesity influences this relationship. Methods Neonate body composition and skinfold thicknesses were assessed in healthy neonates (n=371; 1-3 days old). Linear regression models examined the relationship between total FM and location of FM (central vs. peripheral). Location of FM was calculated by skinfolds: peripheral was the sum of (biceps and triceps)/2 and central was represented by the subscapular skinfold. Results A significant interaction was found for location of FM and maternal obesity. Holding all predictors constant, in offspring born to non-obese mothers, a 0.5 mm increase in central FM predicted a 15 g greater total FM whereas a 0.5 mm increase in peripheral FM predicted a 66 g greater total FM. However, in offspring born to obese mothers, a 0.5 mm increase in central FM predicted a 56 g total FM whereas a 0.5 mm increase in peripheral FM predicted a 14 g greater total FM. Conclusions The relationship between total FM and location of FM is influenced by maternal obesity. PMID:25088238

  7. Impact of maternal obesity on inhaled corticosteroid use in childhood: a registry based analysis of first born children and a sibling pair analysis.

    PubMed

    Lowe, Adrian J; Ekeus, Cecilia; Bråbäck, Lennart; Rajaleid, Kristiina; Forsberg, Bertil; Hjern, Anders

    2013-01-01

    It has been proposed that maternal obesity during pregnancy may increase the risk that the child develops allergic disease and asthma, although the mechanisms underpinning this relationship are currently unclear. We sought to assess if this association may be due to confounding by genetic or environmental risk factors that are common to maternal obesity and childhood asthma, using a sibling pair analysis. The study population comprised a Swedish national cohort of term children born between 1992 and 2008 to native Swedish parents. Maternal body mass index (BMI) was measured at 8-10 weeks gestation. Unconditional logistic regression models were used to determine if maternal obesity was associated with increased risk of inhaled corticosteroid (ICS) in 431,718 first-born children, while adjusting for potential confounders. An age-matched discordant sib-pair analysis was performed, taking into account shared genetic and environmental risk factors. Maternal over-weight and obesity were associated with increased risk that the child would require ICS (for BMI≥35 kg/m(2), aOR = 1.30, 95%CI = 1.10-1.52 compared with normal weight mothers) in children aged 6-12 years. Similar effects were seen in younger children, but in children aged 13-16 years, maternal obesity (BMI≥30) was related to increased risk of ICS use in girls (aOR = 1.28, 95%CI = 1.07-1.53) but not boys (OR = 1.05, 95%CI = 0.87-1.26). The sib-pair analysis, which included 2,034 sib-pairs older than six years who were discordant for both ICS use and maternal BMI category, failed to find any evidence that increasing maternal weight was related to increased risk of ICS use. Maternal obesity is associated with increased risk of childhood ICS use up to approximately 12 years of age, but only in girls after this age. These effects could not be confirmed in a sib pair analysis, suggesting either limited statistical power, or the effects of maternal BMI may be due to shared genetic or

  8. Joint effects of child temperament and maternal sensitivity on the development of childhood obesity.

    PubMed

    Wu, Tiejian; Dixon, Wallace E; Dalton, William T; Tudiver, Fred; Liu, Xuefeng

    2011-05-01

    The interplay between child characteristics and parenting is increasingly implicated as crucial to child health outcomes. This study assessed the joint effects of children's temperamental characteristics and maternal sensitivity on children's weight status. Data from the National Institute of Child Health and Human Development's Study of Early Child Care and Youth Development were utilized. Infant temperament, assessed at child's age of 6 months by maternal report, was categorized into three types: easy, average, and difficult. Maternal sensitivity, assessed at child's age of 6 months by observing maternal behaviors during mother-child semi-structured interaction, was categorized into two groups: sensitive and insensitive. Children's height and weight were measured longitudinally from age 2 years to Grade 6, and body mass index (BMI) was calculated. BMI percentile was obtained based on the Centers for Disease Control and Prevention's BMI charts. Children, who had a BMI ≥ the 85th percentile, were defined as overweight-or-obese. Generalized estimating equations were used to analyze the data. The proportions of children overweight-or-obese increased with age, 15.58% at 2 years old to 34.34% by Grade 6. The joint effects of children's temperament and maternal sensitivity on a child's body mass status depended on the child's age. For instance, children with difficult temperament and insensitive mothers had significantly higher risks for being overweight-or-obese during the school age phase but not during early childhood. Specific combinations of child temperament and maternal sensitivity were associated with the development of obesity during childhood. Findings may hold implications for childhood obesity prevention/intervention programs targeting parents.

  9. Persistent influence of maternal obesity on offspring health: Mechanisms from animal models and clinical studies

    USDA-ARS?s Scientific Manuscript database

    The consequences of excessive maternal weight and adiposity at conception for the offspring are now well recognized. Maternal obesity increases the risk of overweight and obesity even in children born with appropriate-for-gestational age (AGA) birth weights. Studies in animal models have employed bo...

  10. Maternal obesity alters immune cell frequencies and responses in umbilical cord blood samples.

    PubMed

    Wilson, Randall M; Marshall, Nicole E; Jeske, Daniel R; Purnell, Jonathan Q; Thornburg, Kent; Messaoudi, Ilhem

    2015-06-01

    Maternal obesity is one of the several key factors thought to modulate neonatal immune system development. Data from murine studies demonstrate worse outcomes in models of infection, autoimmunity, and allergic sensitization in offspring of obese dams. In humans, children born to obese mothers are at increased risk for asthma. These findings suggest a dysregulation of immune function in the children of obese mothers; however, the underlying mechanisms remain poorly understood. The aim of this study was to examine the relationship between maternal body weight and the human neonatal immune system. Umbilical cord blood samples were collected from infants born to lean, overweight, and obese mothers. Frequency and function of major innate and adaptive immune cell populations were quantified using flow cytometry and multiplex analysis of circulating factors. Compared to babies born to lean mothers, babies of obese mothers had fewer eosinophils and CD4 T helper cells, reduced monocyte and dendritic cell responses to Toll-like receptor ligands, and increased plasma levels of IFN-α2 and IL-6 in cord blood. These results support the hypothesis that maternal obesity influences programming of the neonatal immune system, providing a potential link to increased incidence of chronic inflammatory diseases such as asthma and cardiovascular disease in the offspring. © 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

  11. Obesity and pregnancy: a transversal study from a low-risk maternity.

    PubMed

    Calderon, Ana Carolina S; Quintana, Silvana M; Marcolin, Alessandra C; Berezowski, Aderson T; Brito, Luiz Gustavo O; Duarte, Geraldo; Cavalli, Ricardo C

    2014-07-28

    Obesity is a public health problem and is increasing in all populations, including pregnant women. It influences maternal and neonatal outcomes; however, data are scarce in developing countries. We aimed to compare perinatal results between obese and non-obese pregnant women in a low-risk maternity. Transversal study of 1,779 40-week-pregnancies from 2005 to 2009 that completed a standard questionnaire with sociodemographic, obstetrical and neonatal variables and performed an ultrasound with amniotic fluid index (AFI) measurement and foetal vitality (FBP, non-stress test). They were analysed about their association with obesity on pregnancy. When compared with non-obese women, the group of obese patients had higher systolic (118.1 vs 109.2 mmHg; p < 0.01) and diastolic (76.6 vs 70.4 mmHg; p < 0.01) pressure levels, AFI (12.52 vs. 9.61 cm; p = 0.02), presence of meconium on labour (20.52 vs. 14.67%; p = 0.02), birthweight (3602 vs. 3437 g; p < 0.01) and caesarean section (39.74 vs. 29.98%, p < 0.01). Labour induction before 40 weeks in the antenatal period associated with foetal weight estimation should be considered as a recommendation for decreasing high percentages of caesarean delivery found in obese women.

  12. Maternal overweight and obesity are associated with increased risk of type 1 diabetes in offspring of parents without diabetes regardless of ethnicity.

    PubMed

    Hussen, Hozan I; Persson, Martina; Moradi, Tahereh

    2015-07-01

    The incidence of type 1 diabetes in children is increasing in Sweden, as is the prevalence of maternal overweight/obesity. Therefore, the aim of this study was to investigate if maternal overweight/obesity increases the risk of type 1 diabetes in offspring of parents with and without diabetes, and of different ethnicities. The study cohort comprised 1,263,358 children, born in Sweden between 1992 and 2004. Children were followed from birth until diagnosis of type 1 diabetes, emigration, death or end of follow-up in 2009, whichever occurred first. First trimester maternal BMI was calculated (kg/m(2)). Poisson regression was used to calculate incidence rate ratios (IRRs) with 95% CI for type 1 diabetes in the offspring. The risk of type 1 diabetes was increased in offspring of parents with any type of diabetes regardless of parental ethnicity. High first trimester maternal BMI was associated with increased risk of type 1 diabetes only in offspring of parents without diabetes (IRR 1.33 [95% CI 1.20, 1.48]). Increasing incidence of type 1 diabetes in children with non-diabetic parents may partly be explained by increasing prevalence of maternal overweight/obesity.

  13. Epigenetic changes in fetal hypothalamic energy regulating pathways are associated with maternal undernutrition and twinning

    PubMed Central

    Begum, Ghazala; Stevens, Adam; Smith, Emma Bolton; Connor, Kristin; Challis, John R. G.; Bloomfield, Frank; White, Anne

    2012-01-01

    Undernutrition during pregnancy is implicated in the programming of offspring for the development of obesity and diabetes. We hypothesized that maternal programming causes epigenetic changes in fetal hypothalamic pathways regulating metabolism. This study used sheep to examine the effect of moderate maternal undernutrition (60 d before to 30 d after mating) and twinning to investigate changes in the key metabolic regulators proopiomelanocortin (POMC) and the glucocorticoid receptor (GR) in fetal hypothalami. Methylation of the fetal hypothalamic POMC promoter was reduced in underfed singleton, fed twin, and underfed twin groups (60, 73, and 63% decrease, respectively). This was associated with reduced DNA methyltransferase activity and altered histone methylation and acetylation. Methylation of the hypothalamic GR promoter was decreased in both twin groups and in maternally underfed singleton fetuses (52, 65, and 55% decrease, respectively). This correlated with changes in histone methylation and acetylation and increased GR mRNA expression in the maternally underfed singleton group. Alterations in GR were hypothalamic specific, with no changes in hippocampi. Unaltered levels of OCT4 promoter methylation indicated gene-specific effects. In conclusion, twinning and periconceptional undernutrition are associated with epigenetic changes in fetal hypothalamic POMC and GR genes, potentially resulting in altered energy balance regulation in the offspring.—Begum, G., Stevens, A., Smith, E. B., Connor, K., Challis, J. R. G., Bloomfield, F., White, A. Epigenetic changes in fetal hypothalamic energy regulating pathways are associated with maternal undernutrition and twinning. PMID:22223754

  14. Childhood cardiometabolic outcomes of maternal obesity during pregnancy: the Generation R Study.

    PubMed

    Gaillard, Romy; Steegers, Eric A P; Duijts, Liesbeth; Felix, Janine F; Hofman, Albert; Franco, Oscar H; Jaddoe, Vincent W V

    2014-04-01

    Maternal prepregnancy obesity is associated with impaired cardiometabolic health in offspring. Whether these associations reflect direct intrauterine causal mechanisms remains unclear. In a population-based prospective cohort study among 4871 mothers, fathers, and their children, we examined the associations of both maternal and paternal prepregnancy body mass index (BMI) with childhood body fat distribution and cardiometabolic outcomes and explored whether any association was explained by pregnancy, birth, and childhood factors. We measured childhood BMI, total body and abdominal fat distribution, blood pressure, and blood levels of lipids, insulin, and C-peptide at the age of 6 years. We observed that higher maternal and paternal prepregnancy BMI were associated with higher childhood BMI, total body and abdominal fat mass measures, systolic blood pressure, and insulin levels and lower high-density lipoprotein cholesterol levels (P<0.05). Stronger associations were present for maternal than paternal BMI, with statistical support for heterogeneity between these associations. The associations for childhood fat mass and cardiometabolic outcomes attenuated after adjustment for childhood current BMI. Compared with children from normal-weight mothers, those from obese mothers had increased risks of childhood overweight (odds ratio, 3.84 [95% confidence interval, 3.01-4.90]) and clustering of cardiometabolic risk factors (odds ratio, 3.00 [95% confidence interval, 2.09-4.34]). Smaller effect estimates for these outcomes were observed for paternal obesity. In conclusion, higher maternal and paternal prepregnancy BMI were associated with an adverse cardiometabolic profile in offspring, with stronger associations present for maternal prepregnancy BMI. These findings suggest that maternal prepregnancy BMI may influence the cardiometabolic health of offspring through direct intrauterine mechanisms.

  15. Fetal myocardial deformation in maternal diabetes mellitus and obesity.

    PubMed

    Kulkarni, A; Li, L; Craft, M; Nanda, M; Lorenzo, J M M; Danford, D; Kutty, S

    2017-05-01

    Experimental evidence suggests that changes in the fetal myocardium result from intrauterine effects of maternal diabetes mellitus and obesity. The aim of this study was to assess fetal cardiac function using two-dimensional speckle-tracking echocardiography to determine the effects of maternal diabetes and obesity on the fetal myocardium. Comparative cross-sectional evaluation of myocardial function in fetuses of mothers with diabetes mellitus (FDM) or obesity (FO) and normal gestational age-matched control fetuses (FC) was performed using two-dimensional speckle-tracking echocardiography at two centers. In total, 178 fetuses (82 FDM, 26 FO and 70 FC) met the enrolment criteria. Mean gestational age at assessment was similar among groups: 25.3 ± 5.1 weeks for FDM, 25.0 ± 4.6 weeks for FO and 25.1 ± 4.9 weeks for FC. Mean maternal body mass index was significantly higher in FDM and FO groups compared with the FC group. Statistically significant differences in fetal cardiac function were detected between FDM and FC for global longitudinal strain (mean ± SD, -21.4 ± 6.5% vs -27.0 ± 5.2%; P < 0.001), global circumferential strain (mean ± SD, -22.6 ± 6.5% vs -26.2 ± 6.8%; P = 0.002), average longitudinal systolic strain rate (median, -1.4 (interquartile range (IQR), -1.7 to -1.1)/s vs -1.6 (IQR, -2.0 to -1.4)/s; P = 0.001) and average circumferential systolic strain rate (median, -1.4 (IQR, -1.9 to -1.1)/s vs -1.6 (IQR, -2.1 to -1.3)/s; P = 0.006). Cases of non-obese FDM also had abnormal strain parameters compared with FC. Global longitudinal strain (mean ± SD, -21.1 ± 7.5%) and average circumferential systolic strain rate (median, -1.3 (IQR, -1.8 to -1.1)/s) were significantly lower in FO compared with FC. Unfavorable changes occur in the fetal myocardium in response to both maternal diabetes mellitus and obesity. The long-term prognostic implications of these changes require further study

  16. Maternal Obesity Induces Sustained Inflammation in Both Fetal and Offspring Large Intestine of Sheep

    PubMed Central

    Yan, Xu; Huang, Yan; Wang, Hui; Du, Min; Hess, Bret W.; Ford, Stephen P.; Nathanielsz, Peter W.; Zhu, Mei-Jun

    2010-01-01

    Background Both maternal obesity and inflammatory bowel diseases (IBDs) are increasing. It was hypothesized that maternal obesity induces an inflammatory response in the fetal large intestine, predisposing offspring to IBDs. Methods Nonpregnant ewes were assigned to a control (Con, 100% of National Research Council [NRC] recommendations) or obesogenic (OB, 150% of NRC) diet from 60 days before conception. The large intestine was sampled from fetuses at 135 days (term 150 days) after conception and from offspring lambs at 22.5 ± 0.5 months of age. Results Maternal obesity enhanced mRNA expression tumor necrosis factor (TNF)α, interleukin (IL)1α, IL1β, IL6, IL8, and monocyte/macrophage chemotactic protein-1 (MCP1), as well as macrophage markers, CD11b, CD14, and CD68 in fetal gut. mRNA expression of Toll-like receptor (TLR) 2 and TLR4 was increased in OB versus Con fetuses; correspondingly, inflammatory NF-κB and JNK signaling pathways were also upregulated. Both mRNA expression and protein content of transforming growth factor (TGF) β was increased. The IL-17A mRNA expression and protein content was higher in OB compared to Con samples, which was associated with fibrosis in the large intestine of OB fetuses. Similar inflammatory responses and enhanced fibrosis were detected in OB compared to Con offspring. Conclusions Maternal obesity induced inflammation and enhanced expression of proinflammatory cytokines in fetal and offspring large intestine, which correlated with increased TGFβ and IL17 expression. These data show that maternal obesity may predispose offspring gut to IBDs. PMID:21674707

  17. CCAAT-enhancer-binding protein β (C/EBPβ) and downstream human placental growth hormone genes are targets for dysregulation in pregnancies complicated by maternal obesity.

    PubMed

    Vakili, Hana; Jin, Yan; Menticoglou, Savas; Cattini, Peter A

    2013-08-02

    Human chorionic somatomammotropin (CS) and placental growth hormone variant (GH-V) act as metabolic adaptors in response to maternal insulin resistance, which occurs in "normal" pregnancy. Maternal obesity can exacerbate this "resistance," suggesting that CS, GH-V, or transcription factors that regulate their production might be targets. The human CS genes, hCS-A and hCS-B, flank the GH-V gene. A significant decrease in pre-term placental CS/GH-V RNA levels was observed in transgenic mice containing the CS/GH-V genes in a model of high fat diet (HFD)-induced maternal obesity. Similarly, a decrease in CS/GH-V RNA levels was detected in term placentas from obese (body mass index (BMI) ≥ 35 kg/m(2)) versus lean (BMI 20-25 kg/m(2)) women. A specific decrease in transcription factor CCAAT-enhancer-binding protein β (C/EBPβ) RNA levels was also seen with obesity; C/EBPβ is required for mouse placenta development and is expressed, like CS and GH-V, in syncytiotrophoblasts. Binding of C/EBPβ to the CS gene downstream enhancer regions, which by virtue of their position distally flank the GH-V gene, was reduced in placenta chromatin from mice on a HFD and in obese women; a corresponding decrease in RNA polymerase II associated with CS/GH-V promoters was also observed. Detection of decreased endogenous CS/GH-V RNA levels in human placental tumor cells treated with C/EBPβ siRNA is consistent with a direct effect. These data provide evidence for CS/GH-V dysregulation in acute HFD-induced obesity in mouse pregnancy and chronic obesity in human pregnancy and implicate C/EBPβ, a factor associated with CS regulation and placental development.

  18. Effect of GLP-1 Receptor Activation on Offspring Kidney Health in a Rat Model of Maternal Obesity.

    PubMed

    Glastras, Sarah J; Chen, Hui; McGrath, Rachel T; Zaky, Amgad A; Gill, Anthony J; Pollock, Carol A; Saad, Sonia

    2016-03-23

    Maternal obesity is associated with an increased risk of chronic disease in offspring, including type 2 diabetes (T2D). Exendin-4 (Exd-4) activates the glucagon like peptide-1 (GLP-1) receptor thereby decreasing serum glucose levels and body weight. In addition, Exd-4 has been shown to reduce renal and cardiac complications in experimental models of T2D. We hypothesized that treatment with Exd-4 would ameliorate the detrimental effects of maternal and diet-induced obesity on renal characteristics in offspring. Female Sprague-Dawley rats were fed either normal or high-fat diet (HFD) for 6 weeks prior to pregnancy, during pregnancy and lactation, and their offspring were weaned to normal or HFD. The offspring were randomized to Exd-4 or placebo from weaning and their kidneys harvested at Week 9. We found that the kidneys of offspring from obese mothers, regardless of postnatal diet, had significantly increased markers of inflammation, oxidative stress and fibrosis. Exd-4 ameliorated the negative renal effects of maternal obesity and in particular, reduced renal inflammation, oxidative stress and fibrosis. In conclusion, maternal obesity has persisting effects on renal structure in the offspring. GLP-1 analogues are potentially useful for protecting against the deleterious effects of maternal obesity on renal physiology in offspring.

  19. Interventions to prevent adverse fetal programming due to maternal obesity during pregnancy.

    PubMed

    Nathanielsz, Peter W; Ford, Stephen P; Long, Nathan M; Vega, Claudia C; Reyes-Castro, Luis A; Zambrano, Elena

    2013-10-01

    Maternal obesity is a global epidemic affecting both developed and developing countries. Human and animal studies indicate that maternal obesity adversely programs the development of offspring, predisposing them to chronic diseases later in life. Several mechanisms act together to produce these adverse health effects. There is a consequent need for effective interventions that can be used in the management of human pregnancy to prevent these outcomes. The present review analyzes the dietary and exercise intervention studies performed to date in both altricial and precocial animals, rats and sheep, with the aim of preventing adverse offspring outcomes. The results of these interventions present exciting opportunities to prevent, at least in part, adverse metabolic and other outcomes in obese mothers and their offspring. © 2013 International Life Sciences Institute.

  20. Differential hypothalamic leptin sensitivity in obese rat offspring exposed to maternal and postnatal intake of chocolate and soft drink.

    PubMed

    Kjaergaard, M; Nilsson, C; Secher, A; Kildegaard, J; Skovgaard, T; Nielsen, M O; Grove, K; Raun, K

    2017-01-16

    Intake of high-energy foods and maternal nutrient overload increases the risk of metabolic diseases in the progeny such as obesity and diabetes. We hypothesized that maternal and postnatal intake of chocolate and soft drink will affect leptin sensitivity and hypothalamic astrocyte morphology in adult rat offspring. Pregnant Sprague-Dawley rats were fed ad libitum chow diet only (C) or with chocolate and high sucrose soft drink supplement (S). At birth, litter size was adjusted into 10 male offspring per mother. After weaning, offspring from both dietary groups were assigned to either S or C diet, giving four groups until the end of the experiment at 26 weeks of age. As expected, adult offspring fed the S diet post weaning became obese (body weight: P<0.01, %body fat per kg: P<0.001) and this was due to the reduced energy expenditure (P<0.05) and hypothalamic astrogliosis (P<0.001) irrespective of maternal diet. Interesting, offspring born to S-diet-fed mothers and fed the S diet throughout postnatal life became obese despite lower energy intake than controls (P<0.05). These SS offspring showed increased feed efficiency (P<0.001) and reduced fasting pSTAT3 activity (P<0.05) in arcuate nucleus (ARC) compared with other groups. The findings indicated that the combination of the maternal and postnatal S-diet exposure induced persistent changes in leptin signalling, hence affecting energy balance. Thus, appetite regulation was more sensitive to the effect of leptin than energy expenditure, suggesting differential programming of leptin sensitivity in ARC in SS offspring. Effects of the maternal S diet were normalized when offspring were fed a chow diet after weaning. Maternal intake of chocolate and soft drink had long-term consequences for the metabolic phenotype in the offspring if they continued on the S diet in postnatal life. These offspring displayed obesity despite lowered energy intake associated with alterations in hypothalamic leptin signalling.

  1. Differential hypothalamic leptin sensitivity in obese rat offspring exposed to maternal and postnatal intake of chocolate and soft drink

    PubMed Central

    Kjaergaard, M; Nilsson, C; Secher, A; Kildegaard, J; Skovgaard, T; Nielsen, M O; Grove, K; Raun, K

    2017-01-01

    Background/objective: Intake of high-energy foods and maternal nutrient overload increases the risk of metabolic diseases in the progeny such as obesity and diabetes. We hypothesized that maternal and postnatal intake of chocolate and soft drink will affect leptin sensitivity and hypothalamic astrocyte morphology in adult rat offspring. Methods: Pregnant Sprague-Dawley rats were fed ad libitum chow diet only (C) or with chocolate and high sucrose soft drink supplement (S). At birth, litter size was adjusted into 10 male offspring per mother. After weaning, offspring from both dietary groups were assigned to either S or C diet, giving four groups until the end of the experiment at 26 weeks of age. Results: As expected, adult offspring fed the S diet post weaning became obese (body weight: P<0.01, %body fat per kg: P<0.001) and this was due to the reduced energy expenditure (P<0.05) and hypothalamic astrogliosis (P<0.001) irrespective of maternal diet. Interesting, offspring born to S-diet-fed mothers and fed the S diet throughout postnatal life became obese despite lower energy intake than controls (P<0.05). These SS offspring showed increased feed efficiency (P<0.001) and reduced fasting pSTAT3 activity (P<0.05) in arcuate nucleus (ARC) compared with other groups. The findings indicated that the combination of the maternal and postnatal S-diet exposure induced persistent changes in leptin signalling, hence affecting energy balance. Thus, appetite regulation was more sensitive to the effect of leptin than energy expenditure, suggesting differential programming of leptin sensitivity in ARC in SS offspring. Effects of the maternal S diet were normalized when offspring were fed a chow diet after weaning. Conclusions: Maternal intake of chocolate and soft drink had long-term consequences for the metabolic phenotype in the offspring if they continued on the S diet in postnatal life. These offspring displayed obesity despite lowered energy intake associated with

  2. Maternal obesity programs mitochondrial and lipid metabolism gene expression in infant umbilical vein endothelial cells

    PubMed Central

    Ramos Costa, Suzana Maria; Isganaitis, Elvira; Matthews, Tucker; Hughes, Katelyn; Daher, Grace; Dreyfuss, Jonathan M.; Pontes da Silva, Giselia Alves; Patti, Mary-Elizabeth

    2016-01-01

    Background/Objectives Maternal obesity increases risk for childhood obesity, but molecular mechanisms are not well understood. We hypothesized that primary umbilical vein endothelial cells (HUVEC) from infants of overweight and obese mothers would harbor transcriptional patterns reflecting offspring obesity risk. Subjects/Methods In this observational cohort study, we recruited 13 lean (pre-pregnancy BMI <25.0 kg/m2) and 24 overweight-obese (‘ov-ob’, BMI ≥25.0 kg/m2) women. We isolated primary HUVEC, and analyzed both gene expression (Primeview, Affymetrix) and cord blood levels of hormones and adipokines. Results 142 transcripts were differentially expressed in HUVEC from infants of overweight-obese mothers (false discovery rate, FDR <0.05). Pathway analysis revealed that genes involved in mitochondrial and lipid metabolism were negatively correlated with maternal BMI (FDR <0.05). To test whether these transcriptomic patterns were associated with distinct nutrient exposures in the setting of maternal obesity, we analyzed the cord blood lipidome and noted significant increases in levels of total free fatty acids (lean: 95.5 ± 37.1 ug/ml, ov-ob: 124.1 ± 46.0 ug/ml, P=0.049), palmitate (lean: 34.5 ± 12.7 ug/ml, ov-ob: 46.3 ± 18.4 ug/ml, P=0.03) and stearate (lean: 20.8 ± 8.2 ug/ml, ov-ob: 29.7 ± 17.2 ug/ml, P=0.04), in infants of overweight-obese mothers. Conclusion Prenatal exposure to maternal obesity alters HUVEC expression of genes involved in mitochondrial and lipid metabolism, potentially reflecting developmentally-programmed differences in oxidative and lipid metabolism. PMID:27531045

  3. Combined parental obesity augments single-parent obesity effects on hypothalamus inflammation, leptin signaling (JAK/STAT), hyperphagia, and obesity in the adult mice offspring.

    PubMed

    Ornellas, Fernanda; Souza-Mello, Vanessa; Mandarim-de-Lacerda, Carlos Alberto; Aguila, Marcia Barbosa

    2016-01-01

    We aimed to evaluate the effects of maternal and/or paternal obesity on offspring body mass, leptin signaling, appetite-regulating neurotransmitters and local inflammatory markers. C57BL/6 mice received standard chow (SC, lean groups) or high-fat diet (HF, obese groups) starting from one month of age. At three months, HF mice became obese relative to SC mice. They were then mated as follows: lean mother and lean father, lean mother and obese father, obese mother and lean father, and obese mother and obese father. The offspring received the SC diet from weaning until three months of age, when they were sacrificed. In the offspring, paternal obesity did not lead to changes in the Janus kinase (JAK)/signal transducer and activation of the transcription (STAT) pathway or feeding behavior but did induce hypothalamic inflammation. On the other hand, maternal obesity resulted in increased weight gain, hyperleptinemia, decreased leptin OBRb receptor expression, JAK/STAT pathway impairment, and increased SOCS3 signaling in the offspring. In addition, maternal obesity elevated inflammatory markers and altered NPY and POMC expression in the hypothalamus. Interestingly, combined parental obesity exacerbated the deleterious outcomes compared to single-parent obesity. In conclusion, while maternal obesity is known to program metabolic changes and obesity in offspring, the current study demonstrated that obese fathers induce hypothalamus inflammation in offspring, which may contribute to the development of metabolic syndromes in adulthood.

  4. Epigenetic changes in fetal hypothalamic energy regulating pathways are associated with maternal undernutrition and twinning.

    PubMed

    Begum, Ghazala; Stevens, Adam; Smith, Emma Bolton; Connor, Kristin; Challis, John R G; Bloomfield, Frank; White, Anne

    2012-04-01

    Undernutrition during pregnancy is implicated in the programming of offspring for the development of obesity and diabetes. We hypothesized that maternal programming causes epigenetic changes in fetal hypothalamic pathways regulating metabolism. This study used sheep to examine the effect of moderate maternal undernutrition (60 d before to 30 d after mating) and twinning to investigate changes in the key metabolic regulators proopiomelanocortin (POMC) and the glucocorticoid receptor (GR) in fetal hypothalami. Methylation of the fetal hypothalamic POMC promoter was reduced in underfed singleton, fed twin, and underfed twin groups (60, 73, and 63% decrease, respectively). This was associated with reduced DNA methyltransferase activity and altered histone methylation and acetylation. Methylation of the hypothalamic GR promoter was decreased in both twin groups and in maternally underfed singleton fetuses (52, 65, and 55% decrease, respectively). This correlated with changes in histone methylation and acetylation and increased GR mRNA expression in the maternally underfed singleton group. Alterations in GR were hypothalamic specific, with no changes in hippocampi. Unaltered levels of OCT4 promoter methylation indicated gene-specific effects. In conclusion, twinning and periconceptional undernutrition are associated with epigenetic changes in fetal hypothalamic POMC and GR genes, potentially resulting in altered energy balance regulation in the offspring.

  5. Maternal obesity and Caesarean delivery in sub-Saharan Africa.

    PubMed

    Cresswell, Jenny A; Campbell, Oona M R; De Silva, Mary J; Slaymaker, Emma; Filippi, Veronique

    2016-07-01

    To quantify maternal obesity as a risk factor for Caesarean delivery in sub-Saharan Africa. Multivariable logistic regression analysis using 31 nationally representative cross-sectional data sets from the Demographic and Health Surveys (DHS). Maternal obesity was a risk factor for Caesarean delivery in sub-Saharan Africa; a clear dose-response relationship (where the magnitude of the association increased with increasing BMI) was observable. Compared to women of optimal weight, overweight women (BMI 25-29 kg/m(2) ) were significantly more likely to deliver by Caesarean (OR: 1.54; 95% CI: 1.33, 1.78), as were obese women (30-34.9 kg/m(2) (OR: 2.39; 95%CI: 1.96-2.90); 35-39.9 kg/m(2) (OR: 2.47 95%CI: 1.78-3.43)) and morbidly obese women (BMI ≥40 kg/m(2) OR: 3.85; 95% CI: 2.46-6.00). BMI is projected to rise substantially in sub-Saharan Africa over the next few decades and demand for Caesarean sections already exceeds available capacity. Overweight women should be advised to lose weight prior to pregnancy. Furthermore, culturally appropriate prevention strategies to discourage further population-level rises in BMI need to be designed and implemented. © 2016 The Authors. Tropical Medicine & International Health Published by John Wiley & Sons Ltd.

  6. Maternal Obesity, 25-Hydroxy Vitamin D Concentration, and Bone Density in Breastfeeding Dyads.

    PubMed

    Sen, Sarbattama; Penfield-Cyr, Annie; Hollis, Bruce W; Wagner, Carol L

    2017-08-01

    To examine the association between maternal body mass index (BMI) and serum 25-hydroxy vitamin D [25(OH)D] concentration and bone density in mother-infant pairs. The study was a secondary analysis of 234 exclusively breastfeeding dyads who were recruited in the first postpartum month for a randomized controlled trial of maternal vs infant vitamin D supplementation. Mean 25(OH)D concentrations and bone mineral density (BMD) were compared by BMI group. The adjusted association between maternal BMI and 25(OH)D and bone density was examined at 1, 4, and 7 months postpartum. Obese breastfeeding women had lower 25(OH)D concentrations and higher BMD than lean women at all 3 time points (P  <  .01). Higher maternal BMI was associated with lower maternal serum levels of 25(OH)D at 1, 4, and 7 months postpartum (adjusted β = -0.45 ng/ml per kg/m 2 , 95% CI -.076, -0.14, at 1 month) and higher BMD at the same time points (β = 0.006 BMD z score; 95% CI 0.003, 0.01 at 1 month). Seventy-six percent of infants were vitamin D deficient at 1 month of age. Infants born to overweight and obese mothers had lower 25(OH)D concentrations than infants of lean mothers (P < .01). For infants in the maternal supplementation group, higher maternal BMI was associated with lower 25(OH)D concentrations at 4 months (β = -0.68; 95% CI -1.17, -0.20) and lower bone density at 7 months (β = -0.001; 95% CI -0.002, -0.0001). In exclusively breastfeeding dyads, maternal obesity is associated with lower maternal and infant serum 25(OH)D concentrations, which may impact infant bone density. ClinicalTrials.gov: NCT00412074. Copyright © 2017 Elsevier Inc. All rights reserved.

  7. Overnutrition and maternal obesity in sheep pregnancy alter the JNK-IRS-1 signaling cascades and cardiac function in the fetal heart

    PubMed Central

    Wang, Jingying; Ma, Heng; Tong, Chao; Zhang, Hanying; Lawlis, Gavin B.; Li, Yuanda; Zang, Mengwei; Ren, Jun; Nijland, Mark J.; Ford, Stephen P.; Nathanielsz, Peter W.; Li, Ji

    2010-01-01

    Maternal obesity in pregnancy predisposes offspring to insulin resistance and associated cardiovascular disease. Here, we used a well-established sheep model to investigate the effects of maternal obesity on cardiac functions. Multiparous ewes were assigned to a control (CON) diet [100% of National Research Council (NRC) recommendations] or an obesogenic (OB) diet (150% of NRC recommendations) from 60 d before conception to necropsy on d 135 of pregnancy. Fetal blood glucose and insulin were increased (P<0.01, n=8) in OB (35.09±2.03 mg/dl and 3.40±1.43 μU/ml, respectively) vs. CON ewes (23.80±1.38 mg/dl and 0.769±0.256 μU/ml). Phosphorylation of AMP-activated protein kinase (AMPK), a cardioprotective signaling pathway, was reduced (P<0.05), while the stress signaling pathway, p38 MAPK, was up-regulated (P<0.05) in OB maternal and fetal hearts. Phosphorylation of c-Jun N-terminal kinase (JNK) and insulin receptor substrate-1 (IRS-1) at Ser-307 were increased (P<0.05) in OB fetal heart associated with lower downstream PI3K-Akt activity (P<0.05), indicating impaired cardiac insulin signaling. Although OB fetal hearts exhibited a normal contractile function vs. CON fetal hearts during basal perfusion, they developed an impaired heart-rate-left-ventricular-developed pressure product in response to high workload stress. Taken together, fetuses of OB mothers demonstrate alterations in cardiac PI3K-Akt, AMPK, and JNK-IRS-1 signaling pathways that would predispose them to insulin resistance and cardiac dysfunction.—Wang, J., Ma, H., Tong, C., Zhang, H., Lawlis, G. B., Li, Y., Zang, M., Ren, J., Nijland, M. J., Ford, S. P., Nathanielsz, P. W., Li, J. Overnutrition and maternal obesity in sheep pregnancy alter the JNK-IRS-1 signaling cascades and cardiac function in the fetal heart. PMID:20110268

  8. Maternal obesity induces sustained inflammation in both fetal and offspring large intestine of sheep.

    PubMed

    Yan, Xu; Huang, Yan; Wang, Hui; Du, Min; Hess, Bret W; Ford, Stephen P; Nathanielsz, Peter W; Zhu, Mei-Jun

    2011-07-01

    Both maternal obesity and inflammatory bowel diseases (IBDs) are increasing. It was hypothesized that maternal obesity induces an inflammatory response in the fetal large intestine, predisposing offspring to IBDs. Nonpregnant ewes were assigned to a control (Con, 100% of National Research Council [NRC] recommendations) or obesogenic (OB, 150% of NRC) diet from 60 days before conception. The large intestine was sampled from fetuses at 135 days (term 150 days) after conception and from offspring lambs at 22.5 ± 0.5 months of age. Maternal obesity enhanced mRNA expression tumor necrosis factor (TNF)α, interleukin (IL)1α, IL1β, IL6, IL8, and monocyte/macrophage chemotactic protein-1 (MCP1), as well as macrophage markers, CD11b, CD14, and CD68 in fetal gut. mRNA expression of Toll-like receptor (TLR) 2 and TLR4 was increased in OB versus Con fetuses; correspondingly, inflammatory NF-κB and JNK signaling pathways were also upregulated. Both mRNA expression and protein content of transforming growth factor (TGF) β was increased. The IL-17A mRNA expression and protein content was higher in OB compared to Con samples, which was associated with fibrosis in the large intestine of OB fetuses. Similar inflammatory responses and enhanced fibrosis were detected in OB compared to Con offspring. Maternal obesity induced inflammation and enhanced expression of proinflammatory cytokines in fetal and offspring large intestine, which correlated with increased TGFβ and IL17 expression. These data show that maternal obesity may predispose offspring gut to IBDs. Copyright © 2010 Crohn's & Colitis Foundation of America, Inc.

  9. Neonatal maternal separation up-regulates protein signalling for cell survival in rat hypothalamus.

    PubMed

    Irles, Claudine; Nava-Kopp, Alicia T; Morán, Julio; Zhang, Limei

    2014-05-01

    We have previously reported that in response to early life stress, such as maternal hyperthyroidism and maternal separation (MS), the rat hypothalamic vasopressinergic system becomes up-regulated, showing enlarged nuclear volume and cell number, with stress hyperresponsivity and high anxiety during adulthood. The detailed signaling pathways involving cell death/survival, modified by adverse experiences in this developmental window remains unknown. Here, we report the effects of MS on cellular density and time-dependent fluctuations of the expression of pro- and anti-apoptotic factors during the development of the hypothalamus. Neonatal male rats were exposed to 3 h-daily MS from postnatal days 2 to 15 (PND 2-15). Cellular density was assessed in the hypothalamus at PND 21 using methylene blue staining, and neuronal nuclear specific protein and glial fibrillary acidic protein immunostaining at PND 36. Expression of factors related to apoptosis and cell survival in the hypothalamus was examined at PND 1, 3, 6, 9, 12, 15, 20 and 43 by Western blot. Rats subjected to MS exhibited greater cell-density and increased neuronal density in all hypothalamic regions assessed. The time course of protein expression in the postnatal brain showed: (1) decreased expression of active caspase 3; (2) increased Bcl-2/Bax ratio; (3) increased activation of ERK1/2, Akt and inactivation of Bad; PND 15 and PND 20 were the most prominent time-points. These data indicate that MS can induce hypothalamic structural reorganization by promoting survival, suppressing cell death pathways, increasing cellular density which may alter the contribution of these modified regions to homeostasis.

  10. Dietary alleviation of maternal obesity and diabetes: increased resistance to diet-induced obesity transcriptional and epigenetic signatures.

    PubMed

    Attig, Linda; Vigé, Alexandre; Gabory, Anne; Karimi, Moshen; Beauger, Aurore; Gross, Marie-Sylvie; Athias, Anne; Gallou-Kabani, Catherine; Gambert, Philippe; Ekstrom, Tomas J; Jais, Jean-Philippe; Junien, Claudine

    2013-01-01

    According to the developmental origins of health and diseases (DOHaD), and in line with the findings of many studies, obesity during pregnancy is clearly a threat to the health and well-being of the offspring, later in adulthood. We previously showed that 20% of male and female inbred mice can cope with the obesogenic effects of a high-fat diet (HFD) for 20 weeks after weaning, remaining lean. However the feeding of a control diet (CD) to DIO mice during the periconceptional/gestation/lactation period led to a pronounced sex-specific shift (17% to 43%) from susceptibility to resistance to HFD, in the female offspring only. Our aim in this study was to determine how, in the context of maternal obesity and T2D, a CD could increase resistance on female fetuses. Transcriptional analyses were carried out with a custom-built mouse liver microarray and by quantitative RT-PCR for muscle and adipose tissue. Both global DNA methylation and levels of pertinent histone marks were assessed by LUMA and western blotting, and the expression of 15 relevant genes encoding chromatin-modifying enzymes was analyzed in tissues presenting global epigenetic changes. Resistance was associated with an enhancement of hepatic pathways protecting against steatosis, the unexpected upregulation of neurotransmission-related genes and the modulation of a vast imprinted gene network. Adipose tissue displayed a pronounced dysregulation of gene expression, with an upregulation of genes involved in lipid storage and adipocyte hypertrophy or hyperplasia in obese mice born to lean and obese mothers, respectively. Global DNA methylation, several histone marks and key epigenetic regulators were also altered. Whether they were themselves lean (resistant) or obese (sensitive), the offspring of lean and obese mice clearly differed in terms of several metabolic features and epigenetic marks suggesting that the effects of a HFD depend on the leanness or obesity of the mother.

  11. Maternal obesity programs mitochondrial and lipid metabolism gene expression in infant umbilical vein endothelial cells.

    PubMed

    Costa, S M R; Isganaitis, E; Matthews, T J; Hughes, K; Daher, G; Dreyfuss, J M; da Silva, G A P; Patti, M-E

    2016-11-01

    Maternal obesity increases risk for childhood obesity, but molecular mechanisms are not well understood. We hypothesized that primary umbilical vein endothelial cells (HUVEC) from infants of overweight and obese mothers would harbor transcriptional patterns reflecting offspring obesity risk. In this observational cohort study, we recruited 13 lean (pre-pregnancy body mass index (BMI) <25.0 kg m -2 ) and 24 overweight-obese ('ov-ob', BMI⩾25.0 kg m -2 ) women. We isolated primary HUVEC, and analyzed both gene expression (Primeview, Affymetrix) and cord blood levels of hormones and adipokines. A total of 142 transcripts were differentially expressed in HUVEC from infants of overweight-obese mothers (false discovery rate, FDR<0.05). Pathway analysis revealed that genes involved in mitochondrial and lipid metabolism were negatively correlated with maternal BMI (FDR<0.05). To test whether these transcriptomic patterns were associated with distinct nutrient exposures in the setting of maternal obesity, we analyzed the cord blood lipidome and noted significant increases in the levels of total free fatty acids (lean: 95.5±37.1 μg ml -1 , ov-ob: 124.1±46.0 μg ml -1 , P=0.049), palmitate (lean: 34.5±12.7 μg ml -1 , ov-ob: 46.3±18.4 μg ml -1 , P=0.03) and stearate (lean: 20.8±8.2 μg ml -1 , ov-ob: 29.7±17.2 μg ml -1 , P=0.04), in infants of overweight-obese mothers. Prenatal exposure to maternal obesity alters HUVEC expression of genes involved in mitochondrial and lipid metabolism, potentially reflecting developmentally programmed differences in oxidative and lipid metabolism.

  12. Gestational diabetes predicts the risk of childhood overweight and abdominal circumference independent of maternal obesity.

    PubMed

    Nehring, I; Chmitorz, A; Reulen, H; von Kries, R; Ensenauer, R

    2013-12-01

    Gestational diabetes mellitus is believed to be a risk factor for childhood overweight/obesity. We aimed to assess whether this association is either a reflection or independent of confounding by maternal BMI. Data from 7355 mother-child dyads of the German Perinatal Prevention of Obesity cohort with full anthropometric information on mothers and children, gestational diabetes and confounding factors were obtained at school entry health examination. We calculated crude and adjusted logistic regression models for the association of gestational diabetes and childhood overweight/obesity and abdominal adiposity defined by age- and sex-specific percentiles for BMI and waist circumference. Among all children (mean age 5.8 years), 8.1% were overweight, 2.6% were obese and 15.5% had abdominal adiposity. The prevalence of overweight (obesity) was 21% (8.2%) in children of mothers with gestational diabetes and 10.4% (2.4%) in children of healthy mothers. Analyses with adjustment for maternal BMI and other potential confounders yielded an odds ratio of 1.81 (95% CI 1.23-2.65) and 2.80 (95% CI 1.58-4.99) for the impact of gestational diabetes on childhood overweight and obesity, respectively. Similar results were obtained for the risk of childhood abdominal adiposity (odds ratio 1.64, 95% CI 1.16-2.33) by maternal gestational diabetes. The postulated increased risk of overweight and abdominal adiposity in offspring of mothers with gestational diabetes cannot be explained by maternal BMI alone and may be stronger for childhood obesity than for overweight. © 2013 The Authors. Diabetic Medicine © 2013 Diabetes UK.

  13. Preventing maternal and early childhood obesity: the fetal flaw in Australian perinatal care.

    PubMed

    Miller, Margaret; Hearn, Lydia; van der Pligt, Paige; Wilcox, Jane; Campbell, Karen J

    2014-01-01

    Almost half of Australian women of child-bearing age are overweight or obese, with a rate of 30-50% reported in early pregnancy. Maternal adiposity is a costly challenge for Australian obstetric care, with associated serious maternal and neonatal complications. Excess gestational weight gain is an important predictor of offspring adiposity into adulthood and higher maternal weight later in life. Current public health and perinatal care approaches in Australia do not adequately address excess perinatal maternal weight or gestational weight gain. This paper argues that the failure of primary health-care providers to offer systematic advice and support regarding women's weight and related lifestyle behaviours in child-bearing years is an outstanding 'missed opportunity' for prevention of inter-generational overweight and obesity. Barriers to action could be addressed through greater attention to: clinical guidelines for maternal weight management for the perinatal period, training and support of maternal health-care providers to develop skills and confidence in raising weight issues with women, a variety of weight management programs provided by state maternal health services, and clear referral pathways to them. Attention is also required to service systems that clearly define roles in maternal weight management and ensure consistency and continuity of support across the perinatal period.

  14. The impact of maternal obesity on iron status, placental transferrin receptor expression and hepcidin expression in human pregnancy.

    PubMed

    Garcia-Valdes, L; Campoy, C; Hayes, H; Florido, J; Rusanova, I; Miranda, M T; McArdle, H J

    2015-04-01

    Obesity is associated with decreased iron status, possibly due to a rise in hepcidin, an inflammatory protein known to reduce iron absorption. In animals, we have shown that maternal iron deficiency is minimised in the foetus by increased expression of placental transferrin receptor (pTFR1), resulting in increased iron transfer at the expense of maternal iron stores. This study examines the effect of obesity during pregnancy on maternal and neonatal iron status in human cohorts and whether the placenta can compensate for decreased maternal iron stores by increasing pTFR1 expression. A total of 240 women were included in this study. One hundred and fifty-eight placentas (Normal: 90; Overweight: 37; Obese: 31) were collected at delivery. Maternal iron status was measured by determining serum transferrin receptor (sTFR) and ferritin levels at 24 and 34 weeks and at delivery. Hepcidin in maternal and cord blood was measured by ELISA and pTFR1 in placentas by western blotting and real-time RT-PCR. Low iron stores were more common in obese women. Hepcidin levels (ng ml(-1)) at the end of the pregnancy were higher in obese than normal women (26.03±12.95 vs 18.00±10.77, P<0.05). Maternal hepcidin levels were correlated with maternal iron status (sTFR r=0.2 P=0.025), but not with neonatal values. mRNA and protein levels of pTFR1 were both inversely related to maternal iron status. For mRNA and all women, sTFR r=0.2 P=0.044. Ferritin mRNA levels correlated only in overweight women r=-0.5 P=0.039 with hepcidin (r=0.1 P=0.349), irrespective of maternal body mass index (BMI). The data support the hypothesis that obese pregnant women have a greater risk of iron deficiency and that hepcidin may be a regulatory factor. Further, we show that the placenta responds to decreased maternal iron status by increasing pTFR1 expression.

  15. Maternal and fetal outcomes in pregnancies complicated by overweight and obesity.

    PubMed

    Vernini, Joice Monaliza; Moreli, Jusciele Brogin; Magalhães, Claudia Garcia; Costa, Roberto Antônio Araújo; Rudge, Marilza Vieira Cunha; Calderon, Iracema Mattos Paranhos

    2016-08-27

    Overweight and obesity are associated with pregnancy complications and adverse perinatal outcomes, posing short and long-term risks for maternal and child health. This study evaluated maternal, delivery and neonatal outcomes in pregnancies complicated by overweight and obesity. This prospective cross-sectional study included 258 pregnant women. According to prepregnancy body mass index (BMI), participants were classified as normal weight, overweight, or obese. Data were analyzed using the chi-square test and analysis of variance followed by the Tukey test. Logistic regression was performed to calculate odds ratios and 95 % confidence intervals (p < 0.05). Most women ≥ 35 years old were overweight (22.7 %) and obese (27.6 %). Prepregnancy diabetes was significantly associated with obesity (15.7 %, p < 0.000). Obese women showed the lowest weight gain (9.6 ± 7.5Kg). Overweight and obese women practiced physical exercise more frequently (p = 0.010) than normal weight women. A greater proportion of obese mothers (13.4 %) had large for gestational age babies (p = 0.021), with higher thoracic circumference (33.6 ± 2.0 cm) and abdominal circumference (31.6 ± 2.3 cm). Obesity increased the risk of developing hypertension (OR = 7.0; 3.1-15.9), hyperglycemic disturbances (OR = 5.5; 2.9-10.6) and HbA1c ≥ 6.5 % (OR = 3.7; 1.2-11.1). The infants born to obese mothers had longer hospital stay (3.9 ± 3.9 days) (p = 0.005). Our results confirm that obesity in pregnancy can lead to adverse outcomes, and underscore the importance of identifying and treating inadequate weight status during pregnancy.

  16. Impact of Low Maternal Education on Early Childhood Overweight and Obesity in Europe.

    PubMed

    Ruiz, Milagros; Goldblatt, Peter; Morrison, Joana; Porta, Daniela; Forastiere, Francesco; Hryhorczuk, Daniel; Antipkin, Youriy; Saurel-Cubizolles, Marie-Josèphe; Lioret, Sandrine; Vrijheid, Martine; Torrent, Maties; Iñiguez, Carmen; Larrañaga, Isabel; Bakoula, Chryssa; Veltsista, Alexandra; van Eijsden, Manon; Vrijkotte, Tanja G M; Andrýsková, Lenka; Dušek, Ladislav; Barros, Henrique; Correia, Sofia; Järvelin, Marjo-Riitta; Taanila, Anja; Ludvigsson, Johnny; Faresjö, Tomas; Marmot, Michael; Pikhart, Hynek

    2016-05-01

    Comparable evidence on adiposity inequalities in early life is lacking across a range of European countries. This study investigates whether low maternal education is associated with overweight and obesity risk in children from distinct European settings during early childhood. Prospective data of 45 413 children from 11 European cohorts were used. Children's height and weight obtained at ages 4-7 years were used to assess prevalent overweight and obesity according to the International Obesity Task Force definition. The Relative/Slope Indices of Inequality (RII/SII) were estimated within each cohort and by gender to investigate adiposity risk among children born to mothers with low education as compared to counterparts born to mothers with high education. Individual-data meta-analyses were conducted to obtain aggregate estimates and to assess heterogeneity between cohorts. Low maternal education yielded a substantial risk of early childhood adiposity across 11 European countries. Low maternal education yielded a mean risk ratio of 1.58 (95% confidence interval (CI) 1.34, 1.85) and a mean risk difference of 7.78% (5.34, 10.22) in early childhood overweight, respectively, measured by the RII and SII. Early childhood obesity risk by low maternal education was as substantial for all cohorts combined (RII = 2.61 (2.10, 3.23)) and (SII = 4.01% (3.14, 4.88)). Inequalities in early childhood adiposity were consistent among boys, but varied among girls in a few cohorts. Considerable inequalities in overweight and obesity are evident among European children in early life. Tackling early childhood adiposity is necessary to promote children's immediate health and well-being and throughout the life course. © 2016 John Wiley & Sons Ltd.

  17. The role of gut microbiota in the effects of maternal obesity during pregnancy on offspring metabolism.

    PubMed

    Zhou, Liyuan; Xiao, Xinhua

    2018-04-27

    Obesity is considered a global epidemic. Specifically, obesity during pregnancy programs an increased risk of the offspring developing metabolic disorders in addition to the adverse effects on the mother per se Large numbers of human and animal studies have demonstrated that the gut microbiota plays a pivotal role in obesity and metabolic diseases. Similarly, maternal obesity during pregnancy is associated with alterations in the composition and diversity of the intestine microbial community. Recently, the microbiota in the placenta, amniotic fluid, and meconium in healthy gestations has been investigated, and the results supported the "in utero colonization hypothesis" and challenged the traditional "sterile womb" that has been acknowledged worldwide for more than a century. Thus, the offspring microbiota, which is crucial for the immune and metabolic function and further health in the offspring, might be established prior to birth. As a detrimental intrauterine environment, maternal obesity influences the microbial colonization and increases the risk of metabolic diseases in offspring. This review discusses the role of the microbiota in the impact of maternal obesity during pregnancy on offspring metabolism and further analyzes related probiotic or prebiotic interventions to prevent and treat obesity and metabolic diseases. © 2018 The Author(s).

  18. The role of gut microbiota in the effects of maternal obesity during pregnancy on offspring metabolism

    PubMed Central

    Zhou, Liyuan; Xiao, Xinhua

    2017-01-01

    Obesity is considered a global epidemic. Specifically, obesity during pregnancy programs an increased risk of the offspring developing metabolic disorders in addition to the adverse effects on the mother per se. Large numbers of human and animal studies have demonstrated that the gut microbiota plays a pivotal role in obesity and metabolic diseases. Similarly, maternal obesity during pregnancy is associated with alterations in the composition and diversity of the intestine microbial community. Recently, the microbiota in the placenta, amniotic fluid, and meconium in healthy gestations has been investigated, and the results supported the “in utero colonization hypothesis” and challenged the traditional “sterile womb” that has been acknowledged worldwide for more than a century. Thus, the offspring microbiota, which is crucial for the immune and metabolic function and further health in the offspring, might be established prior to birth. As a detrimental intrauterine environment, maternal obesity influences the microbial colonization and increases the risk of metabolic diseases in offspring. This review discusses the role of the microbiota in the impact of maternal obesity during pregnancy on offspring metabolism and further analyzes related probiotic or prebiotic interventions to prevent and treat obesity and metabolic diseases. PMID:29208770

  19. Maternal Obesity and Occurrence of Fetal Macrosomia: A Systematic Review and Meta-Analysis

    PubMed Central

    Gaudet, Laura; Ferraro, Zachary M.; Walker, Mark

    2014-01-01

    Objective. To determine a precise estimate for the contribution of maternal obesity to macrosomia. Data Sources. The search strategy included database searches in 2011 of PubMed, Medline (In-Process & Other Non-Indexed Citations and Ovid Medline, 1950–2011), and EMBASE Classic + EMBASE. Appropriate search terms were used for each database. Reference lists of retrieved articles and review articles were cross-referenced. Methods of Study Selection. All studies that examined the relationship between maternal obesity (BMI ≥30 kg/m2) (pregravid or at 1st prenatal visit) and fetal macrosomia (birth weight ≥4000 g, ≥4500 g, or ≥90th percentile) were considered for inclusion. Tabulation, Integration, and Results. Data regarding the outcomes of interest and study quality were independently extracted by two reviewers. Results from the meta-analysis showed that maternal obesity is associated with fetal overgrowth, defined as birth weight ≥ 4000 g (OR 2.17, 95% CI 1.92, 2.45), birth weight ≥4500 g (OR 2.77,95% CI 2.22, 3.45), and birth weight ≥90% ile for gestational age (OR 2.42, 95% CI 2.16, 2.72). Conclusion. Maternal obesity appears to play a significant role in the development of fetal overgrowth. There is a critical need for effective personal and public health initiatives designed to decrease prepregnancy weight and optimize gestational weight gain. PMID:25544943

  20. Maternal prepregnancy obesity and achievement of infant motor developmental milestones in the upstate KIDS study.

    PubMed

    Wylie, Amanda; Sundaram, Rajeshwari; Kus, Christopher; Ghassabian, Akhgar; Yeung, Edwina H

    2015-04-01

    Maternal prepregnancy obesity is associated with several poor infant health outcomes; however, studies that investigated motor development have been inconsistent. Thus, maternal prepregnancy weight status and infants' gross motor development were examined. Participants consisted of 4,901 mother-infant pairs from the Upstate KIDS study, a longitudinal cohort in New York. Mothers indicated dates when infants achieved each of six gross motor milestones when infants were 4, 8, 12, 18, and 24 months old. Failure time modeling under a Weibull distribution was utilized to compare time to achievement across three levels of maternal prepregnancy BMI. Hazard ratios (HR) below one indicate a lower "risk" of achieving the milestone and translate to later achievement. Compared to infants born to thin and normal-weight mothers (BMI < 25), infants born to mothers with obesity (BMI > 30) were slower to sit without support (HR = 0.91, P = 0.03) and crawl on hands and knees (HR = 0.86, P < 0.001), after adjusting for maternal and birth characteristics. Increased gestational age was associated with faster achievement of all milestones, but additional adjustment did not impact results. Maternal prepregnancy obesity was associated with a slightly longer time for infant to sit and crawl, potentially due to a compromised intrauterine environment or reduced physically active play. © 2015 The Obesity Society.

  1. Pathways from Maternal Effortful Control to Child Self-Regulation: The Role of Maternal Emotional Support

    PubMed Central

    Zeytinoglu, Selin; Calkins, Susan D.; Swingler, Margaret M.; Leerkes, Esther M.

    2016-01-01

    This study examined the direct and indirect pathways from maternal effortful control to two aspects of children’s self-regulation – executive functioning and behavioral regulation – via maternal emotional support. Two hundred and seventy eight children and their primary caregivers (96% mothers) participated in laboratory visits when children were 4 and 5 years, and teachers reported on children’s behavior at kindergarten. At the 4-year assessment, maternal effortful control was measured using the Adult Temperament Questionnaire (ATQ; Evans & Rothbart, 2007) and maternal emotional support was observed during a semi-structured mother-child problem-solving task. At the 5-year assessment, children’s executive functioning was measured using laboratory tasks designed to assess updating/working memory, inhibitory control, and cognitive flexibility, whereas behavioral regulation was assessed via teacher-report questionnaires on children’s attention control, discipline and persistence, and work habits. Results from structural equation modeling indicated that, after controlling for child gender and minority status, and maternal education, maternal effortful control was indirectly associated with both child executive functioning and behavioral regulation through maternal emotional support. Maternal effortful control had a direct association with children’s teacher-reported behavioral regulation but not observed executive functioning. These findings suggest that maternal effortful control may be a key contributing factor to the development of children’s self-regulatory competencies through its impact on maternal emotional support. PMID:27929315

  2. Pathways from maternal effortful control to child self-regulation: The role of maternal emotional support.

    PubMed

    Zeytinoglu, Selin; Calkins, Susan D; Swingler, Margaret M; Leerkes, Esther M

    2017-03-01

    This study examined the direct and indirect pathways from maternal effortful control to 2 aspects of children's self-regulation-executive functioning and behavioral regulation-via maternal emotional support. Two hundred seventy-eight children and their primary caregivers (96% mothers) participated in laboratory visits when children were 4 and 5 years, and teachers reported on children's behavior at kindergarten. At the 4-year assessment, maternal effortful control was measured using the Adult Temperament Questionnaire (Evans & Rothbart, 2007) and maternal emotional support was observed during a semistructured mother-child problem-solving task. At the 5-year assessment, children's executive functioning was measured using laboratory tasks designed to assess updating/working memory, inhibitory control, and cognitive flexibility, whereas behavioral regulation was assessed via teacher-report questionnaires on children's attention control, discipline and persistence, and work habits. Results from structural equation modeling indicated that, after controlling for child gender and minority status, and maternal education, maternal effortful control was indirectly associated with both child executive functioning and behavioral regulation through maternal emotional support. Maternal effortful control had a direct association with children's teacher-reported behavioral regulation but not observed executive functioning. These findings suggest that maternal effortful control may be a key contributing factor to the development of children's self-regulatory competencies through its impact on maternal emotional support. (PsycINFO Database Record (c) 2017 APA, all rights reserved).

  3. Examining Maternal Psychopathology, Family Functioning and Coping Skills in Childhood Obesity: A Case-Control Study.

    PubMed

    Blanco, Miriam; Sepulveda, Ana R; Lacruz, Tatiana; Parks, Melissa; Real, Beatriz; Martin-Peinador, Yolanda; Román, Francisco J

    2017-09-01

    The shared family environment is an important risk factor in the development of childhood obesity. This study aims to examine differences in maternal psychopathology, family functioning, expressed emotion and coping skills between families of a child with obesity and those with a normal-weight child. This case-control study consisted of 50 mothers with a child (age 8-12 years) with obesity (p ≥ 97) and a control group of 50 mothers of a child with normal weight (p < 85), matched for age, sex and socio-economic status. Compared with families with normal-weight children, those with children with obesity showed significant differences in levels of trait anxiety, criticism and over-protectiveness, and maladaptive coping skills. Structural equation modelling revealed that the mothers' psychopathology predicted children's body mass index (BMI) z-scores through expressed emotion and maladaptive coping scores. There were significant direct and indirect relations among maternal BMI, psychopathology, expressed emotion and coping, which all together explained 26.5% of variance of children's BMI z-scores. Considering this relation between maternal variables and child weight status, childhood obesity intervention programs may benefit from targeting maternal BMI, psychopathology, expressed emotion and coping skills. Copyright © 2017 John Wiley & Sons, Ltd and Eating Disorders Association. Copyright © 2017 John Wiley & Sons, Ltd and Eating Disorders Association.

  4. Dysregulation of Placental miRNA in Maternal Obesity Is Associated With Pre- and Postnatal Growth.

    PubMed

    Carreras-Badosa, Gemma; Bonmatí, Alexandra; Ortega, Francisco-Jose; Mercader, Josep-Maria; Guindo-Martínez, Marta; Torrents, David; Prats-Puig, Anna; Martinez-Calcerrada, Jose-Maria; de Zegher, Francis; Ibáñez, Lourdes; Fernandez-Real, Jose-Manuel; Lopez-Bermejo, Abel; Bassols, Judit

    2017-07-01

    Human placenta exhibits a specific microRNA (miRNA) expression pattern. Some of these miRNAs are dysregulated in pregnancy disorders such as preeclampsia and intrauterine growth restriction and are potential biomarkers for these pathologies. To study the placental miRNA profile in pregnant women with pregestational overweight/obesity (preOB) or gestational obesity (gestOB) and explore the associations between placental miRNAs dysregulated in maternal obesity and prenatal and postnatal growth. TaqMan Low Density Arrays and real-time polymerase chain reaction were used to profile the placental miRNAs in 70 pregnant women (20 preOB, 25 gestOB, and 25 control). Placentas and newborns were weighed at delivery, and infants were weighed at 1, 4, and 12 months of age. Eight miRNAs were decreased in placentas from preOB or gestOB (miR-100, miR-1269, miR-1285, miR-181, miR-185, miR-214, miR-296, and miR-487) (all P < 0.05). Among them, miR-100, miR-1285, miR-296, and miR-487 were associated with maternal metabolic parameters (all P < 0.05) and were predictors of lower birth weight (all P < 0.05; R2 > 30%) and increased postnatal weight gain (all P < 0.05; R2 > 20%). In silico analysis showed that these miRNAs were related to cell proliferation and insulin signaling pathways. miR-296 was also present in plasma samples and associated with placental expression and prenatal and postnatal growth parameters (all P < 0.05). We identified a specific placental miRNA profile in maternal obesity. Placental miRNAs dysregulated in maternal obesity may be involved in mediation of growth-promoting effects of maternal obesity on offspring and could be used as early markers of prenatal and postnatal growth. Copyright © 2017 Endocrine Society

  5. Association between maternal obesity and offspring Apgar score or cord pH: a systematic review and meta-analysis.

    PubMed

    Zhu, Tingting; Tang, Jun; Zhao, Fengyan; Qu, Yi; Mu, Dezhi

    2015-12-22

    Previous results are inconsistent regarding the association between maternal obesity and Apgar score or cord pH in humans. The aim of this study was to investigate the association between maternal pre-pregnancy and pregnancy body mass index (BMI) and infant Apgar score or cord pH. We conducted a systematic review of studies published in English before 20 August 2015 using PubMed, EMBASE, and Cochrane Library. Eleven cohort studies with a total of 2,586,265 participants finally met our inclusion criteria. Pooled results revealed the following factors associated with Apgar score <7 at 5 minutes: overweight (odds ratio [OR] 1.13; 95% confidence interval [CI], 1.08-1.20), obese (OR 1.40; 95% CI, 1.27-1.54), and very obese (OR 1.71; 95% CI, 1.55-1.89). The pooled analysis also revealed that maternal overweight or obesity increased the risk for Apgar score <7 at 1 minute. There was no association between maternal BMI and neonatal cord pH. Thus, this study suggests that maternal overweight and obesity affect baby's condition immediately after birth in general. More studies are needed to confirm these results and detect the influence of variables across studies.

  6. Obesity promotes resistance to anti-VEGF therapy in breast cancer by up-regulating IL-6 and potentially FGF-2.

    PubMed

    Incio, Joao; Ligibel, Jennifer A; McManus, Daniel T; Suboj, Priya; Jung, Keehoon; Kawaguchi, Kosuke; Pinter, Matthias; Babykutty, Suboj; Chin, Shan M; Vardam, Trupti D; Huang, Yuhui; Rahbari, Nuh N; Roberge, Sylvie; Wang, Dannie; Gomes-Santos, Igor L; Puchner, Stefan B; Schlett, Christopher L; Hoffmman, Udo; Ancukiewicz, Marek; Tolaney, Sara M; Krop, Ian E; Duda, Dan G; Boucher, Yves; Fukumura, Dai; Jain, Rakesh K

    2018-03-14

    Anti-vascular endothelial growth factor (VEGF) therapy has failed to improve survival in patients with breast cancer (BC). Potential mechanisms of resistance to anti-VEGF therapy include the up-regulation of alternative angiogenic and proinflammatory factors. Obesity is associated with hypoxic adipose tissues, including those in the breast, resulting in increased production of some of the aforementioned factors. Hence, we hypothesized that obesity could contribute to anti-VEGF therapy's lack of efficacy. We found that BC patients with obesity harbored increased systemic concentrations of interleukin-6 (IL-6) and/or fibroblast growth factor 2 (FGF-2), and their tumor vasculature was less sensitive to anti-VEGF treatment. Mouse models revealed that obesity impairs the effects of anti-VEGF on angiogenesis, tumor growth, and metastasis. In one murine BC model, obesity was associated with increased IL-6 production from adipocytes and myeloid cells within tumors. IL-6 blockade abrogated the obesity-induced resistance to anti-VEGF therapy in primary and metastatic sites by directly affecting tumor cell proliferation, normalizing tumor vasculature, alleviating hypoxia, and reducing immunosuppression. Similarly, in a second mouse model, where obesity was associated with increased FGF-2, normalization of FGF-2 expression by metformin or specific FGF receptor inhibition decreased vessel density and restored tumor sensitivity to anti-VEGF therapy in obese mice. Collectively, our data indicate that obesity fuels BC resistance to anti-VEGF therapy via the production of inflammatory and angiogenic factors. Copyright © 2018 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.

  7. Maternal BMI as a predictor of methylation of obesity-related genes in saliva samples from preschool-age Hispanic children at-risk for obesity.

    PubMed

    Oelsner, Kathryn Tully; Guo, Yan; To, Sophie Bao-Chieu; Non, Amy L; Barkin, Shari L

    2017-01-09

    The study of epigenetic processes and mechanisms present a dynamic approach to assess complex individual variation in obesity susceptibility. However, few studies have examined epigenetic patterns in preschool-age children at-risk for obesity despite the relevance of this developmental stage to trajectories of weight gain. We hypothesized that salivary DNA methylation patterns of key obesogenic genes in Hispanic children would 1) correlate with maternal BMI and 2) allow for identification of pathways associated with children at-risk for obesity. Genome-wide DNA methylation was conducted on 92 saliva samples collected from Hispanic preschool children using the Infinium Illumina HumanMethylation 450 K BeadChip (Illumina, San Diego, CA, USA), which interrogates >484,000 CpG sites associated with ~24,000 genes. The analysis was limited to 936 genes that have been associated with obesity in a prior GWAS Study. Child DNA methylation at 17 CpG sites was found to be significantly associated with maternal BMI, with increased methylation at 12 CpG sites and decreased methylation at 5 CpG sites. Pathway analysis revealed methylation at these sites related to homocysteine and methionine degradation as well as cysteine biosynthesis and circadian rhythm. Furthermore, eight of the 17 CpG sites reside in genes (FSTL1, SORCS2, NRF1, DLC1, PPARGC1B, CHN2, NXPH1) that have prior known associations with obesity, diabetes, and the insulin pathway. Our study confirms that saliva is a practical human tissue to obtain in community settings and in pediatric populations. These salivary findings indicate potential epigenetic differences in Hispanic preschool children at risk for pediatric obesity. Identifying early biomarkers and understanding pathways that are epigenetically regulated during this critical stage of child development may present an opportunity for prevention or early intervention for addressing childhood obesity. The clinical trial protocol is available at Clinical

  8. Central role for melanocortin-4 receptors in offspring hypertension arising from maternal obesity

    PubMed Central

    Samuelsson, Anne-Maj S.; Mullier, Amandine; Maicas, Nuria; Oosterhuis, Nynke R.; Eun Bae, Sung; Novoselova, Tatiana V.; Chan, Li F.; Pombo, Joaquim M.; Taylor, Paul D.; Joles, Jaap A.; Coen, Clive W.; Balthasar, Nina; Poston, Lucilla

    2016-01-01

    Melanocortin-4 receptor (Mc4r)–expressing neurons in the autonomic nervous system, particularly in the paraventricular nucleus of the hypothalamus (PVH), play an essential role in blood pressure (BP) control. Mc4r-deficient (Mc4rKO) mice are severely obese but lack obesity-related hypertension; they also show a reduced pressor response to salt loading. We have previously reported that lean juvenile offspring born to diet-induced obese rats (OffOb) exhibit sympathetic-mediated hypertension, and we proposed a role for postnatally raised leptin in its etiology. Here, we test the hypothesis that neonatal hyperleptinemia due to maternal obesity induces persistent changes in the central melanocortin system, thereby contributing to offspring hypertension. Working on the OffOb paradigm in both sexes and using transgenic technology to restore Mc4r in the PVH of Mc4rKO (Mc4rPVH) mice, we have now shown that these mice develop higher BP than Mc4rKO or WT mice. We have also found that experimental hyperleptinemia induced in the neonatal period in Mc4rPVH and WT mice, but not in the Mc4rKO mice, leads to heightened BP and severe renal dysfunction. Thus, Mc4r in the PVH appears to be required for early-life programming of hypertension arising from either maternal obesity or neonatal hyperleptinemia. Early-life exposure of the PVH to maternal obesity through postnatal elevation of leptin may have long-term consequences for cardiovascular health. PMID:27791019

  9. RNA-seq analysis of the rat placentation site reveals maternal obesity-associated changes in placental and offspring thyroid hormone signaling

    USDA-ARS?s Scientific Manuscript database

    Introduction In animal models, maternal obesity (OB) leads to augmented risk of offspring OB. While placental function is influenced by maternal habitus, the effect of maternal obesity on the interacting zones of the placenta [the labyrinth (LZ), junctional (JZ) and metrial gland (MG)] remains unkno...

  10. Persistent influence of maternal obesity on offspring health: Mechanisms from animal models and clinical studies.

    PubMed

    Wankhade, Umesh D; Thakali, Keshari M; Shankar, Kartik

    2016-11-05

    The consequences of excessive maternal weight and adiposity at conception for the offspring are now well recognized. Maternal obesity increases the risk of overweight and obesity even in children born with appropriate-for-gestational age (AGA) birth weights. Studies in animal models have employed both caloric excess and manipulation of macronutrients (especially high-fat) to mimic hypercaloric intake present in obesity. Findings from these studies show transmission of susceptibility to obesity, metabolic dysfunction, alterations in glucose homeostasis, hepatic steatosis, skeletal muscle metabolism and neuroendocrine changes in the offspring. This review summarizes the essential literature in this area in both experimental and clinical domains and focuses on the translatable aspects of these experimental studies. Moreover this review highlights emerging mechanisms broadly explaining maternal obesity-associated developmental programming. The roles of early developmental alterations and placental adaptations are also reviewed. Increasing evidence also points to changes in the epigenome and other emerging mechanisms such as alterations in the microbiome that may contribute to persistent changes in the offspring. Finally, we examine potential interventions that have been employed in clinical cohorts. Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.

  11. Sexual dimorphism in the effect of maternal obesity on antioxidant defense mechanisms in the human placenta.

    PubMed

    Evans, LaShauna; Myatt, Leslie

    2017-03-01

    Maternal obesity creates an adverse intrauterine environment, negatively impacts placental respiration, is associated with a higher incidence of pregnancy complications and programs the offspring for disease in adult life in a sexually dimorphic manner. We defined the effect of maternal obesity and fetal sex on pro- and anti-oxidant status in placenta and placental mitochondria. Placental villous tissue was collected at term via c-section prior to labor from four groups of patients based on fetal sex and prepregnancy/1st trimester body mass index: lean - BMI 22.1 ± 0.3 (6 male, 6 female) and obese - BMI 36.3 ± 0.4 (6 male, 6 female). Antioxidant enzyme activity, mitochondrial protein carbonyls, nitrotyrosine residues, total and nitrated superoxide dismutase (SOD) and nitric oxide synthesis were measured. Maternal obesity was associated with decreased SOD and catalase activity, and total antioxidant capacity (TAC), but increased oxidative (protein carbonyls) and nitrative (nitrotyrosine) stress in a sexually dimorphic manner. Placentas of lean women with a male fetus had higher SOD activity and TAC (p < 0.05) than other groups whereas obese women with a male fetus had highest carbonyls and nitrotyrosine (p < 0.05). Glutathione peroxidase and thioredoxin reductase activity increased with obesity, significantly with a male fetus, perhaps as a compensatory response. Maternal obesity affects oxidative stress and antioxidant activity in the placenta in a sexually dimorphic manner. The male fetus of a lean women has the highest antioxidant activity, a protection which is lost with obesity perhaps contributing to the increased incidence of adverse outcomes with a male fetus. Copyright © 2017 Elsevier Ltd. All rights reserved.

  12. The impact of maternal obesity and race/ethnicity on perinatal outcomes: independent and joint effects

    PubMed Central

    Snowden, Jonathan M; Mission, John F; Marshall, Nicole E; Quigley, Brian; Main, Elliott; Gilbert, William M; Chung, Judith H; Caughey, Aaron B

    2016-01-01

    Objective We characterized independent and joint impacts of maternal race/ethnicity and obesity on adverse birth outcomes, including preeclampsia, low birthweight (LBW), and macrosomia. Methods Retrospective cohort study of all 2007 California births using vital records and claims data. Maternal race/ethnicity and maternal BMI were the key exposures; we analyzed their independent and joint impact on outcomes using regression models. Results Racial/ethnic minority women of normal weight generally had higher risk as compared to white women of normal weight (e.g., African-American women, preeclampsia aOR, 1.60, 95% CI: 1.48 – 1.74, versus white women). However, elevated BMI did not usually confer additional risk (e.g., preeclampsia aOR comparing African-American women with morbid obesity to white women with morbid obesity; 1.17, 95% CI: 0.89 – 1.54). Obesity was a risk factor for LBW only among white women (morbid obesity aOR, 95% CI: 1.24, 1.04 – 1.49, versus white women of normal weight), and not among racial/ethnic minority women (e.g., African-American women, 0.95, 0.83 – 1.08). Conclusions These findings add nuance to our understanding of the interplay between maternal race/ethnicity, BMI, and perinatal outcomes. While the BMI/adverse outcome gradient appears weaker in racial/ethnic minority women, this reflects the overall risk increase in racial/ethnic minority women of all body sizes. PMID:27222008

  13. Effect of diet-induced maternal obesity on fetal skeletal development

    USDA-ARS?s Scientific Manuscript database

    The maternal environment, in particular nutritional status and diet composition during pregnancy, can alter the developmental trajectory of the fetus and change the risk for chronic disease processes such as cardiovascular disease, obesity, diabetes and cancer in the offspring. This knowledge suppor...

  14. Disturbed nitric oxide and homocysteine production are involved in the increased risk of cardiovascular diseases in the F1 offspring of maternal obesity and malnutrition.

    PubMed

    Moussa, Y Y; Tawfik, S H; Haiba, M M; Saad, M I; Hanafi, M Y; Abdelkhalek, T M; Oriquat, G A; Kamel, M A

    2017-06-01

    The present study aimed to evaluate the changes in levels of different independent risk factors for vascular diseases in the rat offspring of maternal obesity and malnutrition as maternal health disturbances are thought to have direct consequences on the offspring health. The effect of postnatal diet on the offspring was also assessed. Three groups of female Wistar rats were used (control, obese and malnourished). After the pregnancy and delivery, the offspring were weaned to control diet or high-caloric (HCD) diet and followed up for 30 weeks. Every 5 weeks postnatal, 20 pups (10 males and 10 females) of each subgroup were sacrificed after overnight fasting, the blood sample was obtained, and the rats were dissected out to obtain heart muscle. The following parameters were assessed; lipid profile, NEFA, homocysteine (Hcy), nitric oxide end product (NOx) and myocardial triglyceride content. Maternal obesity and malnutrition caused significant elevation in the body weight, triglycerides, NEFA, Hcy and NOx in the F1 offspring especially those maintained under HCD. Also, the male offspring showed more prominent changes than female offspring. Maternal malnutrition and obesity may increase the risk of the development of cardiovascular diseases in the offspring, especially the male ones.

  15. No Association between Maternal Pre-pregnancy Obesity and Risk of Hypospadias or Cryptorchidism in Male Newborns

    PubMed Central

    Adams, Scott V.; Hastert, Theresa A.; Huang, Yi; Starr, Jacqueline R.

    2011-01-01

    BACKGROUND Hypospadias and cryptorchidism, two relatively common male genital anomalies, may be caused by altered maternal hormone levels, blood glucose levels, or nutritional deficiencies. Maternal obesity, which increases risk of diabetes and could influence hormone levels, may therefore be associated with risk of hypospadias and cryptorchidism. The purpose of this study was to assess the association between pre-pregnancy maternal obesity and hypospadias and cryptorchidism. METHODS We conducted a case-control study of hypospadias and cryptorchidism in male singleton newborns using Washington State birth records from 1992 to 2008 linked to birth-hospitalization discharge records. Maternal pre-pregnancy body mass index (BMI) was calculated from pre-pregnancy weight and height. Adjusted odds ratios (aORs) and 95% confidence intervals (95% CIs) for hypospadias or cryptorchidism were estimated by fitting multivariable logistic regression models adjusted for year of birth, and maternal age, education, parity, race, and cigarette smoking during pregnancy. RESULTS The complete-case analysis included 2,219 hypospadias cases, 2,563 cryptorchidism cases, and 32,734 controls. Maternal obesity (BMI ≥ 30 kg/m2) was not associated with risk of hypospadias or cryptorchidism in male offspring (aOR(95% CI), hypospadias: 1.07(0.95–1.21); cryptorchidism: 0.99(0.89–1.11)), and no trend in risk with increasing maternal BMI was found. There was little indication of risk associated with BMI among any sub-group of mothers examined, including women with pre-existing diabetes or hypertension, women who developed preeclampsia, non-Hispanic white women, first-time mothers, or mothers aged ≥30 years. CONCLUSIONS The results of this study do not support the hypothesis that pre-pregnancy maternal obesity is a cause of hypospadias or cryptorchidism in male infants. PMID:21462299

  16. Effect of breastfeeding on obesity of schoolchildren: influence of maternal education

    PubMed Central

    Pudla, Katia Jakovljevic; Gonzaléz-Chica, David Alejandro; de Vasconcelos, Francisco de Assis Guedes

    2015-01-01

    Abstract Objective: To evaluate the association between duration of breastfeeding (BF) and obesity in schoolchildren of Florianópolis (SC), and the role of possible effect modifiers. Methods: Cross-sectional study with a random sample of 2826 schoolchildren (7-14 years). Weight and height were measured according to standardized procedures. Data concerning BF and sociodemographic variables were obtained from a questionnaire sent to parents/guardians. Children's nutritional status was evaluated by BMI-for-age z-score for gender (WHO reference curves). Adjusted analyses were performed through logistic regression, considering a possible interaction among variables. Results: Prevalence of obesity was 8.6% (95% CI: 7.6-9.7%) and 55.7% (95% CI: 53.8-57.6%) received breastmilk for ≥6 months. BF was not associated with obesity, even in the adjusted analysis. Stratified analysis according to maternal schooling showed that, in children aged 7-10 years and children whose mothers had 0-8 years of schooling, the chance of obesity was lower among those breastfeed for >1 month, especially among those who received breastmilk for 1-5 months (OR=0.22; 95% CI 0.08-0.62). Among children of women with higher schooling (>8 years), the chance of obesity was 44% lower in those who were breastfed for >12 months (p-value for interaction <0.01). This interaction was not found in older children (11-14 years). Conclusions: Among children of women with lower schooling, BF for any period longer than 1 month is protective against obesity; however, for a higher maternal schooling, BF for less than 12 months increases the odds of obesity. PMID:26100592

  17. Maternal gestational diabetes mellitus and overweight and obesity in offspring: a study in Chinese children.

    PubMed

    Zhao, Y L; Ma, R M; Lao, T T; Chen, Z; Du, M Y; Liang, K; Huang, Y K; Zhang, L; Yang, M H; Sun, Y H; Li, H; Ding, Z B

    2015-12-01

    The purpose of this study was to investigate the effects of maternal gestational diabetes mellitus (GDM) and breast feeding on childhood overweight and obesity in a mainland Chinese population. The incidence of and factors associated with overweight and obesity were compared between children of mothers with (n=1068) and without (n=1756) GDM. The independent roles of the associated factors were examined by multiple logistic regression analysis. The incidence of overweight was higher (16.6 v. 12.6%, P=0.002) in the GDM group, but that of obesity was not different (10.7 v. 12.0%, P=0.315). At age 1-2 and 2-5 years, no difference in overweight (11.0 v. 12.0%, P=0.917, and 15.7 v. 14.6%, P=0.693, respectively) was found, while obesity (8.0 v. 13.6%, P=0.019, and 8.4 v. 13.4%, P=0.014, respectively) was less frequent in the GDM offspring. At age 5-10 years, increased overweight (22.2 v. 12.1%, P<0.001) and obesity (15.9 v. 9.0%, P=0.001) were found in the GDM group, which was associated with maternal obesity, being born large-for-gestational age, male gender and formula feeding. After adjusting for confounding factors, GDM remained an independent determinant of offspring overweight and obesity (aOR 2.28, 95% CI 1.61-3.22), suggesting that the effects of GDM were independent of breast feeding, as well as of maternal obesity and birth size.

  18. Maternal History of Child Abuse and Obesity Risk in Offspring: Mediation by Weight in Pregnancy.

    PubMed

    Leonard, Stephanie A; Petito, Lucia C; Rehkopf, David H; Ritchie, Lorrene D; Abrams, Barbara

    2017-08-01

    Women's experience of childhood adversity may contribute to their children's risk of obesity. Possible causal pathways include higher maternal weight and gestational weight gain, which have been associated with both maternal childhood adversity and obesity in offspring. This study included 6718 mother-child pairs from the National Longitudinal Survey of Youth 1979 in the United States (1979-2012). We applied multiple log-binomial regression models to estimate associations between three markers of childhood adversity (physical abuse, household alcoholism, and household mental illness) and offspring obesity in childhood. We estimated natural direct effects to evaluate mediation by prepregnancy BMI and gestational weight gain. Among every 100 mothers who reported physical abuse in childhood, there were 3.7 (95% confidence interval: -0.1 to 7.5) excess cases of obesity in 2- to 5-year olds compared with mothers who did not report physical abuse. Differences in prepregnancy BMI, but not gestational weight gain, accounted for 25.7% of these excess cases. There was no evidence of a similar relationship for household alcoholism or mental illness or for obesity in older children. In this national, prospective cohort study, prepregnancy BMI partially explained an association between maternal physical abuse in childhood and obesity in preschool-age children. These findings underscore the importance of life-course exposures in the etiology of child obesity and the potential multi-generational consequences of child abuse. Research is needed to determine whether screening for childhood abuse and treatment of its sequelae could strengthen efforts to prevent obesity in mothers and their children.

  19. Nicotinamide mononucleotide (NMN) supplementation ameliorates the impact of maternal obesity in mice: comparison with exercise.

    PubMed

    Uddin, Golam Mezbah; Youngson, Neil A; Doyle, Bronte M; Sinclair, David A; Morris, Margaret J

    2017-11-08

    Maternal overnutrition increases the risk of long-term metabolic dysfunction in offspring. Exercise improves metabolism partly by upregulating mitochondrial biogenesis or function, via increased levels of nicotinamide adenine dinucleotide (NAD + ). We have shown that the NAD + precursor, nicotinamide mononucleotide (NMN) can reverse some of the negative consequences of high fat diet (HFD) consumption. To investigate whether NMN can impact developmentally-set metabolic deficits, we compared treadmill exercise and NMN injection in offspring of obese mothers. Five week old lean and obese female C57BL6/J mice were mated with chow fed males. Female offspring weaned onto HFD were given treadmill exercise for 9 weeks, or NMN injection daily for 18 days. Maternal obesity programmed increased adiposity and liver triglycerides, with decreased glucose tolerance, liver NAD + levels and citrate synthase activity in offspring. Both interventions reduced adiposity, and showed a modest improvement in glucose tolerance and improved markers of mitochondrial function. NMN appeared to have stronger effects on liver fat catabolism (Hadh) and synthesis (Fasn) than exercise. The interventions appeared to exert the most global benefit in mice that were most metabolically challenged (HFD-consuming offspring of obese mothers). This work encourages further study to confirm the suitability of NMN for use in reversing metabolic dysfunction linked to programming by maternal obesity.

  20. Childhood overweight and obesity among Kenyan pre-school children: association with maternal and early child nutritional factors.

    PubMed

    Gewa, Constance A

    2010-04-01

    To report on the prevalence of overweight and obesity among pre-school children in Kenya and examine the associations between childhood overweight and selected maternal and child-related factors. Demographic Health Survey data, multistage stratified cluster sampling methodology. Rural and urban areas of Kenya. A total of 1495 children between the ages of 3 and 5 years in Kenya. Over 30 % of the children were stunted, approximately 16 % were underweight, 4 % were wasted, approximately 18 % were overweight and 4 % were obese; 8 % were both overweight/obese and stunted. Maternal overweight and obesity, higher levels of maternal education, being a large or very large child at birth, and being stunted were each associated with higher odds of overweight and obesity among Kenyan children. Older children and large household size were each associated with lower odds of overweight and obesity among Kenyan children. The analysis demonstrates the presence of under- and overnutrition among Kenyan pre-school children and the importance of focusing on expanding efforts to prevent and treat malnutrition within this population. It also identifies some of the modifiable factors that can be targeted in these efforts.

  1. A Review of the Impact of Maternal Obesity on the Cognitive Function and Mental Health of the Offspring.

    PubMed

    Contu, Laura; Hawkes, Cheryl A

    2017-05-19

    Globally, more than 20% of women of reproductive age are currently estimated to be obese. Children born to obese mothers are at higher risk of developing obesity, coronary heart disease, diabetes, stroke, and asthma in adulthood. Increasing clinical and experimental evidence suggests that maternal obesity also affects the health and function of the offspring brain across the lifespan. This review summarizes the current findings from human and animal studies that detail the impact of maternal obesity on aspects of learning, memory, motivation, affective disorders, attention-deficit hyperactivity disorder, autism spectrum disorders, and neurodegeneration in the offspring. Epigenetic mechanisms that may contribute to this mother-child interaction are also discussed.

  2. Obesity and overweight: Impact on maternal and milk microbiome and their role for infant health and nutrition.

    PubMed

    Garcia-Mantrana, Izaskun; Collado, Maria Carmen

    2016-08-01

    Obesity, particularly in infants, is becoming a significant public health problem that has reached "epidemic" status worldwide. Obese children have an increased risk of developing obesity-related diseases, such as metabolic syndromes and diabetes, as well as increased risk of mortality and adverse health outcomes later in life. Experimental data show that maternal obesity has negative effects on the offspring's health in the short and long term. Increasing evidence suggests a key role for microbiota in host metabolism and energy harvest, providing novel tools for obesity prevention and management. The maternal environment, including nutrition and microbes, influences the likelihood of developing childhood diseases, which may persist and be exacerbated in adulthood. Maternal obesity and weight gain also influence microbiota composition and activity during pregnancy and lactation. They affect microbial diversity in the gut and breast milk. Such microbial changes may be transferred to the offspring during delivery and also during lactation, affecting infant microbial colonisation and immune system maturation. Thus, an adequate nutritional and microbial environment during the peri-natal period may provide a window of opportunity to reduce the risk of obesity and overweight in our infants using targeted strategies aimed at modulating the microbiota during early life. © 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

  3. Maternal Obesity Accelerates Fetal Pancreatic Beta Cell but not Alpha Cell Development in the Sheep: Prenatal and Postnatal Consequences

    USDA-ARS?s Scientific Manuscript database

    Maternal obesity affects offspring weight, body composition and organ function, increasing diabetes and metabolic syndrome risk. We determined effects of maternal obesity and a high energy diet on fetal pancreatic development. Sixty days prior to breeding. ewes were assigned to control (C, 100% of N...

  4. Impact of obesity on maternal and neonatal outcomes in insulin-resistant pregnancy.

    PubMed

    Harper, Lorie M; Renth, Allyson; Cade, W Todd; Colvin, Ryan; Macones, George A; Cahill, Alison G

    2014-05-01

    To determine the impact of obesity on pregnancies complicated by insulin resistance. Secondary analysis of prospective cohort of women with gestational diabetes mellitus (GDM) and type 2 diabetes mellitus (DM). The exclusion criteria were type 1 DM, multiple gestation, fetal anomalies, unknown prepregnancy, and body mass index (BMI). Primary maternal outcome was a composite of any of the following: severe preeclampsia, eclampsia, third- to fourth-degree laceration, readmission, wound infection, or antepartum hospitalization. Primary neonatal outcome was a composite of any of the following: hypoglycemia, preterm delivery, admission to level 3 nursery, oxygen requirement > 6 hours after birth, shoulder dystocia, 5-minute Apgar ≤3, cord pH < 7.0, and cord base excess < -12 mmol/L. Obese women (BMI ≥30.0 kg/m(2)) were compared with nonobese women (BMI < 30.0 kg/m(2)). Of 356 subjects with DM, 233 (66%) were obese. Obese women were not at further increased risk of the composite maternal outcome (adjusted odds ratio [AOR] = 0.68, 95% confidence interval [CI] = 0.43-1.09), the composite neonatal outcome (AOR = 0.76, 95% CI = 0.48-1.21), or cesarean (58.8 vs. 52.9%, p = 0.28, AOR = 1.47, 95% CI = 0.91-2.39). We did not find evidence that obesity worsened pregnancy outcomes in women with GDM and type 2 DM, suggesting that obese women may not require more stringent antepartum treatment strategies. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

  5. [Effect of breastfeeding on obesity of schoolchildren: influence of maternal education].

    PubMed

    Pudla, Katia Jakovljevic; Gonzaléz-Chica, David Alejandro; de Vasconcelos, Francisco de Assis Guedes

    2015-01-01

    To evaluate the association between duration of breastfeeding (BF) and obesity in schoolchildren of Florianópolis (SC), and the role of possible effect modifiers. Cross-sectional study with a random sample of 2,826 schoolchildren (7-14 years). Weight and height were measured according to standardized procedures. Data concerning BF and sociodemographic variables were obtained from a questionnaire sent to parents/guardians. Children's nutritional status was evaluated by BMI-for-age z-score for gender (WHO reference curves). Adjusted analyses were performed through logistic regression, considering a possible interaction among variables. Prevalence of obesity was 8.6% (95% CI: 7.6-9.7%) and 55.7% (95% CI: 53.8-57.6%) received breastmilk for ≥6 months. BF was not associated with obesity, even in the adjusted analysis. Stratified analysis according to maternal schooling showed that, in children aged 7-10 years and children whose mothers had 0-8 years of schooling, the chance of obesity was lower among those breastfeed for >1 month, especially among those who received breastmilk for 1-5 months (OR=0.22; 95% CI 0.08-0.62). Among children of women with higher educational level (>8 years), the chance of obesity was 44% lower in those who were breastfed for >12 months (p-value for interaction <0.01). This interaction was not found in older children (11-14 years). Among children of women with lower schooling, BF for any period longer than 1 month is protective against obesity; however, for a higher maternal schooling, BF for less than 12 months increases the odds of obesity. Copyright © 2015 Sociedade de Pediatria de São Paulo. Publicado por Elsevier Editora Ltda. All rights reserved.

  6. Maternal abuse history and self-regulation difficulties in preadolescence

    PubMed Central

    Delker, Brianna C.; Noll, Laura K.; Kim, Hyoun K.; Fisher, Philip A.

    2014-01-01

    Although poor parenting is known to be closely linked to self-regulation difficulties in early childhood, comparatively little is understood about the role of other risk factors in the early caregiving environment (such as a parent’s own experiences of childhood abuse) in developmental pathways of self-regulation into adolescence. Using a longitudinal design, this study aimed to examine how a mother’s history of abuse in childhood relates to her offspring’s self-regulation difficulties in preadolescence. Maternal controlling parenting and exposure to intimate partner aggression in the child’s first 24–36 months were examined as important early social and environmental influences that may explain the proposed connection between maternal abuse history and preadolescent self-regulation. An ethnically diverse sample of mothers (N = 488) who were identified as at-risk for child maltreatment was recruited at the time of their children’s birth. Mothers and their children were assessed annually from the child’s birth through 36 months, and at age 9–11 years. Structural equation modeling and bootstrap tests of indirect effects were conducted to address the study aims. Findings indicated that maternal abuse history indirectly predicted their children’s self-regulation difficulties in preadolescence mainly through maternal controlling parenting in early childhood, but not through maternal exposure to aggression by an intimate partner. Maternal history of childhood abuse and maternal controlling parenting in her child’s early life may have long-term developmental implications for child self-regulation. PMID:25459984

  7. Programming of Fetal Insulin Resistance in Pregnancies with Maternal Obesity by ER Stress and Inflammation

    PubMed Central

    Sáez, Pablo J.; Villalobos-Labra, Roberto; Farías-Jofré, Marcelo

    2014-01-01

    The global epidemics of obesity during pregnancy and excessive gestational weight gain (GWG) are major public health problems worldwide. Obesity and excessive GWG are related to several maternal and fetal complications, including diabetes (pregestational and gestational diabetes) and intrauterine programming of insulin resistance (IR). Maternal obesity (MO) and neonatal IR are associated with long-term development of obesity, diabetes mellitus, and increased global cardiovascular risk in the offspring. Multiple mechanisms of insulin signaling pathway impairment have been described in obese individuals, involving complex interactions of chronically elevated inflammatory mediators, adipokines, and the critical role of the endoplasmic reticulum (ER) stress-dependent unfolded protein response (UPR). However, the underlying cellular processes linking MO and IR in the offspring have not been fully elucidated. Here, we summarize the state-of-the-art evidence supporting the possibility that adverse metabolic postnatal outcomes such as IR in the offspring of pregnancies with MO and/or excessive GWG may be related to intrauterine activation of ER stress response. PMID:25093191

  8. Males are from Mars, females are from Venus: sex-specific fetal brain gene expression signatures in a mouse model of maternal diet-induced obesity

    PubMed Central

    EDLOW, Andrea G.; GUEDJ, Faycal; PENNINGS, Jeroen L.A.; SVERDLOV, Deanna; NERI, Caterina; BIANCHI, Diana W.

    2016-01-01

    BACKGROUND Maternal obesity is associated with adverse neurodevelopmental outcomes in children, including autism spectrum disorders, developmental delay, and attention deficit hyperactivity disorder. The underlying mechanisms remain unclear. We previously identified second trimester amniotic fluid and term cord blood gene expression patterns suggesting dysregulated brain development in fetuses of obese compared to lean women. OBJECTIVES We sought to investigate the biological significance of these findings in a mouse model of maternal diet-induced obesity. We evaluated sex-specific differences in fetal growth, brain gene expression signatures and associated pathways. STUDY DESIGN Female C57BL/6J mice were fed a 60% high-fat diet or 10% fat control diet for 12–14 weeks prior to mating. During pregnancy, obese dams continued on the high-fat diet (HFD/HFD), or transitioned to the CD (HFD/CD). Lean dams stayed on the control diet. On embryonic day 17.5, embryos were weighed and fetal brains were snap frozen. RNA was extracted from male and female forebrains (10/diet group/sex) and hybridized to whole genome expression arrays. Significantly differentially expressed genes were identified using Welch’s t-test with the Benjamini-Hochberg correction. Functional analyses were performed using Ingenuity Pathways Analysis and Gene Set Enrichment Analysis. RESULTS Embryos of HFD/HFD dams were significantly smaller than controls, with males more severely affected than females (p=0.01). Maternal obesity and maternal obesity with dietary change in pregnancy resulted in significantly more dysregulated genes in male versus female fetal brains (386 vs 66, p<0.001). Maternal obesity with and without dietary change in pregnancy was associated with unique brain gene expression signatures for each sex, with overlap of only one gene. Changing obese dams to a control diet in pregnancy resulted in more differentially expressed genes in the fetal brain than maternal obesity alone

  9. Maternal-infant relationship quality and risk of obesity at age 5.5 years in a national US cohort

    PubMed Central

    2014-01-01

    Background Poor quality relationships between mothers and toddlers have been associated with higher risk for childhood obesity, but few prospective studies of obesity have assessed maternal-child relationship quality in infancy. In addition it is not known whether the increased risk is associated with the mother’s or the child’s contribution to the relationship quality. Methods We analyzed data (n = 5650) from the Early Childhood Longitudinal Study, Birth Cohort, a national study of U.S. children born in 2001 and followed until they entered kindergarten. At 9 months of age, the Nursing Child Assessment Teaching Scale (NCATS) was used to assess the quality of observed playtime interactions between mothers and infants, yielding separate scores for maternal and infant behaviors. Obesity (BMI ≥95th percentile) at age 5.5 years was based on measured weight and height. Results The prevalence (95% confidence interval) of obesity at 5.5 years of age was higher among children in the lowest quartile of maternal NCATS score (20.2% [95% CI: 17.2%, 23.2%]) than in the highest quartile (13.9% [11.3%, 16.5%]), but maternal NCATS score was not significantly associated with obesity after adjustment for race/ethnicity, maternal education and household income. The prevalence of obesity at 5.5 years of age was similar among children in the lowest quartile of infant NCATS score (17.4% [14.4%, 20.3%]) and in the highest quartile (17.6% 14.4%, 20.8%]), and was not changed with covariate adjustment. Conclusions Maternal-infant relationship quality, assessed by direct observation at 9 months of age in a national sample, was not associated with an increased risk of obesity at age 5.5 years after controlling for sociodemographic characteristics. PMID:24564412

  10. Expression of epigenetic machinery genes is sensitive to maternal obesity and weight loss in relation to fetal growth in mice.

    PubMed

    Panchenko, Polina E; Voisin, Sarah; Jouin, Mélanie; Jouneau, Luc; Prézelin, Audrey; Lecoutre, Simon; Breton, Christophe; Jammes, Hélène; Junien, Claudine; Gabory, Anne

    2016-01-01

    Maternal obesity impacts fetal growth and pregnancy outcomes. To counteract the deleterious effects of obesity on fertility and pregnancy issue, preconceptional weight loss is recommended to obese women. Whether this weight loss is beneficial/detrimental for offspring remains poorly explored. Epigenetic mechanisms could be affected by maternal weight changes, perturbing expression of key developmental genes in the placenta or fetus. Our aim was to investigate the effects of chronic maternal obesity on feto-placental growth along with the underlying epigenetic mechanisms. We also tested whether preconceptional weight loss could alleviate these effects. Female mice were fed either a control diet (CTRL group), a high-fat diet (obese (OB) group), or a high-fat diet switched to a control diet 2 months before conception (weight loss (WL) group). At mating, OB females presented an obese phenotype while WL females normalized metabolic parameters. At embryonic day 18.5 (E18.5), fetuses from OB females presented fetal growth restriction (FGR; -13 %) and 28 % of the fetuses were small for gestational age (SGA). Fetuses from WL females normalized this phenotype. The expression of 60 epigenetic machinery genes and 32 metabolic genes was measured in the fetal liver, placental labyrinth, and junctional zone. We revealed 23 genes altered by maternal weight trajectories in at least one of three tissues. The fetal liver and placental labyrinth were more responsive to maternal obesity than junctional zone. One third (18/60) of the epigenetic machinery genes were differentially expressed between at least two maternal groups. Interestingly, genes involved in the histone acetylation pathway were particularly altered (13/18). In OB group, lysine acetyltransferases and Bromodomain-containing protein 2 were upregulated, while most histone deacetylases were downregulated. In WL group, the expression of only a subset of these genes was normalized. This study highlights the high

  11. Stronger influence of maternal than paternal obesity on infant and early childhood body mass index: the Fels Longitudinal Study.

    PubMed

    Linabery, A M; Nahhas, R W; Johnson, W; Choh, A C; Towne, B; Odegaard, A O; Czerwinski, S A; Demerath, E W

    2013-06-01

    Excessive early childhood adiposity is a prevalent and increasing concern in many parts of the world. Parental obesity is one of the several factors previously associated with infant and early childhood weight, length and adiposity. Parental obesity represents a surrogate marker of the complex interplay among genetic, epigenetic and shared environmental factors, and is potentially modifiable. The relative contributions of maternal and paternal body mass index (BMI) to infant and early childhood growth, as well as the timing of such effects, have not been firmly established. Utilizing serial infant measurements and growth curve modelling, this is the largest study to fully characterize and formally compare associations between maternal and paternal BMI and offspring growth across the entire infancy and early childhood period. Maternal obesity is a stronger determinant of offspring BMI than paternal obesity at birth and from 2 to 3 years of age, suggesting that prevention efforts focused particularly on maternal lifestyle and BMI may be important in reducing excess infant BMI. The observation that maternal BMI effects are not constant, but rather present at birth, wane and re-emerge during late infancy, suggests that there is a window of opportunity in early infancy when targeted interventions on children of obese mothers may be most effective. Parental obesity influences infant body size. To fully characterize their relative effects on infant adiposity, associations between maternal and paternal body mass index (BMI) category (normal: ≤25 kg m(-2) , overweight: 25 - <30 kg m(-2) , obese: ≥30 kg m(-2) ) and infant BMI were compared in Fels Longitudinal Study participants. A median of 9 serial weight and length measures from birth to 3.5 years were obtained from 912 European American children born in 1928-2008. Using multivariable mixed effects regression, contributions of maternal vs. paternal BMI status to infant BMI growth curves were evaluated

  12. Differential Effects of Exposure to Maternal Obesity or Maternal Weight Loss during the Periconceptional Period in the Sheep on Insulin Signalling Molecules in Skeletal Muscle of the Offspring at 4 Months of Age

    PubMed Central

    Nicholas, Lisa M.; Morrison, Janna L.; Rattanatray, Leewen; Ozanne, Susan E.; Kleemann, Dave O.; Walker, Simon K.; MacLaughlin, Severence M.; Zhang, Song; Martin-Gronert, Malgorzata S.; McMillen, Isabella C.

    2013-01-01

    Exposure to maternal obesity before and/or throughout pregnancy may increase the risk of obesity and insulin resistance in the offspring in childhood and adult life, therefore, resulting in its transmission into subsequent generations. We have previously shown that exposure to maternal obesity around the time of conception alone resulted in increased adiposity in female lambs. Changes in the abundance of insulin signalling molecules in skeletal muscle and adipose tissue precede the development of insulin resistance and type 2 diabetes. It is not clear, however, whether exposure to maternal obesity results in insulin resistance in her offspring as a consequence of the impact of increased adiposity on skeletal muscle or as a consequence of the programming of specific changes in the abundance of insulin signalling molecules in this tissue. We have used an embryo transfer model in the sheep to investigate the effects of exposure to either maternal obesity or to weight loss in normal and obese mothers preceding and for one week after conception on the expression and abundance of insulin signalling molecules in muscle in the offspring. We found that exposure to maternal obesity resulted in lower muscle GLUT-4 and Ser 9 phospho-GSK3α and higher muscle GSK3α abundance in lambs when compared to lambs conceived in normally nourished ewes. Exposure to maternal weight loss in normal or obese mothers, however, resulted in lower muscle IRS1, PI3K, p110β, aPKCζ, Thr 642 phospho-AS160 and GLUT-4 abundance in the offspring. In conclusion, maternal obesity or weight loss around conception have each programmed specific changes on subsets of molecules in the insulin signalling, glucose transport and glycogen synthesis pathways in offspring. There is a need for a stronger evidence base to ensure that weight loss regimes in obese women seeking to become pregnant minimize the metabolic costs for the next generation. PMID:24386400

  13. Maternal Obesity in Pregnancy, Gestational Weight Gain, and Risk of Childhood Asthma

    PubMed Central

    Young, Omar M.; Kumar, Rajesh; Simhan, Hyagriv; Celedón, Juan C.

    2014-01-01

    BACKGROUND AND OBJECTIVE: Environmental or lifestyle exposures in utero may influence the development of childhood asthma. In this meta-analysis, we aimed to assess whether maternal obesity in pregnancy (MOP) or increased maternal gestational weight gain (GWG) increased the risk of asthma in offspring. METHODS: We included all observational studies published until October 2013 in PubMed, Embase, CINAHL, Scopus, The Cochrane Database, and Ovid. Random effects models with inverse variance weights were used to calculate pooled risk estimates. RESULTS: Fourteen studies were included (N = 108 321 mother–child pairs). Twelve studies reported maternal obesity, and 5 reported GWG. Age of children was 14 months to 16 years. MOP was associated with higher odds of asthma or wheeze ever (OR = 1.31; 95% confidence interval [CI], 1.16–1.49) or current (OR = 1.21; 95% CI, 1.07–1.37); each 1-kg/m2 increase in maternal BMI was associated with a 2% to 3% increase in the odds of childhood asthma. High GWG was associated with higher odds of asthma or wheeze ever (OR = 1.16; 95% CI, 1.001–1.34). Maternal underweight and low GWG were not associated with childhood asthma or wheeze. Meta-regression showed a negative association of borderline significance for maternal asthma history (P = .07). The significant heterogeneity among existing studies indicates a need for standardized approaches to future studies on the topic. CONCLUSIONS: MOP and high GWG are associated with an elevated risk of childhood asthma; this finding may be particularly significant for mothers without asthma history. Prospective randomized trials of maternal weight management are needed. PMID:25049351

  14. Maternal obesity in pregnancy, gestational weight gain, and risk of childhood asthma.

    PubMed

    Forno, Erick; Young, Omar M; Kumar, Rajesh; Simhan, Hyagriv; Celedón, Juan C

    2014-08-01

    Environmental or lifestyle exposures in utero may influence the development of childhood asthma. In this meta-analysis, we aimed to assess whether maternal obesity in pregnancy (MOP) or increased maternal gestational weight gain (GWG) increased the risk of asthma in offspring. We included all observational studies published until October 2013 in PubMed, Embase, CINAHL, Scopus, The Cochrane Database, and Ovid. Random effects models with inverse variance weights were used to calculate pooled risk estimates. Fourteen studies were included (N = 108 321 mother-child pairs). Twelve studies reported maternal obesity, and 5 reported GWG. Age of children was 14 months to 16 years. MOP was associated with higher odds of asthma or wheeze ever (OR = 1.31; 95% confidence interval [CI], 1.16-1.49) or current (OR = 1.21; 95% CI, 1.07-1.37); each 1-kg/m(2) increase in maternal BMI was associated with a 2% to 3% increase in the odds of childhood asthma. High GWG was associated with higher odds of asthma or wheeze ever (OR = 1.16; 95% CI, 1.001-1.34). Maternal underweight and low GWG were not associated with childhood asthma or wheeze. Meta-regression showed a negative association of borderline significance for maternal asthma history (P = .07). The significant heterogeneity among existing studies indicates a need for standardized approaches to future studies on the topic. MOP and high GWG are associated with an elevated risk of childhood asthma; this finding may be particularly significant for mothers without asthma history. Prospective randomized trials of maternal weight management are needed. Copyright © 2014 by the American Academy of Pediatrics.

  15. Programming maternal and child overweight and obesity in the context of undernutrition: current evidence and key considerations for low- and middle-income countries.

    PubMed

    Jaacks, Lindsay M; Kavle, Justine; Perry, Abigail; Nyaku, Albertha

    2017-05-01

    The goals of the present targeted review on maternal and child overweight and obesity were to: (i) understand the current situation in low- and middle-income countries (LMIC) with regard to recent trends and context-specific risk factors; and (ii) building off this, identify entry points for leveraging existing undernutrition programmes to address overweight and obesity in LMIC. Trends reveal that overweight and obesity are a growing problem among women and children in LMIC; as in Ghana, Kenya, Niger, Sierra Leone, Tanzania and Zimbabwe, where the prevalence among urban women is approaching 50 %. Four promising entry points were identified: (i) the integration of overweight and obesity into national nutrition plans; (ii) food systems (integration of food and beverage marketing regulations into existing polices on the marketing of breast-milk substitutes and adoption of policies to promote healthy diets); (iii) education systems (integration of nutrition into school curricula with provision of high-quality foods through school feeding programmes); and (iv) health systems (counselling and social and behaviour change communication to improve maternal diet, appropriate gestational weight gain, and optimal infant and young child feeding practices). We conclude by presenting a step-by-step guide for programme officers and policy makers in LMIC with actionable objectives to address overweight and obesity.

  16. Maternal weight misperceptions and smoking are associated with overweight and obesity in low SES preschoolers.

    PubMed

    Kaufman-Shriqui, V; Fraser, D; Novack, Y; Bilenko, N; Vardi, H; Abu-Saad, K; Elhadad, N; Feine, Z; Mor, K; Shahar, D R

    2012-02-01

    To identify modifiable risk factors for obesity among low socioeconomic status (LSES) children. Cross-sectional data were obtained from 238 4-7-year-old children and 224 mothers from LSES preschools. Anthropometric measurements were obtained; mothers were interviewed about sociodemographic characteristics, health behaviors, perceptions and beliefs. The combined prevalence of overweight and obesity (OWOB) among children was 29.8% based on the new World Health Organization (WHO) growth standard. Prevalence of OWOB (body mass index ≥25) among mothers was 51.8%. Mean age, sleeping hours, gender distribution and poverty level were similar between normal and OWOB children. Over 82% of mothers underestimated their child's weight status. Of the 62 OWOB children, 74.2% were perceived by their mothers as having 'normal weight' (NW) and 8% were perceived as 'thin'. Mothers perceived 67 out of 158 NW children (42.4%) as 'thin' (P<0.001). Mediation analysis indicated that 10% of the effect of maternal underestimation on child's OWOB may be mediated through child's daily sedentary hours (P=0.06). In a multivariable logistic-regression analysis controlling for maternal obesity, knowledge regarding breakfast's importance and child's daily sedentary hours, maternal underestimation of the child's weight status (odds ratio=7.33; 95% confidence interval (CI):2.41-22.37; P<0.0001) and parental smoking (odds ratio=3.25; 95% CI: 1.26-8.40; P=0.015) were the only significant factors associated with OWOB in LSES children. Maternal perception of child's weight status and parental smoking are associated with childhood OWOB among LSES children. These parameters can help identify children at risk for obesity. Maternal perception may be amenable to intervention.

  17. The association between maternal serious psychological distress and child obesity at 3 years: a cross-sectional analysis of the UK Millennium Cohort Data.

    PubMed

    Ramasubramanian, L; Lane, S; Rahman, A

    2013-01-01

      The prevalence of child obesity is increasing rapidly worldwide. Early childhood has been identified as a critical time period for the development of obesity. Maternal mental health and early life environment are crucial factors and have been linked to adverse child outcomes. The objective of the study was to examine the relationship between maternal serious psychological distress and obesity in early childhood.   A cross-sectional analysis of data from the Millennium Cohort Study was conducted. Subjects consisted of all natural mothers (n= 10 465) who had complete and plausible data for Kessler-6 scores, socio-demographic and anthropometric variables, and their children for whom anthropometric measurements were completed at age 3. Maternal serious psychological distress was defined as a score of 13 or more on the Kessler-6 scale. Obesity was defined as body mass index ≥95th centile of the 1990 reference chart for age and sex in children. The data were analysed using spss 16. Maternal socio-demographic factors that are known to influence maternal mental health and child obesity were identified and adjusted using multivariate logistic regression.   Of the 10 465 mother-child dyads, 3.5% of mothers had serious psychological distress and 5.5% of children were obese at 3 years of age. Logistic regression analysis showed that maternal serious psychological distress was associated with early childhood obesity (P= 0.01; OR 1.62, 95% CI 1.11, 2.37). After adjusting for potential confounding factors using multivariate logistic regression, maternal serious psychological distress remained significantly associated with early childhood obesity (P= 0.01; OR 1.59, 95% CI 1.08, 2.34).   The results show that maternal serious psychological distress is independently associated with early childhood obesity. © 2011 Blackwell Publishing Ltd.

  18. Paternal and maternal obesity but not gestational weight gain is associated with type 1 diabetes

    PubMed Central

    Magnus, Maria C; Olsen, Sjurdur F; Granstrom, Charlotta; Lund-Blix, Nicolai A; Svensson, Jannet; Johannesen, Jesper; Fraser, Abigail; Skrivarhaug, Torild; Joner, Geir; Njølstad, Pål R; Størdal, Ketil; Stene, Lars C

    2018-01-01

    Abstract Background Our objective was to examine the associations of parental body mass index (BMI) and maternal gestational weight gain with childhood-onset type 1 diabetes. Comparing the associations of maternal and paternal BMI with type 1 diabetes in the offspring will provide further insight into the role of unmeasured confounding by characteristics linked to BMI in both parents. Methods We studied 132 331 children participating in the Norwegian Mother and Child Cohort Study (MoBa) and the Danish National Birth Cohort (DNBC) who were born between February 1998 and July 2009. Exposures of interest included parental BMI and maternal gestational weight gain obtained by maternal report. We used Cox-proportional hazards regression to examine the risk of type 1 diabetes (n=499 cases), which was ascertained by national childhood diabetes registers. Results The incidence of type 1 diabetes was 32.7 per 100 000 person-years in MoBa and 28.5 per 100 000 person-years in DNBC. Both maternal pre-pregnancy obesity, adjusted hazard ratio (HR) 1.41 [95% confidence interval (CI): 1.06, 1.89] and paternal obesity, adjusted HR 1.51 (95% CI: 1.11, 2.04), were associated with childhood-onset type 1 diabetes. The associations were similar after mutual adjustment. In contrast, maternal total gestational weight gain was not associated with childhood-onset type 1 diabetes, adjusted HR 1.00 (95% CI: 0.99, 1.02) per kilogram increase. Conclusions Our study suggests that the association between maternal obesity and childhood-onset type 1 diabetes is not likely explained by intrauterine mechanisms, but possibly rather by unknown environmental factors influencing BMI in the family. PMID:29415279

  19. Effects of taurine supplementation on hepatic markers of inflammation and lipid metabolism in mothers and offspring in the setting of maternal obesity.

    PubMed

    Li, Minglan; Reynolds, Clare M; Sloboda, Deborah M; Gray, Clint; Vickers, Mark H

    2013-01-01

    Maternal obesity is associated with obesity and metabolic disorders in offspring. However, intervention strategies to reverse or ameliorate the effects of maternal obesity on offspring health are limited. Following maternal undernutrition, taurine supplementation can improve outcomes in offspring, possibly via effects on glucose homeostasis and insulin secretion. The effects of taurine in mediating inflammatory processes as a protective mechanism has not been investigated. Further, the efficacy of taurine supplementation in the setting of maternal obesity is not known. Using a model of maternal obesity, we examined the effects of maternal taurine supplementation on outcomes related to inflammation and lipid metabolism in mothers and neonates. Time-mated Wistar rats were randomised to either: 1) control : control diet during pregnancy and lactation (CON); 2) CON supplemented with 1.5% taurine in drinking water (CT); 3) maternal obesogenic diet (high fat, high fructose) during pregnancy and lactation (MO); or 4) MO supplemented with taurine (MOT). Maternal and neonatal weights, plasma cytokines and hepatic gene expression were analysed. A MO diet resulted in maternal hyperinsulinemia and hyperleptinemia and increased plasma glucose, glutamate and TNF-α concentrations. Taurine normalised maternal plasma TNF-α and glutamate concentrations in MOT animals. Both MO and MOT mothers displayed evidence of fatty liver accompanied by alterations in key markers of hepatic lipid metabolism. MO neonates displayed a pro-inflammatory hepatic profile which was partially rescued in MOT offspring. Conversely, a pro-inflammatory phenotype was observed in MOT mothers suggesting a possible maternal trade-off to protect the neonate. Despite protective effects of taurine in MOT offspring, neonatal mortality was increased in CT neonates, indicating possible adverse effects of taurine in the setting of normal pregnancy. These data suggest that maternal taurine supplementation may

  20. Programming of mouse obesity by maternal exposure to concentrated ambient fine particles.

    PubMed

    Chen, Minjie; Wang, Xiaoke; Hu, Ziying; Zhou, Huifen; Xu, Yanyi; Qiu, Lianglin; Qin, Xiaobo; Zhang, Yuhao; Ying, Zhekang

    2017-06-23

    Many diseases including obesity may originate through alterations in the early-life environment that interrupts fetal development. Increasing evidence has shown that exposure to ambient fine particles (PM 2.5 ) is associated with abnormal fetal development. However, its long-term metabolic effects on offspring have not been systematically investigated. To determine if maternal exposure to PM 2.5 programs offspring obesity, female C57Bl/6j mice were exposed to filtered air (FA) or concentrated ambient PM 2.5 (CAP) during pre-conception, pregnancy, and lactation, and the developmental and metabolic responses of offspring were assessed. The growth trajectory of offspring revealed that maternal exposure to CAP significantly decreased offspring birth weight but increased body weight of adult male but not female offspring, and the latter was expressed as increased adiposity. These adult male offspring had increased food intake, but were sensitive to exogenous leptin. Their hypothalamic expression of Socs3 and Pomc, two target genes of leptin, was not changed, and the hypothalamic expression of NPY, an orexigenic peptide that is inhibited by leptin, was significantly increased. These decreases in central anorexigenic signaling were accompanied by reduced plasma leptin and its expression in adipose tissues, the primary source of circulating leptin. In contrast, maternal exposure did not significantly change any of these indexes in adult female offspring. Pyrosequencing demonstrated that the leptin promoter methylation of adipocytes was significantly increased in CAP-exposed male but not female offspring. Our data indicate that maternal exposure to ambient PM 2.5 programs obesity in male offspring probably through alterations in the methylation of the promoter region of the leptin gene.

  1. Maternal obesity and congenital heart defects: a population-based study123

    PubMed Central

    Mills, James L; Troendle, James; Conley, Mary R; Carter, Tonia; Druschel, Charlotte M

    2010-01-01

    Background: Obesity affects almost one-third of pregnant women and causes many complications, including neural tube defects. It is not clear whether the risk of congenital heart defects, the most common malformations, is also increased. Objective: This study was conducted to determine whether obesity is associated with an increased risk of congenital heart defects. Design: A population-based, nested, case-control study was conducted in infants born with congenital heart defects and unaffected controls from the cohort of all births (n = 1,536,828) between 1993 and 2003 in New York State, excluding New York City. The type of congenital heart defect, maternal body mass index (BMI; in kg/m2), and other risk factors were obtained from the Congenital Malformations Registry and vital records. Mothers of 7392 congenital heart defect cases and 56,304 unaffected controls were studied. Results: All obese women (BMI ≥ 30) were significantly more likely than normal-weight women (BMI: 19–24.9) to have children with a congenital heart defect [odds ratio (OR): 1.15; 95% CI: 1.07, 1.23; P < 0.0001]. Overweight women were not at increased risk (OR: 1.00; 95% CI: 0.94, 1.06). The risk in morbidly obese women (BMI ≥ 40) was higher (OR: 1.33; 95% CI: 1.15, 1.54; P = 0.0001) than that in obese women with a BMI of 30–39.9 (OR: 1.11; 95% CI: 1.04, 1.20; P = 0.004). There was a highly significant trend of increasing OR for congenital heart defects with increasing maternal obesity (P < 0.0001). The offspring of obese women had significantly higher ORs for atrial septal defects, hypoplastic left heart syndrome, aortic stenosis, pulmonic stenosis, and tetralogy of Fallot. Conclusions: Obese, but not overweight, women are at significantly increased risk of bearing children with a range of congenital heart defects, and the risk increases with increasing BMI. Weight reduction as a way to reduce risk should be investigated. PMID:20375192

  2. Prenatal exposure to maternal very severe obesity is associated with impaired neurodevelopment and executive functioning in children.

    PubMed

    Mina, Theresia H; Lahti, Marius; Drake, Amanda J; Denison, Fiona C; Räikkönen, Katri; Norman, Jane E; Reynolds, Rebecca M

    2017-07-01

    BackgroundPrenatal maternal obesity has been associated with an increased risk of neurocognitive problems in childhood, but there are fewer studies on executive functioning.MethodsTests and questionnaires to assess neurodevelopment, executive functioning, and the ability to delay gratification were conducted in 113 children (mean (SD)=4.24 (0.63) years of age) born to mothers with very severe obesity (SO, body mass index (BMI)⩾40 kg/m 2 , n=51) or to lean mothers (BMI⩽25 kg/m 2 , n=62).ResultsPrenatal maternal SO predicted poorer neurodevelopment (unstandardized regression coefficient (B)=-0.42, 95% confidence interval (CI) (-0.82; -0.02)), worse problem-solving (odd ratio (OR)=0.60, 95% CI (1.13; 0.07)), and fine motor skills (OR=4.91, 95% CI (1.27; 19.04)), poorer executive functioning in areas of attention, inhibitory control, and working memory (standardized B=3.75, 95% CI (1.01; 13.93)) but not in self-gratification delay. The effects were independent of maternal concurrent psychological well-being and child's BMI, but not independent of maternal education.ConclusionFuture studies should investigate whether perinatal management of maternal obesity could prevent adverse outcomes in child neurodevelopment.

  3. Swedish and American studies show that initiatives to decrease maternal obesity could play a key role in reducing preterm birth.

    PubMed

    Gould, Jeffrey B; Mayo, Jonathan; Shaw, Gary M; Stevenson, David K

    2014-06-01

    Maternal obesity is a major source of preventable perinatal morbidity, but studies of the relationship between obesity and preterm birth have been inconsistent. This review looks at two major studies covering just under 3.5 million births, from California, USA, and Sweden. Inconsistent findings in previous studies appear to stem from the complex relationship between obesity and preterm birth. Initiatives to decrease maternal obesity represent an important strategy in reducing preterm birth. ©2014 Foundation Acta Paediatrica. Published by John Wiley & Sons Ltd.

  4. Genetic Evidence for Causal Relationships Between Maternal Obesity-Related Traits and Birth Weight.

    PubMed

    Tyrrell, Jessica; Richmond, Rebecca C; Palmer, Tom M; Feenstra, Bjarke; Rangarajan, Janani; Metrustry, Sarah; Cavadino, Alana; Paternoster, Lavinia; Armstrong, Loren L; De Silva, N Maneka G; Wood, Andrew R; Horikoshi, Momoko; Geller, Frank; Myhre, Ronny; Bradfield, Jonathan P; Kreiner-Møller, Eskil; Huikari, Ville; Painter, Jodie N; Hottenga, Jouke-Jan; Allard, Catherine; Berry, Diane J; Bouchard, Luigi; Das, Shikta; Evans, David M; Hakonarson, Hakon; Hayes, M Geoffrey; Heikkinen, Jani; Hofman, Albert; Knight, Bridget; Lind, Penelope A; McCarthy, Mark I; McMahon, George; Medland, Sarah E; Melbye, Mads; Morris, Andrew P; Nodzenski, Michael; Reichetzeder, Christoph; Ring, Susan M; Sebert, Sylvain; Sengpiel, Verena; Sørensen, Thorkild I A; Willemsen, Gonneke; de Geus, Eco J C; Martin, Nicholas G; Spector, Tim D; Power, Christine; Järvelin, Marjo-Riitta; Bisgaard, Hans; Grant, Struan F A; Nohr, Ellen A; Jaddoe, Vincent W; Jacobsson, Bo; Murray, Jeffrey C; Hocher, Berthold; Hattersley, Andrew T; Scholtens, Denise M; Davey Smith, George; Hivert, Marie-France; Felix, Janine F; Hyppönen, Elina; Lowe, William L; Frayling, Timothy M; Lawlor, Debbie A; Freathy, Rachel M

    2016-03-15

    Neonates born to overweight or obese women are larger and at higher risk of birth complications. Many maternal obesity-related traits are observationally associated with birth weight, but the causal nature of these associations is uncertain. To test for genetic evidence of causal associations of maternal body mass index (BMI) and related traits with birth weight. Mendelian randomization to test whether maternal BMI and obesity-related traits are potentially causally related to offspring birth weight. Data from 30,487 women in 18 studies were analyzed. Participants were of European ancestry from population- or community-based studies in Europe, North America, or Australia and were part of the Early Growth Genetics Consortium. Live, term, singleton offspring born between 1929 and 2013 were included. Genetic scores for BMI, fasting glucose level, type 2 diabetes, systolic blood pressure (SBP), triglyceride level, high-density lipoprotein cholesterol (HDL-C) level, vitamin D status, and adiponectin level. Offspring birth weight from 18 studies. Among the 30,487 newborns the mean birth weight in the various cohorts ranged from 3325 g to 3679 g. The maternal genetic score for BMI was associated with a 2-g (95% CI, 0 to 3 g) higher offspring birth weight per maternal BMI-raising allele (P = .008). The maternal genetic scores for fasting glucose and SBP were also associated with birth weight with effect sizes of 8 g (95% CI, 6 to 10 g) per glucose-raising allele (P = 7 × 10(-14)) and -4 g (95% CI, -6 to -2 g) per SBP-raising allele (P = 1×10(-5)), respectively. A 1-SD ( ≈ 4 points) genetically higher maternal BMI was associated with a 55-g higher offspring birth weight (95% CI, 17 to 93 g). A 1-SD ( ≈ 7.2 mg/dL) genetically higher maternal fasting glucose concentration was associated with 114-g higher offspring birth weight (95% CI, 80 to 147 g). However, a 1-SD ( ≈ 10 mm Hg) genetically higher maternal SBP was associated with a 208-g

  5. Males are from Mars, and females are from Venus: sex-specific fetal brain gene expression signatures in a mouse model of maternal diet-induced obesity.

    PubMed

    Edlow, Andrea G; Guedj, Faycal; Pennings, Jeroen L A; Sverdlov, Deanna; Neri, Caterina; Bianchi, Diana W

    2016-05-01

    Maternal obesity is associated with adverse neurodevelopmental outcomes in children, including autism spectrum disorders, developmental delay, and attention-deficit hyperactivity disorder. The underlying mechanisms remain unclear. We previously identified second-trimester amniotic fluid and term cord blood gene expression patterns suggesting dysregulated brain development in fetuses of obese compared with lean women. We sought to investigate the biological significance of these findings in a mouse model of maternal diet-induced obesity. We evaluated sex-specific differences in fetal growth, brain gene expression signatures, and associated pathways. Female C57BL/6J mice were fed a 60% high-fat diet or 10% fat control diet for 12-14 weeks prior to mating. During pregnancy, obese dams continued on the high-fat diet or transitioned to the control diet. Lean dams stayed on the control diet. On embryonic day 17.5, embryos were weighed and fetal brains were snap frozen. RNA was extracted from male and female forebrains (10 per diet group per sex) and hybridized to whole-genome expression arrays. Significantly differentially expressed genes were identified using a Welch's t test with the Benjamini-Hochberg correction. Functional analyses were performed using ingenuity pathways analysis and gene set enrichment analysis. Embryos of dams on the high-fat diet were significantly smaller than controls, with males more severely affected than females (P = .01). Maternal obesity and maternal obesity with dietary change in pregnancy resulted in significantly more dysregulated genes in male vs female fetal brains (386 vs 66, P < .001). Maternal obesity with and without dietary change in pregnancy was associated with unique brain gene expression signatures for each sex, with an overlap of only 1 gene. Changing obese dams to a control diet in pregnancy resulted in more differentially expressed genes in the fetal brain than maternal obesity alone. Functional analyses identified common

  6. Emotion regulation in preschoolers: the roles of behavioral inhibition, maternal affective behavior, and maternal depression.

    PubMed

    Feng, Xin; Shaw, Daniel S; Kovacs, Maria; Lane, Tonya; O'Rourke, Flannery E; Alarcon, Joseph H

    2008-02-01

    This study examined preschoolers' emotion regulation (ER) strategies and the association with temperament, maternal interactive style, and maternal history of childhood-onset depression (COD). Participants were 62 children and their mothers, 37 of whom had mothers with COD. Children's ER was assessed using a disappointment paradigm; temperament assessment also was laboratory-based. Maternal COD was inversely related to offspring's active ER and positive mood. Among children of COD mothers, behavioral inhibition was associated with passive regulation and sadness, and maternal positivity toward these children was associated with child active ER and positive mood. Behavioral inhibition may place children of COD mothers at risk for developing maladaptive ways of regulating negative emotion, whereas mothers' positivity may serve as a protective factor for them.

  7. Effect of maternal obesity on fetal bone development in the rat

    USDA-ARS?s Scientific Manuscript database

    Epidemiological studies show that quality of nutrition during intrauterine and postnatal early life impact the risk of low bone mass and fracture later in life. Maternal consumption of high-fat diets has been demonstrated to affect health outcomes, such as: brain development; obesity; insulin resist...

  8. Maternal low protein diet leads to placental angiogenic compensation via dysregulated M1/M2 macrophages and TNFa expression in Sprague-Dawley rats

    USDA-ARS?s Scientific Manuscript database

    A maternal low-protein (LP) diet results in low birth weight, increased offspring rapid adipose tissue catch-up growth, adult obesity, and insulin resistance in Sprague-Dawley rats. The placenta functions to fulfill the fetus’ nutrient demands. Placental function is dependent on regulation of immune...

  9. Maternal Western diet increases adiposity even in male offspring of obesity-resistant rat dams: early endocrine risk markers.

    PubMed

    Frihauf, Jennifer B; Fekete, Éva M; Nagy, Tim R; Levin, Barry E; Zorrilla, Eric P

    2016-12-01

    Maternal overnutrition or associated complications putatively mediate the obesogenic effects of perinatal high-fat diet on developing offspring. Here, we tested the hypothesis that a Western diet developmental environment increases adiposity not only in male offspring from obesity-prone (DIO) mothers, but also in those from obesity-resistant (DR) dams, implicating a deleterious role for the Western diet per se. Selectively bred DIO and DR female rats were fed chow (17% kcal fat) or Western diet (32%) for 54 days before mating and, thereafter, through weaning. As intended, despite chow-like caloric intake, Western diet increased prepregnancy weight gain and circulating leptin levels in DIO, but not DR, dams. Yet, in both genotypes, maternal Western diet increased the weight and adiposity of preweanlings, as early as in DR offspring, and increased plasma leptin, insulin, and adiponectin of weanlings. Although body weight normalized with chow feeding during adolescence, young adult Western diet offspring subsequently showed decreased energy expenditure and, in DR offspring, decreased lipid utilization as a fuel substrate. By mid-adulthood, maternal Western diet DR offspring ate more chow, weighed more, and were fatter than controls. Thus, maternal Western diet covertly programmed increased adiposity in childhood and adulthood, disrupted relations of energy regulatory hormones with body fat, and decreased energy expenditure in offspring of lean, genetically obesity-resistant mothers. Maternal Western diet exposure alone, without maternal obesity or overnutrition, can promote offspring weight gain. Copyright © 2016 Frihauf et al.

  10. Maternal Western diet increases adiposity even in male offspring of obesity-resistant rat dams: early endocrine risk markers

    PubMed Central

    Frihauf, Jennifer B.; Fekete, Éva M.; Nagy, Tim R.; Levin, Barry E.

    2016-01-01

    Maternal overnutrition or associated complications putatively mediate the obesogenic effects of perinatal high-fat diet on developing offspring. Here, we tested the hypothesis that a Western diet developmental environment increases adiposity not only in male offspring from obesity-prone (DIO) mothers, but also in those from obesity-resistant (DR) dams, implicating a deleterious role for the Western diet per se. Selectively bred DIO and DR female rats were fed chow (17% kcal fat) or Western diet (32%) for 54 days before mating and, thereafter, through weaning. As intended, despite chow-like caloric intake, Western diet increased prepregnancy weight gain and circulating leptin levels in DIO, but not DR, dams. Yet, in both genotypes, maternal Western diet increased the weight and adiposity of preweanlings, as early as in DR offspring, and increased plasma leptin, insulin, and adiponectin of weanlings. Although body weight normalized with chow feeding during adolescence, young adult Western diet offspring subsequently showed decreased energy expenditure and, in DR offspring, decreased lipid utilization as a fuel substrate. By mid-adulthood, maternal Western diet DR offspring ate more chow, weighed more, and were fatter than controls. Thus, maternal Western diet covertly programmed increased adiposity in childhood and adulthood, disrupted relations of energy regulatory hormones with body fat, and decreased energy expenditure in offspring of lean, genetically obesity-resistant mothers. Maternal Western diet exposure alone, without maternal obesity or overnutrition, can promote offspring weight gain. PMID:27654396

  11. Genetic evidence for causal relationships between maternal obesity-related traits and birth weight

    PubMed Central

    Tyrrell, Jessica; Richmond, Rebecca C.; Palmer, Tom M.; Feenstra, Bjarke; Rangarajan, Janani; Metrustry, Sarah; Cavadino, Alana; Paternoster, Lavinia; Armstrong, Loren L.; De Silva, N. Maneka G.; Wood, Andrew R.; Horikoshi, Momoko; Geller, Frank; Myhre, Ronny; Bradfield, Jonathan P.; Kreiner-Møller, Eskil; Huikari, Ville; Painter, Jodie N.; Hottenga, Jouke-Jan; Allard, Catherine; Berry, Diane J.; Bouchard, Luigi; Das, Shikta; Evans, David M.; Hakonarson, Hakon; Hayes, M. Geoffrey; Heikkinen, Jani; Hofman, Albert; Knight, Bridget; Lind, Penelope A.; McCarthy, Mark I.; McMahon, George; Medland, Sarah E.; Melbye, Mads; Morris, Andrew P.; Nodzenski, Michael; Reichetzeder, Christoph; Ring, Susan M.; Sebert, Sylvain; Sengpiel, Verena; Sørensen, Thorkild I.A.; Willemsen, Gonneke; de Geus, Eco J. C.; Martin, Nicholas G.; Spector, Tim D.; Power, Christine; Järvelin, Marjo-Riitta; Bisgaard, Hans; Grant, Struan F.A.; Nohr, Ellen A.; Jaddoe, Vincent W.; Jacobsson, Bo; Murray, Jeffrey C.; Hocher, Berthold; Hattersley, Andrew T.; Scholtens, Denise M.; Smith, George Davey; Hivert, Marie-France; Felix, Janine F.; Hyppönen, Elina; Lowe, William L.; Frayling, Timothy M.; Lawlor, Debbie A.; Freathy, Rachel M.

    2016-01-01

    Structured abstract Importance Neonates born to overweight/obese women are larger and at higher risk of birth complications. Many maternal obesity-related traits are observationally associated with birth weight, but the causal nature of these associations is uncertain. Objective To test for genetic evidence of causal associations of maternal body mass index (BMI) and related traits with birth weight. Design, Setting and Participants We used Mendelian randomization to test whether maternal BMI and obesity-related traits are causally related to offspring birth weight. Mendelian randomization makes use of the fact that genotypes are randomly determined at conception and are thus not confounded by non-genetic factors. Data were analysed on 30,487 women from 18 studies. Participants were of European ancestry from population- or community-based studies located in Europe, North America or Australia and participating in the Early Growth Genetics (EGG) Consortium. Live, term, singleton offspring born between 1929 and 2013 were included. We tested associations between a genetic score of 30 BMI-associated single nucleotide polymorphisms (SNPs) and (i) maternal BMI and (ii) birth weight, to estimate the causal relationship between BMI and birth weight. Analyses were repeated for other obesity-related traits. Exposures Genetic scores for BMI, fasting glucose level, type 2 diabetes, systolic blood pressure (SBP), triglyceride level, HDL-cholesterol level, vitamin D status and adiponectin level. Main Outcome(s) and Measure(s) Offspring birth weight measured by trained study personnel (n=2 studies), from medical records (n= 10 studies) or from maternal report (n=6 studies). Results Among the 30,487 newborns the mean birth weight in the various cohorts ranged from 3325 g to 3679 g. The genetic score for BMI was associated with a 2g (95%CI: 0, 3g) higher offspring birth weight per maternal BMI-raising allele (P=0.008). The maternal genetic scores for fasting glucose and SBP were

  12. Maternal obesity disrupts circadian rhythms of clock and metabolic genes in the offspring heart and liver.

    PubMed

    Wang, Danfeng; Chen, Siyu; Liu, Mei; Liu, Chang

    2015-06-01

    Early life nutritional adversity is tightly associated with the development of long-term metabolic disorders. Particularly, maternal obesity and high-fat diets cause high risk of obesity in the offspring. Those offspring are also prone to develop hyperinsulinemia, hepatic steatosis and cardiovascular diseases. However, the precise underlying mechanisms leading to these metabolic dysregulation in the offspring remain unclear. On the other hand, disruptions of diurnal circadian rhythms are known to impair metabolic homeostasis in various tissues including the heart and liver. Therefore, we investigated that whether maternal obesity perturbs the circadian expression rhythms of clock, metabolic and inflammatory genes in offspring heart and liver by using RT-qPCR and Western blotting analysis. Offspring from lean and obese dams were examined on postnatal day 17 and 35, when pups were nursed by their mothers or took food independently. On P17, genes examined in the heart either showed anti-phase oscillations (Cpt1b, Pparα, Per2) or had greater oscillation amplitudes (Bmal1, Tnf-α, Il-6). Such phase abnormalities of these genes were improved on P35, while defects in amplitudes still existed. In the liver of 17-day-old pups exposed to maternal obesity, the oscillation amplitudes of most rhythmic genes examined (except Bmal1) were strongly suppressed. On P35, the oscillations of circadian and inflammatory genes became more robust in the liver, while metabolic genes were still kept non-rhythmic. Maternal obesity also had a profound influence in the protein expression levels of examined genes in offspring heart and liver. Our observations indicate that the circadian clock undergoes nutritional programing, which may contribute to the alternations in energy metabolism associated with the development of metabolic disorders in early life and adulthood.

  13. Obstructive heart defects associated with candidate genes, maternal obesity, and folic acid supplementation.

    PubMed

    Tang, Xinyu; Cleves, Mario A; Nick, Todd G; Li, Ming; MacLeod, Stewart L; Erickson, Stephen W; Li, Jingyun; Shaw, Gary M; Mosley, Bridget S; Hobbs, Charlotte A

    2015-06-01

    Right-sided and left-sided obstructive heart defects (OHDs) are subtypes of congenital heart defects, in which the heart valves, arteries, or veins are abnormally narrow or blocked. Previous studies have suggested that the development of OHDs involved a complex interplay between genetic variants and maternal factors. Using the data from 569 OHD case families and 1,644 control families enrolled in the National Birth Defects Prevention Study (NBDPS) between 1997 and 2008, we conducted an analysis to investigate the genetic effects of 877 single nucleotide polymorphisms (SNPs) in 60 candidate genes for association with the risk of OHDs, and their interactions with maternal use of folic acid supplements, and pre-pregnancy obesity. Applying log-linear models based on the hybrid design, we identified a SNP in methylenetetrahydrofolate reductase (MTHFR) gene (C677T polymorphism) with a main genetic effect on the occurrence of OHDs. In addition, multiple SNPs in betaine-homocysteine methyltransferase (BHMT and BHMT2) were also identified to be associated with the occurrence of OHDs through significant main infant genetic effects and interaction effects with maternal use of folic acid supplements. We also identified multiple SNPs in glutamate-cysteine ligase, catalytic subunit (GCLC) and DNA (cytosine-5-)-methyltransferase 3 beta (DNMT3B) that were associated with elevated risk of OHDs among obese women. Our findings suggested that the risk of OHDs was closely related to a combined effect of variations in genes in the folate, homocysteine, or glutathione/transsulfuration pathways, maternal use of folic acid supplements and pre-pregnancy obesity. © 2015 Wiley Periodicals, Inc.

  14. Regulation of appetite to treat obesity

    PubMed Central

    Kim, Gilbert W; Lin, Jieru E; Valentino, Michael A; Colon-Gonzalez, Francheska; Waldman, Scott A

    2011-01-01

    Obesity has escalated into a pandemic over the past few decades. In turn, research efforts have sought to elucidate the molecular mechanisms underlying the regulation of energy balance. A host of endogenous mediators regulate appetite and metabolism, and thereby control both short- and long-term energy balance. These mediators, which include gut, pancreatic and adipose neuropeptides, have been targeted in the development of anti-obesity pharmacotherapy, with the goal of amplifying anorexigenic and lipolytic signaling or blocking orexigenic and lipogenic signaling. This article presents the efficacy and safety of these anti-obesity drugs. PMID:21666781

  15. Associations Between Maternal Pregravid Obesity and Gestational Diabetes and the Timing of Pubarche in Daughters

    PubMed Central

    Kubo, Ai; Ferrara, Assiamira; Laurent, Cecile A.; Windham, Gayle C.; Greenspan, Louise C.; Deardorff, Julianna; Hiatt, Robert A.; Quesenberry, Charles P.; Kushi, Lawrence H.

    2016-01-01

    Abstract We investigated whether in utero exposure to maternal pregravid obesity and/or gestational diabetes mellitus (GDM) was associated with early puberty in girls. We used data from a longitudinal study of 421 mother-daughter pairs enrolled in an integrated health services organization, Kaiser Permanente Northern California (2005–2012). Girls aged 6–8 years were followed annually through ages 12–14 years. Onset of puberty was assessed using study clinic-based Tanner staging. We examined associations of self-reported pregravid obesity and maternal GDM with timing of the daughter's transition to pubertal maturation stage 2 or above for development of breasts and pubic hair, using accelerated failure time regression models with interval censoring to estimate time ratios and hazard ratios and corresponding 95% confidence intervals. Maternal obesity (pregravid body mass index (BMI; weight (kg)/height (m)2) ≥30) was associated with a daughter's earlier transition to breast and pubic hair stage 2+ in comparison with girls whose mothers had pregravid BMI <25. These associations were attenuated and not statistically significant after adjustment for covariates. Girls whose mothers had both pregravid BMI ≥25 and GDM were at higher risk of an earlier transition to pubic hair stage 2+ than those whose mothers had neither condition (adjusted time ratio = 0.89, 95% confidence interval: 0.83, 0.96; hazard ratio = 2.97, 95% confidence interval: 1.52, 5.83). These findings suggest that exposure to maternal obesity and hyperglycemia places girls at higher risk of earlier pubarche. PMID:27268032

  16. Management of reproduction and pregnancy complications in maternal obesity: which role for dietary polyphenols?

    PubMed

    Santangelo, Carmela; Varì, Rosaria; Scazzocchio, Beatrice; Filesi, Carmelina; Masella, Roberta

    2014-01-01

    Obesity is a global and dramatic public health problem; maternal obesity represents one of the main risk factors of infertility and pregnancy complications as it is associated with adverse maternal and offspring outcomes. In the last few years, adipose tissue dysfunction associated with altered adipocytokine secretion has been suggested to play a critical role in all the phases of reproductive process. Obesity is a nutrition-related disorder. In this regard, dietary intervention strategies, such as high intake of fruit and vegetables, have shown significant effects in both preserving health and counteracting obesity-associated diseases. Evidence has been provided that polyphenols, important constituents of plant-derived food, can influence developmental program of oocyte and embryo, as well as pregnancy progression by modulating several cellular pathways. This review will examine the controversial results so far obtained on adipocytokine involvement in fertility impairment and pregnancy complications. Furthermore, the different effects exerted by polyphenols on oocyte, embryo, and pregnancy development will be also taken in account. © 2013 International Union of Biochemistry and Molecular Biology.

  17. Methyl donor supplementation prevents transgenerational amplification of obesity

    USDA-ARS?s Scientific Manuscript database

    The obesity epidemic, recognized in developed nations for decades, is now a worldwide phenomenon. All age groups are affected, including women of childbearing age, fueling concern that maternal obesity before and during pregnancy and lactation impairs developmental establishment of body weight regul...

  18. Maternal pre-pregnancy obesity and achievement of infant motor developmental milestones in the Upstate KIDS Study

    PubMed Central

    Wylie, Amanda; Sundaram, Rajeshwari; Kus, Christopher; Ghassabian, Akhgar; Yeung, Edwina H.

    2015-01-01

    Objective Maternal pre-pregnancy obesity is associated with several poor infant health outcomes; however studies that investigated motor development have been inconsistent. Thus, we examined maternal pre-pregnancy weight status and infants’ gross motor development. Design and Methods Participants consisted of 4,901 mother-infant pairs from the Upstate KIDS study, a longitudinal cohort in New York. Mothers indicated dates when infants achieved each of six gross motor milestones when infants were 4, 8, 12, 18, and 24 months old. Failure time modeling under a Weibull distribution was utilized to compare time to achievement across three levels of maternal pre-pregnancy BMI. Hazard ratios below one indicate a lower “risk” of achieving the milestone and translate to later achievement. Results Compared to infants born to thin and normal weight mothers (BMI <25), infants born to obese mothers (BMI>30) were slower to sit without support [HR=0.91, p=0.03] and crawl on hands and knees [HR=0.86, p<0.001], after adjusting for maternal and birth characteristics. Increased gestational age was associated with faster achievement of all milestones but additional adjustment did not impact results. Conclusions Maternal pre-pregnancy obesity was associated with a slightly longer time for infant to sit and crawl, potentially due to a compromised intrauterine environment or reduced physically active play. PMID:25755075

  19. Maternal low protein diet leads to placental angiogenic compensation via dysregulated M1/M2 macrophages and TNFa expression in Sprague-Dawley rats

    USDA-ARS?s Scientific Manuscript database

    A maternal low-protein (LP) diet results in low birth weight, increased offspring rapid adipose tissue catch-up growth, adult obesity, and insulin resistance in Sprague-Dawley rats. The placenta plays key roles in nutrient transport and fetal growth. Placental function is dependent on regulation of ...

  20. Interventions designed to prevent adverse programming outcomes resulting from exposure to maternal obesity during development

    PubMed Central

    Nathanielsz, PW; Ford, SP; Long, NM; Vega, CC; Reyes-Castro, LA; Zambrano, E

    2013-01-01

    Maternal obesity is a global epidemic affecting the developed and developing world. Human and animal studies indicate that maternal obesity programs development predisposing offspring to later-life chronic diseases. Several mechanisms act together to produce these adverse health problems. There is a need for effective interventions that prevent these outcomes and guide management in human pregnancy. We report here dietary and exercise intervention studies in both altricial and precocial species, rats and sheep, designed to prevent adverse offspring outcomes. Both interventions present exciting opportunities to at least in part prevent adverse metabolic and other outcomes in mother and offspring. PMID:24147928

  1. Maternal obesity increases inflammation and exacerbates damage following neonatal hypoxic-ischaemic brain injury in rats.

    PubMed

    Teo, Jonathan D; Morris, Margaret J; Jones, Nicole M

    2017-07-01

    In humans, maternal obesity is associated with an increase in the incidence of birth related difficulties. However, the impact of maternal obesity on the severity of brain injury in offspring is not known. Recent studies have found evidence of increased glial response and inflammatory mediators in the brains as a result of obesity in humans and rodents. We hypothesised that hypoxic-ischaemic (HI) brain injury is greater in neonatal offspring from obese rat mothers compared to lean controls. Female Sprague Dawley rats were randomly allocated to high fat (HFD, n=8) or chow (n=4) diet and mated with lean male rats. On postnatal day 7 (P7), male and female pups were randomly assigned to HI injury or control (C) groups. HI injury was induced by occlusion of the right carotid artery followed by 3h exposure to 8% oxygen, at 37°C. Control pups were removed from the mother for the same duration under ambient conditions. Righting behaviour was measured on day 1 and 7 following HI. The extent of brain injury was quantified in brain sections from P14 pups using cresyl violet staining and the difference in volume between brain hemispheres was measured. Before mating, HFD mothers were 11% heavier than Chow mothers (p<0.05, t-test). Righting reflex was delayed in offspring from HFD-fed mothers compared to the Chow mothers. The Chow-HI pups showed a loss in ipsilateral brain tissue, while the HFD-HI group had significantly greater loss. No significant difference was detected in brain volume between the HFD-C and Chow-C pups. When analysed on a per litter basis, the size of the injury was significantly correlated with maternal weight. Similar observations were made with neuronal staining showing a greater loss of neurons in the brain of offspring from HFD-mothers following HI compared to Chow. Astrocytes appeared to more hypertrophic and a greater number of microglia were present in the injured hemisphere in offspring from mothers on HFD. HI caused an increase in the proportion of

  2. Infant Gut Microbiota Development Is Driven by Transition to Family Foods Independent of Maternal Obesity.

    PubMed

    Laursen, Martin Frederik; Andersen, Louise B B; Michaelsen, Kim F; Mølgaard, Christian; Trolle, Ellen; Bahl, Martin Iain; Licht, Tine Rask

    2016-01-01

    The first years of life are paramount in establishing our endogenous gut microbiota, which is strongly affected by diet and has repeatedly been linked with obesity. However, very few studies have addressed the influence of maternal obesity on infant gut microbiota, which may occur either through vertically transmitted microbes or through the dietary habits of the family. Additionally, very little is known about the effect of diet during the complementary feeding period, which is potentially important for gut microbiota development. Here, the gut microbiotas of two different cohorts of infants, born either of a random sample of healthy mothers (n = 114), or of obese mothers (n = 113), were profiled by 16S rRNA amplicon sequencing. Gut microbiota data were compared to breastfeeding patterns and detailed individual dietary recordings to assess effects of the complementary diet. We found that maternal obesity did not influence microbial diversity or specific taxon abundances during the complementary feeding period. Across cohorts, breastfeeding duration and composition of the complementary diet were found to be the major determinants of gut microbiota development. In both cohorts, gut microbial composition and alpha diversity were thus strongly affected by introduction of family foods with high protein and fiber contents. Specifically, intake of meats, cheeses, and Danish rye bread, rich in protein and fiber, were associated with increased alpha diversity. Our results reveal that the transition from early infant feeding to family foods is a major determinant for gut microbiota development. IMPORTANCE The potential influence of maternal obesity on infant gut microbiota may occur either through vertically transmitted microbes or through the dietary habits of the family. Recent studies have suggested that the heritability of obesity may partly be caused by the transmission of "obesogenic" gut microbes. However, the findings presented here suggest that maternal obesity per

  3. Infant Gut Microbiota Development Is Driven by Transition to Family Foods Independent of Maternal Obesity

    PubMed Central

    Laursen, Martin Frederik; Andersen, Louise B. B.; Michaelsen, Kim F.; Mølgaard, Christian; Trolle, Ellen; Bahl, Martin Iain

    2016-01-01

    ABSTRACT The first years of life are paramount in establishing our endogenous gut microbiota, which is strongly affected by diet and has repeatedly been linked with obesity. However, very few studies have addressed the influence of maternal obesity on infant gut microbiota, which may occur either through vertically transmitted microbes or through the dietary habits of the family. Additionally, very little is known about the effect of diet during the complementary feeding period, which is potentially important for gut microbiota development. Here, the gut microbiotas of two different cohorts of infants, born either of a random sample of healthy mothers (n = 114), or of obese mothers (n = 113), were profiled by 16S rRNA amplicon sequencing. Gut microbiota data were compared to breastfeeding patterns and detailed individual dietary recordings to assess effects of the complementary diet. We found that maternal obesity did not influence microbial diversity or specific taxon abundances during the complementary feeding period. Across cohorts, breastfeeding duration and composition of the complementary diet were found to be the major determinants of gut microbiota development. In both cohorts, gut microbial composition and alpha diversity were thus strongly affected by introduction of family foods with high protein and fiber contents. Specifically, intake of meats, cheeses, and Danish rye bread, rich in protein and fiber, were associated with increased alpha diversity. Our results reveal that the transition from early infant feeding to family foods is a major determinant for gut microbiota development. IMPORTANCE The potential influence of maternal obesity on infant gut microbiota may occur either through vertically transmitted microbes or through the dietary habits of the family. Recent studies have suggested that the heritability of obesity may partly be caused by the transmission of “obesogenic” gut microbes. However, the findings presented here suggest that

  4. Maternal high-fat diet associated with altered gene expression, DNA methylation, and obesity risk in mouse offspring.

    PubMed

    Keleher, Madeline Rose; Zaidi, Rabab; Shah, Shyam; Oakley, M Elsa; Pavlatos, Cassondra; El Idrissi, Samir; Xing, Xiaoyun; Li, Daofeng; Wang, Ting; Cheverud, James M

    2018-01-01

    We investigated maternal obesity in inbred SM/J mice by assigning females to a high-fat diet or a low-fat diet at weaning, mating them to low-fat-fed males, cross-fostering the offspring to low-fat-fed SM/J nurses at birth, and weaning the offspring onto a high-fat or low-fat diet. A maternal high-fat diet exacerbated obesity in the high-fat-fed daughters, causing them to weigh more, have more fat, and have higher serum levels of leptin as adults, accompanied by dozens of gene expression changes and thousands of DNA methylation changes in their livers and hearts. Maternal diet particularly affected genes involved in RNA processing, immune response, and mitochondria. Between one-quarter and one-third of differentially expressed genes contained a differentially methylated region associated with maternal diet. An offspring high-fat diet reduced overall variation in DNA methylation, increased body weight and organ weights, increased long bone lengths and weights, decreased insulin sensitivity, and changed the expression of 3,908 genes in the liver. Although the offspring were more affected by their own diet, their maternal diet had epigenetic effects lasting through adulthood, and in the daughters these effects were accompanied by phenotypic changes relevant to obesity and diabetes.

  5. Maternal high-fat diet associated with altered gene expression, DNA methylation, and obesity risk in mouse offspring

    PubMed Central

    Zaidi, Rabab; Shah, Shyam; Oakley, M. Elsa; Pavlatos, Cassondra; El Idrissi, Samir; Xing, Xiaoyun; Li, Daofeng; Wang, Ting; Cheverud, James M.

    2018-01-01

    We investigated maternal obesity in inbred SM/J mice by assigning females to a high-fat diet or a low-fat diet at weaning, mating them to low-fat-fed males, cross-fostering the offspring to low-fat-fed SM/J nurses at birth, and weaning the offspring onto a high-fat or low-fat diet. A maternal high-fat diet exacerbated obesity in the high-fat-fed daughters, causing them to weigh more, have more fat, and have higher serum levels of leptin as adults, accompanied by dozens of gene expression changes and thousands of DNA methylation changes in their livers and hearts. Maternal diet particularly affected genes involved in RNA processing, immune response, and mitochondria. Between one-quarter and one-third of differentially expressed genes contained a differentially methylated region associated with maternal diet. An offspring high-fat diet reduced overall variation in DNA methylation, increased body weight and organ weights, increased long bone lengths and weights, decreased insulin sensitivity, and changed the expression of 3,908 genes in the liver. Although the offspring were more affected by their own diet, their maternal diet had epigenetic effects lasting through adulthood, and in the daughters these effects were accompanied by phenotypic changes relevant to obesity and diabetes. PMID:29447215

  6. Maternal obesity and tobacco use modify the impact of genetic variants on the occurrence of conotruncal heart defects.

    PubMed

    Tang, Xinyu; Nick, Todd G; Cleves, Mario A; Erickson, Stephen W; Li, Ming; Li, Jingyun; MacLeod, Stewart L; Hobbs, Charlotte A

    2014-01-01

    Conotruncal heart defects (CTDs) are among the most severe birth defects worldwide. Studies of CTDs indicate both lifestyle behaviors and genetic variation contribute to the risk of CTDs. Based on a hybrid design using data from 616 case-parental and 1645 control-parental triads recruited for the National Birth Defects Prevention Study between 1997 and 2008, we investigated whether the occurrence of CTDs is associated with interactions between 921 maternal and/or fetal single nucleotide polymorphisms (SNPs) and maternal obesity and tobacco use. The maternal genotypes of the variants in the glutamate-cysteine ligase, catalytic subunit (GCLC) gene and the fetal genotypes of the variants in the glutathione S-transferase alpha 3 (GSTA3) gene were associated with an elevated risk of CTDs among obese mothers. The risk of delivering infants with CTDs among obese mothers carrying AC genotype for a variant in the GCLC gene (rs6458939) was 2.00 times the risk among those carrying CC genotype (95% confidence interval: 1.41, 2.38). The maternal genotypes of several variants in the glutathione-S-transferase (GST) family of genes and the fetal genotypes of the variants in the GCLC gene interacted with tobacco exposures to increase the risk of CTDs. Our study suggests that the genetic basis underlying susceptibility of the developing heart to the adverse effects of maternal obesity and tobacco use involve both maternal and embryonic genetic variants. These results may provide insights into the underlying pathophysiology of CTDs, and ultimately lead to novel prevention strategies.

  7. In vivo maternal and in vitro BPA exposure effects on hypothalamic neurogenesis and appetite regulators.

    PubMed

    Desai, Mina; Ferrini, Monica G; Han, Guang; Jellyman, Juanita K; Ross, Michael G

    2018-07-01

    In utero exposure to the ubiquitous plasticizer, bisphenol A (BPA) is associated with offspring obesity. As food intake/appetite is one of the critical elements contributing to obesity, we determined the effects of in vivo maternal BPA and in vitro BPA exposure on newborn hypothalamic stem cells which form the arcuate nucleus appetite center. For in vivo studies, female rats received BPA prior to and during pregnancy via drinking water, and newborn offspring primary hypothalamic neuroprogenitor (NPCs) were obtained and cultured. For in vitro BPA exposure, primary hypothalamic NPCs from healthy newborns were utilized. In both cases, we studied the effects of BPA on NPC proliferation and differentiation, including putative signal and appetite factors. Maternal BPA increased hypothalamic NPC proliferation and differentiation in newborns, in conjunction with increased neuroproliferative (Hes1) and proneurogenic (Ngn3) protein expression. With NPC differentiation, BPA exposure increased appetite peptide and reduced satiety peptide expression. In vitro BPA-treated control NPCs showed results that were consistent with in vivo data (increase appetite vs satiety peptide expression) and further showed a shift towards neuronal versus glial fate as well as an increase in the epigenetic regulator lysine-specific histone demethylase1 (LSD1). These findings emphasize the vulnerability of stem-cell populations that are involved in life-long regulation of metabolic homeostasis to epigenetically-mediated endocrine disruption by BPA during early life. Copyright © 2018. Published by Elsevier Inc.

  8. The effect of maternal obesity on the expression and functionality of placental P-glycoprotein: Implications in the individualized transplacental digoxin treatment for fetal heart failure.

    PubMed

    Wang, Chuan; Li, Huaying; Luo, Chunyan; Li, Yifei; Zhang, Yi; Yun, Ding; Mu, Dezhi; Zhou, Kaiyu; Hua, Yimin

    2015-10-01

    Placental P-glycoprotein (P-gp) plays a significant role in controlling digoxin transplacental rate. Investigations on P-gp regulation in placenta of women with different pregnant pathology are of great significance to the individualized transplacental digoxin treatment for fetal heart failure (FHF). This study aimed to explore the effect of maternal obesity on the expression and functionality of placental P-gp both in human and in mice. Placenta tissues from obese and lean women were collected. Female C57BL mice were fed with either a normal chow diet or a high-fat diet for 12 weeks before mating and throughout pregnancy. Maternal plasma glucose, HDL-C, LDL-C, TC, TGs, insulin, IL-1β, IL-6 and TNF-α concentrations was detected. Placental ABCB1/Abcb1a/Abcb1b/IL-1β/IL-6/TNF-α mRNA and P-gp/IL-1β/IL-6/TNF-α protein expression were determined by real-time quantitative PCR and western-blot, respectively. Maternal plasma and fetal-unit digoxin concentrations were detected by a commercial kit assay. Both ABCB1 gene mRNA and protein expression of obesity group was significantly lower than that of control group in human. The high-fat dietary intervention resulted in an overweight phenotype, a significant increased Lee's index, higher levels of plasma glucose, HDL-C, LDL-C, insulin and TGs, increased peri-renal and peri-reproductive gland adipose tissue weight, and larger size of adipose cell. Compared with control group at the same gestational day (E12.5, E15.5, E17.5), placental Abcb1a mRNA and P-gp expression of obese group were significantly decreased in mice, while digoxin transplacental rates were significantly increased. Higher maternal plasma IL-1β/TNF-α concentrations and placental IL-1β/TNF-α expression were observed in obesity groups in comparison with control group at the same gestational age. Maternal obesity could inhibit placental P-gp expression and its functionality both in human and in mice, which might be resulted from a heightened inflammatory

  9. Maternal obesity and post-natal high fat diet disrupt hepatic circadian rhythm in rat offspring

    USDA-ARS?s Scientific Manuscript database

    Offspring of obese (Ob) rat dams gain greater body wt and fat mass when fed high-fat diet (HFD) as compared to controls. Alterations of diurnal circadian rhythm are known to detrimentally impact metabolically active tissues such as liver. We sought to determine if maternal obesity (MOb) leads to p...

  10. Maternal obesity downregulates myogenesis and beta-catenin signaling in fetal skeletal muscle.

    PubMed

    Tong, Jun F; Yan, Xu; Zhu, Mei J; Ford, Stephen P; Nathanielsz, Peter W; Du, Min

    2009-04-01

    Skeletal muscle is one of the primary tissues responsible for insulin resistance and type 2 diabetes (T2D). The fetal stage is crucial for skeletal muscle development. Obesity induces inflammatory responses, which might regulate myogenesis through Wnt/beta-catenin signaling. This study evaluated the effects of maternal obesity (>30% increase in body mass index) during pregnancy on myogenesis and the Wnt/beta-catenin and IKK/NF-kappaB pathways in fetal skeletal muscle using an obese pregnant sheep model. Nonpregnant ewes were assigned to a control group (C; fed 100% of National Research Council recommendations; n=5) or obesogenic (OB; fed 150% of National Research Council recommendations; n=5) diet from 60 days before to 75 days after conception (term approximately 148 days) when fetal semitendenosus skeletal muscle was sampled for analyses. Myogenic markers including MyoD, myogenin, and desmin contents were reduced in OB compared with C fetal semitendenosus, indicating the downregulation of myogenesis. The diameter of primary muscle fibers was smaller in OB fetal muscle. Phosphorylation of GSK3beta was reduced in OB compared with C fetal semitendenosus. Although the beta-catenin level was lower in OB than C fetal muscle, more beta-catenin was associated with FOXO3a in the OB fetuses. Moreover, we found phosphorylation levels of IKKbeta and RelA/p65 were both increased in OB fetal muscle. In conclusion, our data showed that myogenesis and the Wnt/beta-catenin signaling pathway were downregulated, which might be due to the upregulation of inflammatory IKK/NF-kappaB signaling pathways in fetal muscle of obese mothers.

  11. Maternal obesity in early pregnancy and risk of adverse outcomes.

    PubMed

    Bautista-Castaño, Inmaculada; Henriquez-Sanchez, Patricia; Alemán-Perez, Nestor; Garcia-Salvador, Jose J; Gonzalez-Quesada, Alicia; García-Hernández, Jose A; Serra-Majem, Luis

    2013-01-01

    To assess the role of the health consequences of maternal overweight and obesity at the start of pregnancy on gestational pathologies, delivery and newborn characteristics. A cohort of pregnant women (n = 6.558) having delivered at the Maternal & Child University Hospital of Gran Canaria (HUMIGC) in 2008 has been studied. Outcomes were compared using multivariate analyses controlling for confounding variables. Compared to normoweight, overweight and obese women have greater risks of gestational diabetes mellitus (RR = 2.13 (95% CI: 1.52-2.98) and (RR = 2.85 (95% CI: 2.01-4.04), gestational hypertension (RR = 2.01 (95% CI: 1.27-3.19) and (RR = 4.79 (95% CI: 3.13-7.32) and preeclampsia (RR = 3.16 (95% CI: 1.12-8.91) and (RR = 8.80 (95% CI: 3.46-22.40). Obese women have also more frequently oligodramnios (RR = 2.02 (95% CI: 1.25-3.27), polyhydramnios. (RR = 1.76 (95% CI: 1.03-2.99), tearing (RR = 1.24 (95% CI: 1.05-1.46) and a lower risk of induced deliveries (RR = 0.83 (95% CI: 0.72-0.95). Both groups have more frequently caesarean section (RR = 1.36 (95% CI: 1.14-1.63) and (RR = 1.84 (95% CI: 1.53-2.22) and manual placenta extraction (RR = 1.65 (95% CI: 1.28-2.11) and (RR = 1.77 (95% CI: 1.35-2.33). Newborns from overweight and obese women have higher weight (p<0.001) and a greater risk of being macrosomic (RR = 2.00 (95% CI: 1.56-2.56) and (RR = 2.74 (95% CI: 2.12-3.54). Finally, neonates from obese mother have a higher risk of being admitted to special care units (RR = 1.34 (95% CI: 1.01-1.77). Apgar 1 min was significantly higher in newborns from normoweight mothers: 8.65 (95% CI: 8.62-8.69) than from overweight: 8.56 (95% CI: 8.50-8.61) or obese mothers: 8.48 (95% CI: 8.41-8.54). Obesity and overweight status at the beginning of pregnancy increase the adverse outcomes of the pregnancy. It is important to promote the normalization of bodyweight in those women who intend to get pregnant and to

  12. Maternal Depressive Symptoms, Toddler Emotion Regulation, and Subsequent Emotion Socialization

    PubMed Central

    Premo, Julie E.; Kiel, Elizabeth J.

    2015-01-01

    Although many studies have examined how maternal depressive symptoms relate to parenting outcomes, less work has examined how symptoms affect emotion socialization, a parenting construct linked to a myriad of socioemotional outcomes in early childhood. In line with a transactional perspective on the family, it is also important to understand how children contribute to these emotional processes. The current study examined how toddler emotion regulation strategies moderated the relation between maternal depressive symptoms and emotion socialization responses, including non-supportive responses (e.g., minimizing, responding punitively to children’s negative emotions) and wish-granting, or the degree to which mothers give in to their children’s demands in order to decrease their children’s and their own distress. Mothers (n = 91) and their 24-month-old toddlers participated in laboratory tasks from which toddler emotion regulation behaviors were observed. Mothers reported depressive symptoms and use of maladaptive emotion socialization strategies concurrently and at a 1-year follow-up. The predictive relation between maternal depressive symptoms and emotion socialization was then examined in the context of toddlers’ emotion regulation. Toddlers’ increased use of caregiver-focused regulation interacted with depressive symptoms in predicting increased wish-granting socialization responses at 36 months. At high levels of toddlers’ caregiver-focused regulation, depressive symptoms related to increased wish granting socialization at 36 months. There was no relation for non-supportive socialization responses. Results suggest that toddler emotional characteristics influence how depressive symptoms may put mothers at risk for maladaptive parenting. Family psychologists must strive to understand the role of both parent and toddler characteristics within problematic emotional interactions. PMID:26461486

  13. Existing maternal obesity guidelines may increase inequalities between ethnic groups: a national epidemiological study of 502,474 births in England.

    PubMed

    Heslehurst, Nicola; Sattar, Naveed; Rajasingam, Daghni; Wilkinson, John; Summerbell, Carolyn D; Rankin, Judith

    2012-12-18

    Asians are at increased risk of morbidity at a lower body mass index (BMI) than European Whites, particularly relating to metabolic risk. UK maternal obesity guidelines use general population BMI criteria to define obesity, which do not represent the risk of morbidity among Asian populations. This study compares incidence of first trimester obesity using Asian-specific and general population BMI criteria. A retrospective epidemiological study of 502,474 births between 1995 and 2007, from 34 maternity units across England. Data analyses included a comparison of trends over time between ethnic groups using Asian-specific and general population BMI criteria. Logistic regression estimated odds ratios for first trimester obesity among ethnic groups following adjustment for population demographics. Black and South Asian women have a higher incidence of first trimester obesity compared with White women. This is most pronounced for Pakistani women following adjustment for population structure (OR 2.19, 95% C.I. 2.08, 2.31). There is a twofold increase in the proportion of South Asian women classified as obese when using the Asian-specific BMI criteria rather than general population BMI criteria. The incidence of obesity among Black women is increasing at the most rapid rate over time (p=0.01). The twofold increase in maternal obesity among South Asians when using Asian-specific BMI criteria highlights inequalities among pregnant women. A large proportion of South Asian women are potentially being wrongly assigned to low risk care using current UK guidelines to classify obesity and determine care requirements. Further research is required to identify if there is any improvement in pregnancy outcomes if Asian-specific BMI criteria are utilised in the clinical management of maternal obesity to ensure the best quality of care is provided for women irrespective of ethnicity.

  14. Maternal overweight and obesity and risk of pre-eclampsia in women with type 1 diabetes or type 2 diabetes.

    PubMed

    Persson, Martina; Cnattingius, Sven; Wikström, Anna-Karin; Johansson, Stefan

    2016-10-01

    Women with type 1 or type 2 diabetes are at increased risk of pre-eclampsia. Overweight and obesity are associated with an increased risk of pre-eclampsia in women without diabetes. The aim of the study was to investigate the impact of maternal overweight and obesity on the risk of pre-eclampsia in women with type 1 diabetes or type 2 diabetes. In a population-based cohort study including singleton births in Sweden, we estimated the risk of pre-eclampsia among women with type 1 diabetes (n = 7062) and type 2 diabetes (n = 886), and investigated whether maternal overweight (BMI 25-29.9 kg/m(2)) and obesity (BMI ≥30.0 kg/m(2)) modified the risk. Logistic regression analyses were used to estimate crude and adjusted ORs with 95% CIs, using women without diabetes as the reference group (n = 1,509,525). Compared with women without diabetes, the adjusted ORs for pre-eclampsia in women with type 1 and type 2 diabetes were 5.74 (95% CI 5.31, 6.20) and 2.11 (95% CI 1.65, 2.70), respectively. The corresponding risks of pre-eclampsia combined with preterm birth were even higher. Risks of pre-eclampsia increased with maternal overweight (BMI 25-29.9 kg/m(2)) and obesity (BMI ≥30.0 kg/m(2)), foremost in women without diabetes, to a lesser extent in women with type 1 diabetes but not in women with type 2 diabetes. Maternal overweight and obesity increased risks of pre-eclampsia in women with type 1 diabetes but not in women with type 2 diabetes. Even so, considering associations between maternal BMI and overall maternal and offspring risk, all women (with and without diabetes) should aim for a normal weight before pregnancy.

  15. Maternal obesity during gestation impairs fatty acid oxidation and mitochondrial SIRT3 expression in rat offspring at weaning

    USDA-ARS?s Scientific Manuscript database

    In utero exposure to maternal obesity increases the offspring’s risk of obesity in later life. We have also previously reported that offspring of obese rat dams develop hepatic steatosis, mild hyperinsulinemia, and a lipogenic gene signature in the liver at postnatal day (PND) 21. In the current s...

  16. Maternal super-obesity and perinatal outcomes in Australia: a national population-based cohort study.

    PubMed

    Sullivan, Elizabeth A; Dickinson, Jan E; Vaughan, Geraldine A; Peek, Michael J; Ellwood, David; Homer, Caroline S E; Knight, Marian; McLintock, Claire; Wang, Alex; Pollock, Wendy; Jackson Pulver, Lisa; Li, Zhuoyang; Javid, Nasrin; Denney-Wilson, Elizabeth; Callaway, Leonie

    2015-12-02

    Super-obesity is associated with significantly elevated rates of obstetric complications, adverse perinatal outcomes and interventions. The purpose of this study was to determine the prevalence, risk factors, management and perinatal outcomes of super-obese women giving birth in Australia. A national population-based cohort study. Super-obese pregnant women (body mass index (BMI) >50 kg/m(2) or weight >140 kg) who gave birth between January 1 and October 31, 2010 and a comparison cohort were identified using the Australasian Maternity Outcomes Surveillance System (AMOSS). Outcomes included maternal and perinatal morbidity and mortality. Prevalence estimates calculated with 95% confidence intervals (CIs). Adjusted odds ratios (ORs) were calculated using multivariable logistic regression. 370 super-obese women with a median BMI of 52.8 kg/m(2) (range 40.9-79.9 kg/m(2)) and prevalence of 2.1 per 1 000 women giving birth (95% CI: 1.96-2.40). Super-obese women were significantly more likely to be public patients (96.2%), smoke (23.8%) and be socio-economically disadvantaged (36.2%). Compared with other women, super-obese women had a significantly higher risk for obstetric (adjusted odds ratio (AOR) 2.42, 95% CI: 1.77-3.29) and medical (AOR: 2.89, 95% CI: 2.64-4.11) complications during pregnancy, birth by caesarean section (51.6%) and admission to special care (HDU/ICU) (6.2%). The 372 babies born to 365 super-obese women with outcomes known had significantly higher rates of birthweight ≥ 4500 g (AOR 19.94, 95 % CI: 6.81-58.36), hospital transfer (AOR 3.81, 95 % CI: 1.93-7.55) and admission to Neonatal Intensive Care Unit (NICU) (AOR 1.83, 95% CI: 1.27-2.65) compared to babies of the comparison group, but not prematurity (10.5% versus 9.2%) or perinatal mortality (11.0 (95% CI: 4.3-28.0) versus 6.6 (95% CI: 2.6- 16.8) per 1 000 singleton births). Super-obesity in pregnancy in Australia is associated with increased rates of pregnancy and birth complications, and with

  17. Influence of maternal obesity, diet and exercise on epigenetic regulation of adipocytes

    USDA-ARS?s Scientific Manuscript database

    The prevalence of obesity and metabolic syndrome has been increasing at an alarming rate in both children and adults. Obesity is associated with increased risk for development of metabolic syndrome and chronic diseases. Obesity is a leading cause of preventable death so there is an urgent need for u...

  18. The Impact of maternal obesity and race/ethnicity on perinatal outcomes: Independent and joint effects.

    PubMed

    Snowden, Jonathan M; Mission, John F; Marshall, Nicole E; Quigley, Brian; Main, Elliott; Gilbert, William M; Chung, Judith H; Caughey, Aaron B

    2016-07-01

    Independent and joint impacts of maternal race/ethnicity and obesity on adverse birth outcomes, including pre-eclampsia, low birth weight, and macrosomia, were characterized. Retrospective cohort study of all 2007 California births was conducted using vital records and claims data. Maternal race/ethnicity and maternal body mass index (BMI) were the key exposures; their independent and joint impact on outcomes using regression models was analyzed. Racial/ethnic minority women of normal weight generally had higher risk as compared with white women of normal weight (e.g., African-American women, pre-eclampsia adjusted odds ratio [aOR] 1.60, 95% confidence interval [CI]: 1.48-1.74 vs. white women). However, elevated BMI did not usually confer additional risk (e.g., pre-eclampsia aOR comparing African-American women with excess weight with white women with excess weight, 1.17, 95% CI: 0.89-1.54). Obesity was a risk factor for low birth weight only among white women (excess weight aOR, 1.24, 95% CI: 1.04-1.49 vs. white women of normal weight) and not among racial/ethnic minority women (e.g., African-American women, 0.95, 95% CI: 0.83-1.08). These findings add nuance to our understanding of the interplay between maternal race/ethnicity, BMI, and perinatal outcomes. While the BMI/adverse outcome gradient appears weaker in racial/ethnic minority women, this reflects the overall risk increase in racial/ethnic minority women of all body sizes. © 2016 The Obesity Society.

  19. Maternal mentalization affects mothers' - but not children's - weight via emotional eating.

    PubMed

    Keitel-Korndörfer, Anja; Bergmann, Sarah; Nolte, Tobias; Wendt, Verena; von Klitzing, Kai; Klein, Annette M

    2016-10-01

    Previous research on childhood obesity has shown that maternal obesity is an important risk factor for this malady. Because biological and environmental factors are able to explain the transgenerational transmission of obesity only in part, psychological risk factors (e.g., emotional eating) have become more important in recent research. As maternal mentalization - which lays the foundation for the child's ability to regulate his/her emotions - has not yet been investigated, we examined the effects of mentalization on maternal and childhood obesity. By investigating groups of obese (n = 30) and normal-weight (n = 30) mothers and their children aged 18 to 55 months, we found, contrary to our expectations, that obese mothers' mentalization (Reflective Functioning Scale) was similar to that of mothers with normal weight and that mentalization showed no direct effect on the child's weight. However, we found hints of an indirect influence of mentalization via emotional eating on mothers' but not on children's weight and via mother-child attachment (Attachment Q-Set) on children's weight. Possible reasons for these inconclusive effects are discussed.

  20. Lifestyle intervention up-regulates gene and protein levels of molecules involved in insulin signaling in the endometrium of overweight/obese women with polycystic ovary syndrome.

    PubMed

    Ujvari, D; Hulchiy, M; Calaby, A; Nybacka, Å; Byström, B; Hirschberg, A L

    2014-07-01

    Does lifestyle intervention aiming at weight loss influence endometrial insulin signaling in overweight/obese women with polycystic ovary syndrome (PCOS)? Lifestyle intervention up-regulates, both at the mRNA and protein levels, components of insulin signaling in the endometrium of overweight/obese PCOS women, in relation to an improved menstrual pattern. PCOS is a multifactorial endocrine disorder diagnosed by two of the following three criteria: chronic anovulation, hyperandrogenism and polycystic ovaries. Many women with PCOS also have insulin resistance and obesity. The syndrome is furthermore associated with endometrial cancer and possible alterations in endometrial function and receptivity. This study assessed the effects of a combined diet and exercise lifestyle intervention for 3 months. A group of 20 overweight/obese PCOS women with anovulation, hyperandrogenism and polycystic ovaries were subjected to a combined diet and exercise program for 3 months. Ten body mass index (BMI)-matched regularly menstruating overweight/obese controls, nine normal-weight PCOS women and ten normal-weight controls were also included in the study. In an academic clinical setting, women were examined in mid-follicular phase for endocrine assessment and determination of endometrial levels of mRNA and immunohistochemical staining of insulin signaling molecules (the insulin receptor, insulin receptor substrate-1 (IRS1) and glucose transporter (GLUT) 1 and 4). Women with PCOS exhibited lower levels of IRS1 (P < 0.01) and GLUT4 (P < 0.01) mRNA in their proliferative endometrium than BMI-matched controls. After lifestyle intervention, weight loss averaged 4.7% and the menstrual pattern improved in 65% of the overweight/obese women with PCOS. Levels of IRS1 (P < 0.01) and GLUT1 (P < 0.05) mRNA were significantly up-regulated in the endometrium of those women with improved menstrual function, as were the protein expression levels of pY612IRS1 (the activated IRS1 form, P < 0.05), pS312

  1. Childhood obesity is associated with maternal smoking in pregnancy.

    PubMed

    Toschke, André Michael; Koletzko, Berthold; Slikker, William; Hermann, Monika; von Kries, Rüdiger

    2002-08-01

    Overweight and obesity are major public health issues. Childhood obesity often persists throughout adulthood. Recently a higher prevalence of obesity in adults whose mothers smoked during pregnancy was reported. The aim of this study was to assess whether this association is also detectable in pre-school children in a different setting and to identify the critical period for intrauterine exposure to inhaled smoke products in pregnancy. We analysed questionnaire data on early feeding and lifestyle factors of 8,765 German children aged 5.00 to 6.99 years. Obesity was defined as a body mass index >97th percentile. The prevalence estimates for obesity were: mother never smoked 2.8% (95% CI 2.4%-3.2%), smoked after pregnancy only 1.6% (95%CI 0.4%-4.1%), smoked throughout pregnancy 6.2% (95% CI 4.5%-8.3%), smoked before pregnancy, but not throughout 4.5% (95%CI 3.6%-5.7%). These associations could not be explained by confounding due to a number of constitutional, sociodemographic and lifestyle factors. The unadjusted/adjusted odds ratios were: smoked during pregnancy: 2.32 (95% CI 1.63%-3.30%)/1.92 (95% CI 1.29%-2.86%); smoked before, but not throughout pregnancy: 1.67 (95%CI 1.26%-2.22%)/1.74 (95%CI 1.29%-2.34%). the association of maternal smoking in pregnancy and obesity was also detectable in children at school entry. Since smoking after pregnancy was not associated with childhood obesity, intrauterine exposure rather than family lifestyle factors associated with smoking appears to be instrumental. There appears to be a role for early intrauterine exposure.

  2. Maternal Self-Regulation, Relationship Adjustment, and Home Chaos: Contributions to Infant Negative Emotionality

    PubMed Central

    Bridgett, David J.; Burt, Nicole M.; Laake, Lauren M.; Oddi, Kate B.

    2013-01-01

    There has been increasing interest in the direct and indirect effects of parental self-regulation on children’s outcomes. In the present investigation, the effects of maternal self-regulation, home chaos, and inter-parental relationship adjustment on broad and specific indicators of infant negative emotionality (NE) were examined. A sample of maternal caregivers and their 4-month-old infants (N = 85) from a rural community participated. Results demonstrated that better maternal self-regulation was associated with lower infant NE broadly, as well as with lower infant sadness and distress to limitations/frustration and better falling reactivity (i.e. emotion regulation), specifically. Maternal self-regulation also predicted less chaotic home environments and better maternal inter-parental relationship adjustment. Findings also supported the indirect effects of maternal self-regulation on broad and specific indicators of infant NE through home chaos and maternal relationship adjustment. Some differential effects were also identified. Elevated home chaos appeared to specifically affect infant frustration/distress to limitations whereas maternal relationship adjustment affected broad infant NE, as well as several specific indicators of infant NE: frustration/distress to limitations, sadness, and falling reactivity. In conjunction with other recent investigations that have reported the effects of maternal self-regulation on parenting, the findings in the present investigation suggest that parental self-regulation may influence children’s outcomes through several proximal environmental pathways. PMID:23748168

  3. Maternal self-regulation, relationship adjustment, and home chaos: contributions to infant negative emotionality.

    PubMed

    Bridgett, David J; Burt, Nicole M; Laake, Lauren M; Oddi, Kate B

    2013-12-01

    There has been increasing interest in the direct and indirect effects of parental self-regulation on children's outcomes. In the present investigation, the effects of maternal self-regulation, home chaos, and inter-parental relationship adjustment on broad and specific indicators of infant negative emotionality (NE) were examined. A sample of maternal caregivers and their 4-month-old infants (N = 85) from a rural community participated. Results demonstrated that better maternal self-regulation was associated with lower infant NE broadly, as well as with lower infant sadness and distress to limitations/frustration and better falling reactivity (i.e., emotion regulation), specifically. Maternal self-regulation also predicted less chaotic home environments and better maternal inter-parental relationship adjustment. Findings also supported the indirect effects of maternal self-regulation on broad and specific indicators of infant NE through home chaos and maternal relationship adjustment. Some differential effects were also identified. Elevated home chaos appeared to specifically affect infant frustration/distress to limitations whereas maternal relationship adjustment affected broad infant NE, as well as several specific indicators of infant NE: frustration/distress to limitations, sadness, and falling reactivity. In conjunction with other recent investigations that have reported the effects of maternal self-regulation on parenting, the findings in the present investigation suggest that parental self-regulation may influence children's outcomes through several proximal environmental pathways. Copyright © 2013 Elsevier Inc. All rights reserved.

  4. The Impact of Maternal Obesity and Gestational Weight Gain on Early and Mid-Pregnancy Lipid Profiles

    PubMed Central

    Scifres, Christina M.; Catov, Janet M.; Simhan, Hyagriv N.

    2015-01-01

    Objective We evaluated the impact of maternal overweight/obesity and excessive weight gain on maternal serum lipids in the first and second trimester of pregnancy. Design and Methods Prospective data were collected for 225 women. Maternal serum lipids and fatty acids were measured at <13 weeks and between 24–28 weeks. Analyses were stratified by normal weight versus overweight/obese status and excessive vs. non-excessive weight gain. Results Overweight/obese women had higher baseline cholesterol (161.3±29.6 vs 149.4±26.8 mg/dL, p<0.01), LDL (80.0±19.9 vs 72.9 ±18.8 mg/dL, p<0.01) and triglycerides ( 81.7±47.2 vs 69.7±40.3 mg/dL, p=0.05) when compared to normal weight women, while HDL (43.6 ±10.4 47.6±11.5 mg/dL, p<0.01) was lower. However, cholesterol and LDL increased at a higher weekly rate in normal weight women, resulting in higher total cholesterol in normal weight women (184.1±28.1 vs. 176.0 ±32.1 mg/dL, p=0.05) at 24–28 weeks. Excessive weight gain did not affect the rate of change in lipid profiles in either group. Overweight/obese women had higher levels of arachidonic acid at both time points. Conclusions Overweight/obese women have significantly more atherogenic lipid profiles than normal weight women during the period of early pregnancy, delineating one physiologic pathway that could explain differences in pregnancy outcomes between normal weight and overweight/obese women. PMID:23853155

  5. Exercise in obese female rats has beneficial effects on maternal and male and female offspring metabolism

    PubMed Central

    Vega, Claudia C; Reyes-Castro, Luis A; Bautista, Claudia J; Larrea, Fernando; Nathanielsz, Peter W; Zambrano, Elena

    2013-01-01

    BACKGROUND Maternal obesity (MO) impairs maternal and offspring health. Mechanisms and interventions to prevent adverse maternal and offspring outcomes need to be determined. Human studies are confounded by socio-economic status providing the rationale for controlled animal data on effects of maternal exercise (MEx) intervention on maternal (F0) and offspring (F1) outcomes in MO. HYPOTHESIS MO produces metabolic and endocrine dysfunction, increases maternal and offspring glucocorticoid exposure, oxidative stress and adverse offspring outcomes by postnatal day (PND) 36. MEx prevents these outcomes. METHODS F0 female rats ate either control or obesogenic diet from weaning through lactation. Half of each group wheel ran (from day ninety of life through pregnancy beginning day 120) providing four groups (n=8/group) – i) controls, ii) obese, iii) exercised controls and iv) exercised obese. After weaning, PND 21, F1 offspring ate a control diet. Metabolic parameters of F0 prepregnancy and end of lactation and F1 offspring at PND 36 were analyzed. RESULTS Exercise did not change maternal weight. Before breeding, MO elevated F0 glucose, insulin, triglycerides, cholesterol, leptin, fat and oxidative stress. Exercise completely prevented the triglyceride rise and partially glucose, insulin, cholesterol and oxidative stress increases. MO decreased fertility, recovered by exercise. At the end of lactation, exercise returned all metabolic variables except leptin to control levels. Exercise partially prevented MO elevated corticosterone. F1 Offspring weights were similar at birth. At PND 36 MO increased F1 male but not female offspring leptin, triglycerides and fat mass. In controls exercise reduced male and female offspring glucose, prevented the offspring leptin increase and partially the triglyceride rise. CONCLUSIONS MEx before and during pregnancy has beneficial effects on maternal and offspring metabolism and endocrine function occurring with no weight change in mothers

  6. Antenatal exercise in overweight and obese women and its effects on offspring and maternal health: design and rationale of the IMPROVE (Improving Maternal and Progeny Obesity Via Exercise) randomised controlled trial.

    PubMed

    Seneviratne, Sumudu N; Parry, Graham K; McCowan, Lesley Me; Ekeroma, Alec; Jiang, Yannan; Gusso, Silmara; Peres, Geovana; Rodrigues, Raquel O; Craigie, Susan; Cutfield, Wayne S; Hofman, Paul L

    2014-04-26

    Obesity during pregnancy is associated with adverse outcomes for the offspring and mother. Lifestyle interventions in pregnancy such as antenatal exercise, are proposed to improve both short- and long-term health of mother and child. We hypothesise that regular moderate-intensity exercise during the second half of pregnancy will result in improved maternal and offspring outcomes, including a reduction in birth weight and adiposity in the offspring, which may be protective against obesity in later life. The IMPROVE (Improving Maternal and Progeny Risks of Obesity Via Exercise) study is a two-arm parallel randomised controlled clinical trial being conducted in Auckland, New Zealand. Overweight and obese women (BMI ≥25 kg/m2) aged 18-40 years, with a singleton pregnancy of <20 weeks of gestation, from the Auckland region, are eligible for the trial. Exclusion criteria are ongoing smoking or medical contra-indications to antenatal exercise.Participants are randomised with 1:1 allocation ratio to either intervention or control group, using computer-generated randomisation sequences in variable block sizes, stratified on ethnicity and parity, after completion of baseline assessments. The intervention consists of a 16-week structured home-based moderate-intensity exercise programme utilising stationary cycles and heart rate monitors, commencing at 20 weeks of gestation. The control group do not receive any exercise intervention. Both groups undergo regular fetal ultrasonography and receive standard antenatal care. Due to the nature of the intervention, participants are un-blinded to group assignment during the trial.The primary outcome is offspring birth weight. Secondary offspring outcomes include fetal and neonatal body composition and anthropometry, neonatal complications and cord blood metabolic markers. Maternal outcomes include weight gain, pregnancy and delivery complications, aerobic fitness, quality of life, metabolic markers and post-partum body composition

  7. The effect of androgen excess on maternal metabolism, placental function and fetal growth in obese dams.

    PubMed

    Fornes, Romina; Maliqueo, Manuel; Hu, Min; Hadi, Laila; Jimenez-Andrade, Juan M; Ebefors, Kerstin; Nyström, Jenny; Labrie, Fernand; Jansson, Thomas; Benrick, Anna; Stener-Victorin, Elisabet

    2017-08-14

    Pregnant women with polycystic ovary syndrome (PCOS) are often overweight or obese. To study the effects of maternal androgen excess in obese dams on metabolism, placental function and fetal growth, female C57Bl6J mice were fed a control (CD) or a high fat/high sucrose (HF/HS) diet for 4-10 weeks, and then mated. On gestational day (GD) 15.5-17.5, dams were injected with dihydrotestosterone (CD-DHT, HF/HS-DHT) or a vehicle (CD-Veh, HF/HS-Veh). HF/HS dams had higher fat content, both before mating and on GD18.5, with no difference in glucose homeostasis, whereas the insulin sensitivity was higher in DHT-exposed dams. Compared to the CD groups, the livers from HF/HS dams weighed more on GD18.5, the triglyceride content was higher, and there was a dysregulation of liver enzymes related to lipogenesis and higher mRNA expression of Fitm1. Fetuses from HF/HS-Veh dams had lower liver triglyceride content and mRNA expression of Srebf1c. Maternal DHT exposure, regardless of diet, decreased fetal liver Pparg mRNA expression and increased placental androgen receptor protein expression. Maternal diet-induced obesity, together with androgen excess, affects maternal and fetal liver function as demonstrated by increased triglyceride content and dysfunctional expression of enzymes and transcription factors involved in de novo lipogenesis and fat storage.

  8. Maternal obesity is associated with gut microbial metabolic potential in offspring during infancy.

    PubMed

    Cerdó, Tomás; Ruiz, Alicia; Jáuregui, Ruy; Azaryah, Hatim; Torres-Espínola, Francisco José; García-Valdés, Luz; Teresa Segura, M; Suárez, Antonio; Campoy, Cristina

    2018-02-01

    Children born to obese mothers are at increased risk for obesity, but the mechanisms behind this association are not fully understood. Our study aimed to investigate differences in the functions encoded by the microbiome of infants at 18 months of age when the transition from early infant-feeding to solid family foods is established. To investigate the impact of maternal prepregnancy body mass index on infants' gut microbiome, faecal samples from infants born to normoweight (n = 21) and obese mothers (n = 18) were analysed by 16S rRNA gene sequencing and a functional-inference-based microbiome analysis. Our results indicated that Firmicutes was significantly enriched in infants born to normoweight mothers whereas Bacteroidetes was significantly enriched in infants born to obese women. In both microbiomes, the greatest number of genes (>50%) that were assigned a function encoded for proteins involved in "metabolism" among tier 1 KEGG Orthology (KO) categories. At lower KO functional categories, the microbiome of infants born to normoweight mothers was characterized by a significant enrichment in the abundances of "pentose phosphate pathway" (p = 0.037), "lysine biosynthesis" (p = 0.043), "glycerolipid metabolism" (p = 0.042), and "C5-branched dibasic acid metabolism" (p = 0.045). Notably, the microbiome of infants born to obese mothers was significantly enriched in "streptomycin biosynthesis" (p = 0.047), "sulphur metabolism" (p = 0.041), "taurine and hypotaurine metabolism" (p = 0.036), and "lipopolysaccharide biosynthesis" (p = 0.043). In summary, our study showed that maternal prepregnancy obesity may imprint a selective gut microbial composition during late infancy with distinct functional performances.

  9. Maternal Emotion Regulation Strategies, Internalizing Problems and Infant Negative Affect

    PubMed Central

    Edwards, Erin S.; Holzman, Jacob B.; Burt, Nicole M.; Rutherford, Helena J. V.; Mayes, Linda C.; Bridgett, David J.

    2016-01-01

    Recent work has identified links between mothers’ self-regulation and emotion regulation (ER) and children’s social-emotional outcomes. However, associations between maternal ER strategies (e.g., reappraisal, suppression), known to influence internalizing problems in adults, and children’s negative affect (NA) have not been considered. In the current study, the direct and indirect relationships, through maternal internalizing problems, between maternal use of ER strategies and infant NA are examined. The potential effects of infant NA on maternal internalizing difficulties are also considered. Ninety-nine mothers and their infants participated across three time points during the first year postpartum. Higher maternal suppression was indirectly related to higher infant NA, through maternal internalizing problems; lower maternal reappraisal also was indirectly related to higher infant NA through maternal internalizing problems. Infant NA at four months postpartum was related to mothers’ internalizing problems 6 months postpartum. The implications of these findings for future research and intervention are discussed. PMID:28785122

  10. Diet-induced obesity reduces core body temperature across the estrous cycle and pregnancy in the rat.

    PubMed

    Crew, Rachael C; Waddell, Brendan J; Maloney, Shane K; Mark, Peter J

    2018-04-16

    Obesity during pregnancy causes adverse maternal and fetal health outcomes and programs offspring for adult-onset diseases, including cardiovascular disease. Obesity also disrupts core body temperature (T c ) regulation in nonpregnant rodents; however, it is unknown whether obesity alters normal maternal T c adaptations to pregnancy. Since T c is influenced by the circadian system, and both obesity and pregnancy alter circadian biology, it was hypothesized that obesity disrupts the normal rhythmic patterns of T c before and during gestation. Obesity was induced by cafeteria (CAF) feeding in female Wistar rats for 8 weeks prior to and during gestation, whereas control (CON) animals had free access to chow. Intraperitoneal temperature loggers measured daily T c profiles throughout the study, while maternal body composition and leptin levels were assessed near term. Daily temperature profiles were examined for rhythmic features (mesor, amplitude and acrophase) by cosine regression analysis. CAF animals exhibited increased fat mass (93%) and associated hyperleptinemia (3.2-fold increase) compared to CON animals. CAF consumption reduced the average T c (by up to 0.29°C) across the estrous cycle and most of pregnancy; however, T c for CAF and CON animals converged toward the end of gestation. Obesity reduced the amplitude of T c rhythms at estrus and proestrus and on day 8 of pregnancy, but increased the amplitude at day 20 of pregnancy. Photoperiod analysis revealed that obesity reduced T c exclusively in the light period during pre-pregnancy but only during the dark period in late gestation. In conclusion, obesity alters rhythmic T c profiles and reduces the magnitude of the T c decline late in rat gestation, which may have implications for maternal health and fetal development.

  11. A mouse model of pre-pregnancy maternal obesity combined with offspring exposure to a high-fat diet resulted in cognitive impairment in male offspring.

    PubMed

    Zhu, Chen; Han, Ting-Li; Zhao, Yalan; Zhou, Xiaobo; Mao, Xun; Qi, Hongbo; Baker, Philip N; Zhang, Hua

    2018-04-23

    Cognitive impairment is a brain dysfunction characterized by neuropsychological deficits in attention, working memory, and executive function. Maternal obesity and consumption of a high-fat diet (HFD) in the offspring has been suggested to have detrimental consequences for offspring cognitive function through its effect on the hippocampus and prefrontal cortex. Therefore, our study aimed to investigate the effects of maternal obesity and offspring HFD exposure on the brain metabolome of the offspring. In our pilot study, a LepRdb/+ mouse model was used to model pre-pregnancy maternal obesity and the c57bl/6 wildtype was used as a control group. Offspring were fed either a HFD or a low-fat control diet (LFD) after weaning (between 8 and 10 weeks). The Mirrors water maze was performed between 28 and 30 weeks to measure cognitive function. Fatty acid metabolomic profiles of the prefrontal cortex and hippocampus from the offspring at 30-32 weeks were analyzed using gas chromatography-mass spectrometry. The memory of male offspring from obese maternal mice, consuming a HFD post-weaning, was significantly impaired when compared to the control offspring mice. No significant differences were observed in female offspring. In male mice, the fatty acid metabolites in the prefrontal cortex were most affected by maternal obesity, whereas, the fatty acid metabolites in the hippocampus were most affected by the offspring's diet. Hexadecanoic acid and octadecanoic acid were significantly affected in both the hippocampus and pre-frontal cortex, as a result of maternal obesity and a HFD in the offspring. Our findings suggest that the combination of maternal obesity and HFD in the offspring can result in spatial cognitive deficiency in the male offspring, by influencing the fatty acid metabolite profiles in the prefrontal cortex and hippocampus. Further research is needed to validate the results of our pilot study. Copyright © 2018 Elsevier Inc. All rights reserved.

  12. Maternal Scaffolding and Attention Regulation in Children Living in Poverty

    ERIC Educational Resources Information Center

    Robinson, Julia B.; Burns, Barbara M.; Davis, Deborah Winders

    2009-01-01

    This study examines the relation of maternal scaffolding and children's attention regulation abilities in preschool children from low-income families within the context of a parent-child interaction task and in a child-alone task. Maternal scaffolding behaviors differed for mothers of children with different attention regulation skills. Mothers…

  13. Adipose genes down-regulated during experimental endotoxemia are also suppressed in obesity.

    PubMed

    Shah, Rachana; Hinkle, Christine C; Haris, Lalarukh; Shah, Rhia; Mehta, Nehal N; Putt, Mary E; Reilly, Muredach P

    2012-11-01

    Adipose inflammation is a crucial link between obesity and its metabolic complications. Human experimental endotoxemia is a controlled model for the study of inflammatory cardiometabolic responses in vivo. We hypothesized that adipose genes down-regulated during endotoxemia would approximate changes observed with obesity-related inflammation and reveal novel candidates in cardiometabolic disease. Healthy volunteers (n = 14) underwent a 3 ng/kg endotoxin challenge; adipose biopsies were taken at 0, 4, 12, and 24 h for mRNA microarray. A priority list of highly down-regulated and biologically relevant genes was validated by RT-PCR in an independent sample of adipose from healthy subjects (n = 7) undergoing a subclinical 0.6 ng/kg endotoxemia protocol. Expression of validated genes was screened in adipose of lean and severely obese individuals (n = 11 per group), and cellular source was probed in cultured adipocytes and macrophages. Endotoxemia (3 ng/kg) suppressed expression of 353 genes (to <67% of baseline; P < 1 × 10(-5)) of which 68 candidates were prioritized for validation. In low-dose (0.6 ng/kg) endotoxin validation, 22 (32%) of these 68 genes were confirmed. Functional classification revealed that many of these genes are involved in cell development and differentiation. Of validated genes, 59% (13 of 22) were down-regulated more than 1.5-fold in primary human adipocytes after treatment with endotoxin. In human macrophages, 59% (13 of 22) were up-regulated during differentiation to inflammatory M1 macrophages whereas 64% (14 of 22) were down-regulated during transition to homeostatic M2 macrophages. Finally, in obese vs. lean adipose, 91% (20 of 22) tended to have reduced expression (χ(2) = 10.72, P < 0.01) with 50% (11 of 22) reaching P < 0.05 (χ(2) = 9.28, P < 0.01). Exploration of down-regulated mRNA in adipose during human endotoxemia revealed suppression of genes involved in cell development and differentiation. A majority of candidates were also

  14. REGULATION OF OBESITY AND INSULIN RESISTANCE BY NITRIC OXIDE

    PubMed Central

    Sansbury, Brian E.; Hill, Bradford G.

    2014-01-01

    Obesity is a risk factor for developing type 2 diabetes and cardiovascular disease and has quickly become a world-wide pandemic with few tangible and safe treatment options. While it is generally accepted that the primary cause of obesity is energy imbalance, i.e., the calories consumed are greater than are utilized, understanding how caloric balance is regulated has proven a challenge. Many “distal” causes of obesity, such as the structural environment, occupation, and social influences, are exceedingly difficult to change or manipulate. Hence, molecular processes and pathways more proximal to the origins of obesity—those that directly regulate energy metabolism or caloric intake—appear to be more feasible targets for therapy. In particular, nitric oxide (NO) is emerging as a central regulator of energy metabolism and body composition. NO bioavailability is decreased in animal models of diet-induced obesity and in obese and insulin resistant patients, and increasing NO output has remarkable effects on obesity and insulin resistance. This review discusses the role of NO in regulating adiposity and insulin sensitivity and places its modes of action into context with the known causes and consequences of metabolic disease. PMID:24878261

  15. Synergy of nature and nurture in the development of childhood obesity.

    PubMed

    Levin, B E

    2009-04-01

    Epidemiological studies suggest that maternal undernutrition, obesity and diabetes during gestation and lactation can all produce obesity in human offspring. Animal models provide a means of assessing the independent consequences of altering the pre- vs postnatal environments on a variety of metabolic, physiological and neuroendocrine functions, which lead to the development of offspring obesity, diabetes, hypertension and hyperlipidemia. During the gestational period, maternal malnutrition, obesity, type 1 and type 2 diabetes, and psychological and pharmacological stressors can all promote offspring obesity. Normal postnatal nutrition can sometimes reduce the adverse effect of some of these prenatal factors, but may also exacerbate the development of obesity and diabetes in offspring of dams that are malnourished during gestation. The genetic background of the individual is also an important determinant of outcome when the perinatal environment is perturbed. Individuals with an obesity-prone genotype are more likely to be adversely affected by factors such as maternal obesity and high-fat diets. Many perinatal manipulations are associated with reorganization of the central neural pathways which regulate food intake, energy expenditure and storage in ways that enhance the development of obesity and diabetes in offspring. Both leptin and insulin have strong neurotrophic properties so that an excess or an absence of either of them during the perinatal period may underlie some of these adverse developmental changes. As perinatal manipulations can permanently and adversely alter the systems that regulate energy homeostasis, it behooves us to gain a better understanding of the factors during this period that promote the development of offspring obesity as a means of stemming the tide of the emerging worldwide obesity epidemic.

  16. Maternal obesity-impaired insulin signaling in sheep and induced lipid accumulation and fibrosis in skeletal muscle of offspring.

    PubMed

    Yan, Xu; Huang, Yan; Zhao, Jun-Xing; Long, Nathan M; Uthlaut, Adam B; Zhu, Mei-Jun; Ford, Stephen P; Nathanielsz, Peter W; Du, Min

    2011-07-01

    The prevalence of maternal obesity is increasing rapidly in recent decades. We previously showed that maternal obesity affected skeletal muscle development during the fetal stage. The objective of this study was to evaluate the effects of maternal obesity on the skeletal muscle properties of offspring. Ewes were fed a control diet (100% energy requirement, Con) or an obesogenic diet (150% energy requirement, OB) from 2 mo before pregnancy to weaning. After weaning, the offspring lambs were fed a maintenance diet until 19 mo of age and then ad libitum for 12 wk to measure feed intake. At 22 mo old, the longissimus dorsi (LD) muscle was biopsied. The downstream insulin signaling was lower in OB than Con lambs as shown by reduction in the phosphorylation of protein kinase B, mammalian target of rapamycin, and 4-E binding protein 1. On the other hand, the phosphorylation of protein kinase C and insulin receptor substrate 1 was higher in OB compared to Con lambs. More intramuscular adipocytes were observed in OB compared to Con offspring muscle, and the expression of peroxisome proliferator-activated receptor gamma, an adipocyte marker, was also higher, which was consistent with the higher intramuscular triglyceride content. Both fatty acid transport protein 1 and cluster of differentiation 36 (also known as fatty acid translocase) were increased in the OB group. In addition, higher collagen content was also detected in OB compared to Con offspring. In conclusion, our data show that offspring from obese mothers had impaired insulin signaling in muscle compared with control lambs, which correlates with increased intramuscular triglycerides and higher expression of fatty acid transporters. These data clearly show that maternal obesity impairs the function of the skeletal muscle of offspring, supporting the fetal programming of adult metabolic diseases.

  17. [Coexistence of maternal overweight or obesity and stunted children in south-western Benin households].

    PubMed

    Dembélé, Bernard; Sossa Jérôme, Charles; Saizonou, Jacques; Makoutodé, Patrick Charles; Mongbo Adé, Virginie; Guedègbé Capo-Chichi, Justine; Dona Ouendo, Marius-Edgard

    To determine the prevalence and determinants of coexistence of maternal overweight or obesity and stunted children (DBM / SCOM) in south-western Benin households. This cross-sectional study was carried out in June 2015 on 357 mother-child pairs randomly selected by a two-stage sampling technique in the city of Comè and its surroundings. Data on socio-economic factors, family, health care, dietary quality were collected by questionnaires, observation and documentary review. Anthropometric measurements were performed in mothers and children. A logistic regression analysis model was used to search for determinants of the coexistence of the two aspects of malnutrition. 19.3% of mothers were overweight and 5.7% were obese. 46% of children were stunted. The prevalence of DBM / SCOM was 11.5%. The main factors associated with DBM/SCOM were the child's age, the mother's occupation, ethnicity, social status and educational level, and the size, economic level, transportation means and food insecurity of the household. A high frequency of the coexistence of maternal overweight or obesity and stunting was observed in Comè households. Interventions based on the identified determinants are needed to act simultaneously on the double burden of malnutrition in Comè.

  18. Mechanisms involved in epigenetic down-regulation of Gfap under maternal hypothyroidism.

    PubMed

    Kumar, Praveen; Godbole, Nachiket M; Chaturvedi, Chandra P; Singh, Ravi S; George, Nelson; Upadhyay, Aditya; Anjum, B; Godbole, Madan M; Sinha, Rohit A

    2018-07-20

    Thyroid hormones (TH) of maternal origin are crucial regulator of mammalian brain development during embryonic period. Although maternal TH deficiency during the critical periods of embryonic neo-cortical development often results in irreversible clinical outcomes, the fundamental basis of these abnormalities at a molecular level is still obscure. One of the key developmental process affected by maternal TH insufficiency is the delay in astrocyte maturation. Glial fibrillary acidic protein (Gfap) is a predominant cell marker of mature astrocyte and is regulated by TH status. Inspite, of being a TH responsive gene during neocortical development the mechanistic basis of Gfap transcriptional regulation by TH has remained elusive. In this study using rat model of maternal hypothyroidism, we provide evidence for an epigenetic silencing of Gfap under TH insufficiency and its recovery upon TH supplementation. Our results demonstrate increased DNA methylation coupled with decreased histone acetylation at the Gfap promoter leading to suppression of Gfap expression under maternal hypothyroidism. In concordance, we also observed a significant increase in histone deacetylase (HDAC) activity in neocortex of TH deficient embryos. Collectively, these results provide novel insight into the role of TH regulated epigenetic mechanisms, including DNA methylation, and histone modifications, which are critically important in mediating precise temporal neural gene regulation. Copyright © 2018 Elsevier Inc. All rights reserved.

  19. Global Methylation in the Placenta and Umbilical Cord Blood From Pregnancies With Maternal Gestational Diabetes, Preeclampsia, and Obesity

    PubMed Central

    Lambertini, Luca; Rialdi, Alexander; Lee, MenJean; Mystal, Elana Ying; Grabie, Mordy; Manaster, Isaac; Huynh, Nancy; Finik, Jackie; Davey, Mia; Davey, Kei; Ly, Jenny; Stone, Joanne; Loudon, Holly; Eglinton, Gary; Hurd, Yasmin; Newcorn, Jeffrey H.; Chen, Jia

    2014-01-01

    Emerging evidence indicates that maternal medical risk during pregnancy, such as gestational diabetes mellitus (GDM), preeclampsia, and obesity, predisposes the offspring to suboptimal development. However, the underlying biological/epigenetic mechanism in utero is still unknown. The current pilot study (N = 50) compared the levels of global methylation in the placenta and umbilical cord blood among women with and without each risk condition (GDM, preeclampsia, and obesity) and explored whether the levels of global methylation were associated with fetal/infant growth. Results show that global methylation levels in the placenta were lower in patients with gestational diabetes (P = .003) and preeclampsia (P = .05) but higher with obesity (P = .01). Suggestive negative associations were found between global methylation level in the placenta and infant body length and head circumference. While preliminary, it is possible that the placenta tissue, but not umbilical cord blood, may be epigenetically programmed by maternal GDM, preeclampsia, and obesity to carry out its own specific functions that influence fetal growth. PMID:23765376

  20. Transgenic Increase in N-3/N-6 Fatty Acid Ratio Reduces Maternal Obesity-Associated Inflammation and Limits Adverse Developmental Programming in Mice

    PubMed Central

    Heerwagen, Margaret J. R.; Stewart, Michael S.; de la Houssaye, Becky A.; Janssen, Rachel C.; Friedman, Jacob E.

    2013-01-01

    Maternal and pediatric obesity has risen dramatically over recent years, and is a known predictor of adverse long-term metabolic outcomes in offspring. However, which particular aspects of obese pregnancy promote such outcomes is less clear. While maternal obesity increases both maternal and placental inflammation, it is still unknown whether this is a dominant mechanism in fetal metabolic programming. In this study, we utilized the Fat-1 transgenic mouse to test whether increasing the maternal n-3/n-6 tissue fatty acid ratio could reduce the consequences of maternal obesity-associated inflammation and thereby mitigate downstream developmental programming. Eight-week-old WT or hemizygous Fat-1 C57BL/6J female mice were placed on a high-fat diet (HFD) or control diet (CD) for 8 weeks prior to mating with WT chow-fed males. Only WT offspring from Fat-1 mothers were analyzed. WT-HFD mothers demonstrated increased markers of infiltrating adipose tissue macrophages (P<0.02), and a striking increase in 12 serum pro-inflammatory cytokines (P<0.05), while Fat1-HFD mothers remained similar to WT-CD mothers, despite equal weight gain. E18.5 Fetuses from WT-HFD mothers had larger placentas (P<0.02), as well as increased placenta and fetal liver TG deposition (P<0.01 and P<0.02, respectively) and increased placental LPL TG-hydrolase activity (P<0.02), which correlated with degree of maternal insulin resistance (r = 0.59, P<0.02). The placentas and fetal livers from Fat1-HFD mothers were protected from this excess placental growth and fetal-placental lipid deposition. Importantly, maternal protection from excess inflammation corresponded with improved metabolic outcomes in adult WT offspring. While the offspring from WT-HFD mothers weaned onto CD demonstrated increased weight gain (P<0.05), body and liver fat (P<0.05 and P<0.001, respectively), and whole body insulin resistance (P<0.05), these were prevented in WT offspring from Fat1-HFD mothers. Our results suggest that

  1. Transgenic increase in N-3/n-6 Fatty Acid ratio reduces maternal obesity-associated inflammation and limits adverse developmental programming in mice.

    PubMed

    Heerwagen, Margaret J R; Stewart, Michael S; de la Houssaye, Becky A; Janssen, Rachel C; Friedman, Jacob E

    2013-01-01

    Maternal and pediatric obesity has risen dramatically over recent years, and is a known predictor of adverse long-term metabolic outcomes in offspring. However, which particular aspects of obese pregnancy promote such outcomes is less clear. While maternal obesity increases both maternal and placental inflammation, it is still unknown whether this is a dominant mechanism in fetal metabolic programming. In this study, we utilized the Fat-1 transgenic mouse to test whether increasing the maternal n-3/n-6 tissue fatty acid ratio could reduce the consequences of maternal obesity-associated inflammation and thereby mitigate downstream developmental programming. Eight-week-old WT or hemizygous Fat-1 C57BL/6J female mice were placed on a high-fat diet (HFD) or control diet (CD) for 8 weeks prior to mating with WT chow-fed males. Only WT offspring from Fat-1 mothers were analyzed. WT-HFD mothers demonstrated increased markers of infiltrating adipose tissue macrophages (P<0.02), and a striking increase in 12 serum pro-inflammatory cytokines (P<0.05), while Fat1-HFD mothers remained similar to WT-CD mothers, despite equal weight gain. E18.5 Fetuses from WT-HFD mothers had larger placentas (P<0.02), as well as increased placenta and fetal liver TG deposition (P<0.01 and P<0.02, respectively) and increased placental LPL TG-hydrolase activity (P<0.02), which correlated with degree of maternal insulin resistance (r = 0.59, P<0.02). The placentas and fetal livers from Fat1-HFD mothers were protected from this excess placental growth and fetal-placental lipid deposition. Importantly, maternal protection from excess inflammation corresponded with improved metabolic outcomes in adult WT offspring. While the offspring from WT-HFD mothers weaned onto CD demonstrated increased weight gain (P<0.05), body and liver fat (P<0.05 and P<0.001, respectively), and whole body insulin resistance (P<0.05), these were prevented in WT offspring from Fat1-HFD mothers. Our results suggest that

  2. Maternal obesity is the new challenge; a qualitative study of health professionals' views towards suitable care for pregnant women with a Body Mass Index (BMI) ≥ 30 kg/m².

    PubMed

    Smith, Debbie M; Cooke, Alison; Lavender, Tina

    2012-12-19

    An increase in the number of women with maternal obesity (Body Mass Index [BMI] ≥30 kg/m2) has had a huge impact on the delivery of maternity services. As part of a programme of feasibility work to design an antenatal lifestyle programme for women with a BMI ≥30 kg/m2, the current study explored health professionals' experiences of caring for women with a BMI ≥30 kg/m2 and their views of the proposed lifestyle programme. Semi-structured interviews with 30 health professionals (including midwives, sonographers, anaesthetists and obstetricians) were conducted and analysed using thematic analysis. Recruitment occurred in two areas in the North West of England in early 2011. Three themes were evident. Firstly, obesity was seen as a conversation stopper; obesity can be a challenge to discuss. Secondly, obesity was seen as a maternity issue; obesity has a direct impact on maternity care and therefore intervention is needed. Finally, the long-term impact of maternal obesity intervention; lifestyle advice in pregnancy has the potential to break the cyclic obesity relationship. The health professionals believed that antenatal lifestyle advice can play a key role in addressing the public health issue of obesity as pregnancy is a time of increased motivation for women with a BMI ≥30 kg/m2. Maternal obesity is a challenge and details of the training content required for health professionals to feel confident to approach the issue of maternal obesity with women are presented. Support for the antenatal lifestyle programme for women with a BMI ≥30 kg/m2 highlights the need for further exploration of the impact of interventions on health promotion.

  3. Maternal Posttraumatic Stress Symptoms and Infant Emotional Reactivity and Emotion Regulation

    PubMed Central

    Enlow, Michelle Bosquet; Kitts, Robert L.; Blood, Emily; Bizarro, Andrea; Hofmeister, Michelle; Wright, Rosalind J.

    2011-01-01

    The current study examined associations between maternal posttraumatic stress disorder (PTSD) symptoms and infant emotional reactivity and emotion regulation during the first year of life in a primarily low-income, urban, ethnic/racial minority sample of 52 mother-infant dyads. Mothers completed questionnaires assessing their own trauma exposure history and current PTSD and depressive symptoms and their infants’ temperament when the infants were 6 months old. Dyads participated in the repeated Still-Face Paradigm (SFP-R) when the infants were 6 months old, and infant affective states were coded for each SFP-R episode. Mothers completed questionnaires assessing infant trauma exposure history and infant current emotional and behavioral symptoms when the infants were 13 months old. Maternal PTSD symptoms predicted infants’ emotion regulation at 6 months as assessed by (a) infant ability to recover from distress during the SFP-R and (b) maternal report of infant rate of recovery from distress/arousal in daily life. Maternal PTSD symptoms also predicted maternal report of infant externalizing, internalizing, and dysregulation symptoms at 13 months. Maternal PTSD was not associated with measures of infant emotional reactivity. Neither maternal depressive symptoms nor infant direct exposure to trauma accounted for the associations between maternal PTSD symptoms and infant outcomes. These findings suggest that maternal PTSD is associated with offspring emotion regulation difficulties as early as infancy. Such difficulties may contribute to increased risk of mental health problems among children of mothers with PTSD. PMID:21862136

  4. Maternal Emotion Regulation and Adolescent Behaviors: The Mediating Role of Family Functioning and Parenting.

    PubMed

    Crandall, AliceAnn; Ghazarian, Sharon R; Day, Randal D; Riley, Anne W

    2016-11-01

    Prior research links poor maternal emotion regulation to maladaptive parenting and child behaviors, but little research is available on these relationships during the adolescent period. We use structural equation modeling to assess the influence of poor maternal emotion regulation, measured as emotional reactivity and distancing, on adolescent behaviors (measured as aggression and prosocial behaviors) among 478 adolescents (53 % female; baseline age 10-13 years) and their mothers over a 5 year period. We also tested the possible mediating roles of family functioning and parenting behaviors between maternal emotion regulation and adolescent behaviors. Results indicated that higher baseline maternal emotional distancing and reactivity were not directly predictive of adolescents' behaviors, but they were indirectly related through family functioning and parenting. Specifically, indulgent parenting mediated the relationship between maternal emotional reactivity and adolescent aggression. Maternal-reported family functioning significantly mediated the relationship between maternal emotional distancing and adolescent aggression. Family functioning also mediated the relationship between emotional distancing and regulation parenting. The results imply that poor maternal emotion regulation during their child's early adolescence leads to more maladaptive parenting and problematic behaviors during the later adolescent period. However, healthy family processes may ameliorate the negative impact of low maternal emotion regulation on parenting and adolescent behavioral outcomes. The implications for future research and interventions to improve parenting and adolescent outcomes are discussed.

  5. Impact of Maternal Glucose and Gestational Weight Gain on Child Obesity over the First Decade of Life in Normal Birth Weight Infants.

    PubMed

    Hillier, Teresa A; Pedula, Kathryn L; Vesco, Kimberly K; Oshiro, Caryn E S; Ogasawara, Keith K

    2016-08-01

    Objective To determine, among children with normal birth weight, if maternal hyperglycemia and weight gain independently increase childhood obesity risk in a very large diverse population. Methods Study population was 24,141 individuals (mothers and their normal birth weight offspring, born 1995-2003) among a diverse population with universal GDM screening [50-g glucose-challenge test (GCT); 3 h. 100 g oral glucose tolerance test (OGTT) if GCT+]. Among the 13,037 full-term offspring with normal birth weight (2500-4000 g), annual measured height/weight was ascertained between ages 2 and 10 years to calculate gender-specific BMI-for-age percentiles using USA norms (1960-1995 standard). Results Among children who began life with normal birth weight, we found a significant trend for developing both childhood overweight (>85 %ile) and obesity (>95 %ile) during the first decade of life with both maternal hyperglycemia (normal GCT, GCT+ but no GDM, GDM) and excessive gestational weight gain [>40 pounds (18.1 kg)]; p < 0.0001 for both trends. These maternal glucose and/or weight gain effects to imprint for childhood obesity in the first decade remained after adjustment for potential confounders including maternal age, parity, as well as pre-pregnancy BMI. The attributable risk (%) for childhood obesity was 28.5 % (95 % CI 15.9-41.1) for GDM and 16.4 % (95 % CI 9.4-23.2) for excessive gestational weight gain. Conclusions for Practice Both maternal hyperglycemia and excessive weight gain have independent effects to increase childhood obesity risk. Future research should focus on prevention efforts during pregnancy as a potential window of opportunity to reduce childhood obesity.

  6. Risk of major congenital malformations in relation to maternal overweight and obesity severity: cohort study of 1.2 million singletons

    PubMed Central

    Cnattingius, Sven; Villamor, Eduardo; Söderling, Jonas; Pasternak, Björn; Stephansson, Olof; Neovius, Martin

    2017-01-01

    Objective To estimate the risks of major congenital malformations in the offspring of mothers who are underweight (body mass index (BMI) <18.5), overweight (BMI 25 to <30), or in obesity classes I (BMI 30 to <35), II (35 to <40), or III (≥40) compared with offspring of normal weight mothers (BMI 18.5 to <25) in early pregnancy. Design Population based cohort study. Setting Nationwide Swedish registries. Participants 1 243 957 liveborn singleton infants from 2001 to 2014 in Sweden. Data on maternal and pregnancy characteristics were obtained by individual record linkages. Exposure Maternal BMI at the first prenatal visit. Main outcome measures Offspring with any major congenital malformation, and subgroups of organ specific malformations diagnosed during the first year of life. Risk ratios were estimated using generalised linear models adjusted for maternal factors, sex of offspring, and birth year. Results A total of 43 550 (3.5%) offspring had any major congenital malformation, and the most common subgroup was for congenital heart defects (n=20 074; 1.6%). Compared with offspring of normal weight mothers (risk of malformations 3.4%), the proportions and adjusted risk ratios of any major congenital malformation among the offspring of mothers with higher BMI were: overweight, 3.5% and 1.05 (95% confidence interval 1.02 to 1.07); obesity class I, 3.8% and 1.12 (1.08 to 1.15), obesity class II, 4.2% and 1.23 (1.17 to 1.30), and obesity class III, 4.7% and 1.37 (1.26 to 1.49). The risks of congenital heart defects, malformations of the nervous system, and limb defects also progressively increased with BMI from overweight to obesity class III. The largest organ specific relative risks related to maternal overweight and increasing obesity were observed for malformations of the nervous system. Malformations of the genital and digestive systems were also increased in offspring of obese mothers. Conclusions Risks of any major congenital malformation and

  7. Risk of major congenital malformations in relation to maternal overweight and obesity severity: cohort study of 1.2 million singletons.

    PubMed

    Persson, Martina; Cnattingius, Sven; Villamor, Eduardo; Söderling, Jonas; Pasternak, Björn; Stephansson, Olof; Neovius, Martin

    2017-06-14

    Objective  To estimate the risks of major congenital malformations in the offspring of mothers who are underweight (body mass index (BMI) <18.5), overweight (BMI 25 to <30), or in obesity classes I (BMI 30 to <35), II (35 to <40), or III (≥40) compared with offspring of normal weight mothers (BMI 18.5 to <25) in early pregnancy. Design  Population based cohort study. Setting  Nationwide Swedish registries. Participants  1 243 957 liveborn singleton infants from 2001 to 2014 in Sweden. Data on maternal and pregnancy characteristics were obtained by individual record linkages. Exposure  Maternal BMI at the first prenatal visit. Main outcome measures  Offspring with any major congenital malformation, and subgroups of organ specific malformations diagnosed during the first year of life. Risk ratios were estimated using generalised linear models adjusted for maternal factors, sex of offspring, and birth year. Results  A total of 43 550 (3.5%) offspring had any major congenital malformation, and the most common subgroup was for congenital heart defects (n=20 074; 1.6%). Compared with offspring of normal weight mothers (risk of malformations 3.4%), the proportions and adjusted risk ratios of any major congenital malformation among the offspring of mothers with higher BMI were: overweight, 3.5% and 1.05 (95% confidence interval 1.02 to 1.07); obesity class I, 3.8% and 1.12 (1.08 to 1.15), obesity class II, 4.2% and 1.23 (1.17 to 1.30), and obesity class III, 4.7% and 1.37 (1.26 to 1.49). The risks of congenital heart defects, malformations of the nervous system, and limb defects also progressively increased with BMI from overweight to obesity class III. The largest organ specific relative risks related to maternal overweight and increasing obesity were observed for malformations of the nervous system. Malformations of the genital and digestive systems were also increased in offspring of obese mothers. Conclusions  Risks of any major congenital

  8. Maternal obesity in singleton versus twin gestations: a population-based matched case-control study.

    PubMed

    Lucovnik, Miha; Blickstein, Isaac; Verdenik, Ivan; Trojner-Bregar, Andreja; Tul, Natasa

    2015-04-01

    To examine the impact of pre-pregnancy obesity on adverse outcomes in twin compared to singleton pregnancies. Dichorionic twin gestations with maternal body mass index >30 were matched to three singleton controls. Both obese groups were matched (1:3) with non-obese controls. Rates of preeclampsia, gestational diabetes, cesarean section, and preterm birth were compared. One hundred eighty-nine dichorionic twin pregnancies in obese mothers were matched to 567 twin pregnancies in non-obese mothers, and to 567 singleton pregnancies in obese mothers. The latter were matched to 1701 non-obese mothers with singletons. Preeclampsia was more common in obese mothers with both twins and singletons (odds ratio (OR) 3.95, 95% confidence interval (CI) 2.18-7.16 and OR 6.53, 95% CI 3.75-11.4, respectively) as was gestational diabetes (OR 4.35, 95% CI 2.18-8.69; OR 5.53 95% CI 3.60-8.50). Obese mothers with singletons were more likely to deliver abdominally, but the cesarean rates were obesity independent in twins. Obese mothers were more likely to deliver at < 34 weeks in both twin and singleton groups (OR 1.65, 95% CI 1.10-2.48, and OR 2.41, 95% CI 1.21-4.77, respectively). Obesity-attributable adverse outcomes are lower in twins compared to singletons. Obesity increases the risk of preterm birth regardless of plurality.

  9. Adipose Genes Down-Regulated During Experimental Endotoxemia Are Also Suppressed in Obesity

    PubMed Central

    Hinkle, Christine C.; Haris, Lalarukh; Shah, Rhia; Mehta, Nehal N.; Putt, Mary E.; Reilly, Muredach P.

    2012-01-01

    Context: Adipose inflammation is a crucial link between obesity and its metabolic complications. Human experimental endotoxemia is a controlled model for the study of inflammatory cardiometabolic responses in vivo. Objective: We hypothesized that adipose genes down-regulated during endotoxemia would approximate changes observed with obesity-related inflammation and reveal novel candidates in cardiometabolic disease. Design, Subjects, and Intervention: Healthy volunteers (n = 14) underwent a 3 ng/kg endotoxin challenge; adipose biopsies were taken at 0, 4, 12, and 24 h for mRNA microarray. A priority list of highly down-regulated and biologically relevant genes was validated by RT-PCR in an independent sample of adipose from healthy subjects (n = 7) undergoing a subclinical 0.6 ng/kg endotoxemia protocol. Expression of validated genes was screened in adipose of lean and severely obese individuals (n = 11 per group), and cellular source was probed in cultured adipocytes and macrophages. Results: Endotoxemia (3 ng/kg) suppressed expression of 353 genes (to <67% of baseline; P < 1 × 10−5) of which 68 candidates were prioritized for validation. In low-dose (0.6 ng/kg) endotoxin validation, 22 (32%) of these 68 genes were confirmed. Functional classification revealed that many of these genes are involved in cell development and differentiation. Of validated genes, 59% (13 of 22) were down-regulated more than 1.5-fold in primary human adipocytes after treatment with endotoxin. In human macrophages, 59% (13 of 22) were up-regulated during differentiation to inflammatory M1 macrophages whereas 64% (14 of 22) were down-regulated during transition to homeostatic M2 macrophages. Finally, in obese vs. lean adipose, 91% (20 of 22) tended to have reduced expression (χ2 = 10.72, P < 0.01) with 50% (11 of 22) reaching P < 0.05 (χ2 = 9.28, P < 0.01). Conclusions: Exploration of down-regulated mRNA in adipose during human endotoxemia revealed suppression of genes involved in

  10. High fat diet and in utero exposure to maternal obesity disrupts circadian rhythm and leads to metabolic programming of liver in rat offspring

    USDA-ARS?s Scientific Manuscript database

    The risk of obesity in adulthood is subject to programming beginning at conception. In animal models, exposure to maternal obesity and high fat diets influences the risk of obesity in the offspring. Among other long-term changes, offspring from obese rats develop hyperinsulinemia, hepatic steatosi...

  11. Maternal recalled gestational weight gain, pre-pregnancy body mass index, and obesity in the daughter

    PubMed Central

    Stuebe, Alison M.; Forman, Michele R.; Michels, Karin B.

    2009-01-01

    Objective Emerging evidence suggests that exposures during fetal life affect adult metabolism. We assessed the relation between recalled maternal pre-pregnancy body mass, gestational weight gain (GWG), and adiposity in the daughter. Design Retrospective cohort study among mother-nurse daughter dyads in the Nurses’ Health Study II and the Nurses’ Mothers’ Cohort. Mothers of participants completed questionnaires regarding their nurse-daughter in 2001. Participants 26,506 mother-nurse daughter dyads born between 1946 and 1964. Main outcome measures Body mass index of the nurse-daughter at age 18 and in 2001. Results At age 18, 561 (2.1%) daughters were obese (BMI greater than 30), and in 2001, 5,442 (22.0%) were obese. Adjusting for covariates, women whose mothers had a recalled pre-pregnancy BMI of 29 had a 6.1-fold increased risk of obesity at age 18 and a 3.4-fold risk of obesity in 2001, compared with women whose mothers had a pre-pregnancy BMI of 21. We found a U-shaped association between recalled GWG and offspring obesity. Compared with a maternal weight gain of 15–19 lb, GWG <10 lbs was associated with a significant increase in obesity risk at age 18 (odds ratio[OR] 1.54, 95% confidence interval[CI] 1.02–2.34) and in 2001 (OR 1.27, 95%CI 1.05–1.53). High weight gain (40+ lbs) was also associated with obesity risk at age 18 (OR 1.81, 95%CI 1.22–2.69) and in 2001 (OR 1.74, 95%CI 1.48–2.04). These associations were stronger among mothers who were overweight prior to pregnancy (p for interaction = 0.03), and they persisted with adjustment for birth weight. Conclusion A high recalled pre-pregnancy BMI and extremes of recalled GWG are associated with an increased risk of adolescent and adult obesity in offspring, particularly when the mother is overweight. Pre-pregnancy weight and GWG may be modifiable fetal origins of overweight and obesity in women. PMID:19528964

  12. Melatonin protects against maternal obesity-associated oxidative stress and meiotic defects in oocytes via the SIRT3-SOD2-dependent pathway.

    PubMed

    Han, Longsen; Wang, Haichao; Li, Ling; Li, Xiaoyan; Ge, Juan; Reiter, Russel J; Wang, Qiang

    2017-10-01

    Maternal obesity in humans is associated with poor outcomes across the reproductive spectrum. Emerging evidence indicates that these defects are likely attributed to factors within the oocyte. Although various molecules and pathways may contribute to impaired oocyte quality, prevention of fertility issues associated with maternal obesity is a challenge. Using mice fed a high-fat diet (HFD) as an obesity model, we document spindle disorganization, chromosome misalignment, and elevated reactive oxygen species (ROS) levels in oocytes from obese mice. Oral administration of melatonin to HFD mice not only reduces ROS generation, but also prevents spindle/chromosome anomalies in oocytes, consequently promoting the developmental potential of early embryos. Consistent with this finding, we find that melatonin supplement during in vitro maturation also markedly attenuates oxidative stress and meiotic defects in HFD oocytes. Finally, by performing morpholino knockdown and acetylation-mimetic mutant overexpression assays, we reveal that melatonin ameliorates maternal obesity-induced defective phenotypes in oocytes through the SIRT3-SOD2-dependent mechanism. In sum, our data uncover the marked beneficial effects of melatonin on oocyte quality from obese females; this opens a new area for optimizing culture system as well as fertility management. © 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

  13. Maternal work and children's diet, activity, and obesity.

    PubMed

    Datar, Ashlesha; Nicosia, Nancy; Shier, Victoria

    2014-04-01

    Mothers' work hours are likely to affect their time allocation towards activities related to children's diet, activity and well-being. For example, mothers who work more may be more reliant on processed foods, foods prepared away from home and school meal programs for their children's meals. A greater number of work hours may also lead to more unsupervised time for children that may, in turn, allow for an increase in unhealthy behaviors among their children such as snacking and sedentary activities such as TV watching. Using data on a national cohort of children, we examine the relationship between mothers' average weekly work hours during their children's school years on children's dietary and activity behaviors, BMI and obesity in 5th and 8th grade. Our results are consistent with findings from the literature that maternal work hours are positively associated with children's BMI and obesity especially among children with higher socioeconomic status. Unlike previous papers, our detailed data on children's behaviors allow us to speak directly to affected behaviors that may contribute to the increased BMI. We show that children whose mothers work more consume more unhealthy foods (e.g. soda, fast food) and less healthy foods (e.g. fruits, vegetables, milk) and watch more television. Although they report being slightly more physically active, likely due to organized physical activities, the BMI and obesity results suggest that the deterioration in diet and increase in sedentary behaviors dominate. Copyright © 2014 Elsevier Ltd. All rights reserved.

  14. Maternal Obesity-Impaired Insulin Signaling in Sheep and Induced Lipid Accumulation and Fibrosis in Skeletal Muscle of Offspring1

    PubMed Central

    Yan, Xu; Huang, Yan; Zhao, Jun-Xing; Long, Nathan M.; Uthlaut, Adam B.; Zhu, Mei-Jun; Ford, Stephen P.; Nathanielsz, Peter W.; Du, Min

    2011-01-01

    The prevalence of maternal obesity is increasing rapidly in recent decades. We previously showed that maternal obesity affected skeletal muscle development during the fetal stage. The objective of this study was to evaluate the effects of maternal obesity on the skeletal muscle properties of offspring. Ewes were fed a control diet (100% energy requirement, Con) or an obesogenic diet (150% energy requirement, OB) from 2 mo before pregnancy to weaning. After weaning, the offspring lambs were fed a maintenance diet until 19 mo of age and then ad libitum for 12 wk to measure feed intake. At 22 mo old, the longissimus dorsi (LD) muscle was biopsied. The downstream insulin signaling was lower in OB than Con lambs as shown by reduction in the phosphorylation of protein kinase B, mammalian target of rapamycin, and 4-E binding protein 1. On the other hand, the phosphorylation of protein kinase C and insulin receptor substrate 1 was higher in OB compared to Con lambs. More intramuscular adipocytes were observed in OB compared to Con offspring muscle, and the expression of peroxisome proliferator-activated receptor gamma, an adipocyte marker, was also higher, which was consistent with the higher intramuscular triglyceride content. Both fatty acid transport protein 1 and cluster of differentiation 36 (also known as fatty acid translocase) were increased in the OB group. In addition, higher collagen content was also detected in OB compared to Con offspring. In conclusion, our data show that offspring from obese mothers had impaired insulin signaling in muscle compared with control lambs, which correlates with increased intramuscular triglycerides and higher expression of fatty acid transporters. These data clearly show that maternal obesity impairs the function of the skeletal muscle of offspring, supporting the fetal programming of adult metabolic diseases. PMID:21349823

  15. Perinatal maternal high-fat diet induces early obesity and sex-specific alterations of the endocannabinoid system in white and brown adipose tissue of weanling rat offspring.

    PubMed

    Almeida, Mariana M; Dias-Rocha, Camilla P; Souza, André S; Muros, Mariana F; Mendonca, Leonardo S; Pazos-Moura, Carmen C; Trevenzoli, Isis H

    2017-11-01

    Perinatal maternal high-fat (HF) diet programmes offspring obesity. Obesity is associated with overactivation of the endocannabinoid system (ECS) in adult subjects, but the role of the ECS in the developmental origins of obesity is mostly unknown. The ECS consists of endocannabinoids, cannabinoid receptors (cannabinoid type-1 receptor (CB1) and cannabinoid type-2 receptor (CB2)) and metabolising enzymes. We hypothesised that perinatal maternal HF diet would alter the ECS in a sex-dependent manner in white and brown adipose tissue of rat offspring at weaning in parallel to obesity development. Female rats received standard diet (9 % energy content from fat) or HF diet (29 % energy content from fat) before mating, during pregnancy and lactation. At weaning, male and female offspring were killed for tissue harvest. Maternal HF diet induced early obesity, white adipocyte hypertrophy and increased lipid accumulation in brown adipose tissue associated with sex-specific changes of the ECS's components in weanling rats. In male pups, maternal HF diet decreased CB1 and CB2 protein in subcutaneous adipose tissue. In female pups, maternal HF diet increased visceral and decreased subcutaneous CB1. In brown adipose tissue, maternal HF diet increased CB1 regardless of pup sex. In addition, maternal HF diet differentially changed oestrogen receptor across the adipose depots in male and female pups. The ECS and oestrogen signalling play an important role in lipogenesis, adipogenesis and thermogenesis, and we observed early changes in their targets in adipose depots of the offspring. The present findings provide insights into the involvement of the ECS in the developmental origins of metabolic disease induced by inadequate maternal nutrition in early life.

  16. Parental smoking and childhood obesity: higher effect estimates for maternal smoking in pregnancy compared with paternal smoking--a meta-analysis.

    PubMed

    Riedel, Christina; Schönberger, Katharina; Yang, Seungmi; Koshy, Gibby; Chen, Yang-Ching; Gopinath, Bamini; Ziebarth, Stephanie; von Kries, Rüdiger

    2014-10-01

    Some studies reported similar effect estimates for the impact of maternal smoking in pregnancy and paternal smoking on childhood obesity, whereas others suggested higher effects for maternal smoking. We performed a meta-analysis to compare the effect of in utero exposure to maternal smoking and that of paternal or household smoking exposure in utero or after birth with mutual adjustment. Meta-analysis of observational studies identified in MEDLINE, EMBASE and Web of Knowledge published in 1900-2013. Study inclusion criterion was assessment of the association of maternal smoking during pregnancy and paternal or household smoking (anyone living in the household who smokes) at any time with childhood overweight and obesity. The analyses were based on all studies with mutually adjusted effect estimates for maternal and paternal/household smoking applying a random-effects model. Data for 109,838 mother/child pairs were reported in 12 studies. The pooled odds ratios (ORs) for overweight 1.33 [95% confidence interval (CI) 1.23;1.44] (n=6, I2=0.00%) and obesity 1.60 (95% CI 1.37;1.88) (n=4, I2=32.47%) for maternal smoking during pregnancy were higher than for paternal smoking: 1.07 (95% CI 1.00;1.16) (n=6, I2=41.34%) and 1.23 (95% CI 1.10;1.38) (n=4, I2=14.61%), respectively. Similar estimates with widely overlapping confidence limits were found for maternal smoking during pregnancy and childhood overweight and obesity: 1.35 (95% CI 1.20;1.51) (n=3, I2=0.00%) and 1.28 (95% CI 1.07;1.54) (n=3, I2=0.00%) compared with household smoking 1.22 (95% CI 1.06;1.39) (n=3, I2=72.14%) and 1.31 (95% CI 1.15;1.50)] (n=3, I2=0.00%). Higher effect estimates for maternal smoking in pregnancy compared with paternal smoking in mutually adjusted models may suggest a direct intrauterine effect. © The Author 2014; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.

  17. Maternal BMI and migration status as predictors of childhood obesity in Mexico.

    PubMed

    Jiménez-Cruz, A; Wojcicki, J M; Bacardí-Gascón, M; Castellón-Zaragoza, A; García-Gallardo, J L; Schwartz, N; Heyman, M B

    2011-01-01

    To assess the association of maternal migration to Baja California, body mass index (BMI) status, children's perceived food insecurity, and childhood lifestyle behaviors with overweight (BMI > 85% ile), obesity (BMI > 95% ile) and abdominal obesity (Waist Circumference > 90% ile). Convenience sampling methods were used to recruit a cross-sectional sample of 4th, 5th and 6th grade children and their parents at Tijuana and Tecate Public Schools. Children's and parents' weights and heights were measured. Children were considered to have migrant parents if parents were not born in Baja California. One hundred and twenty-two children and their parents were recruited. The mean age of the children was 10.1 ± 1.0 years. Forty nine per cent of children were overweight or obese. Children with obese parents (BMI > 30) had greater odds of being obese, Odds Ratio (OR) 4.9 (95% Confidence Interval (CI), 1.2-19, p = 0.03). Children with migrant parents had greater odds of being obese, OR= 3.7 (95% CI, 1.6-8.3), p = 0.01) and of having abdominal obesity, OR = 3.2 (95% CI, 1.4-7.1, p = 0.01). Children from migrant parents have greater risk of higher consumption of potato chips, OR = 8.0 (95% CI, 2.1-29.1, p = 0.01). Children from non-migrant parents had greater odds of being at risk of hunger. Parental obesity and migration are associated with increased risk of obesity among Mexican children. Children whose parents were born in Baja California have greater odds of being at risk of hunger. Further studies should evaluate the role of migration on risk for childhood obesity.

  18. Maternal omega-3 fatty acids regulate offspring obesity through persistent modulation of gut microbiota.

    PubMed

    Robertson, Ruairi C; Kaliannan, Kanakaraju; Strain, Conall R; Ross, R Paul; Stanton, Catherine; Kang, Jing X

    2018-05-24

    The early-life gut microbiota plays a critical role in host metabolism in later life. However, little is known about how the fatty acid profile of the maternal diet during gestation and lactation influences the development of the offspring gut microbiota and subsequent metabolic health outcomes. Here, using a unique transgenic model, we report that maternal endogenous n-3 polyunsaturated fatty acid (PUFA) production during gestation or lactation significantly reduces weight gain and markers of metabolic disruption in male murine offspring fed a high-fat diet. However, maternal fatty acid status appeared to have no significant effect on weight gain in female offspring. The metabolic phenotypes in male offspring appeared to be mediated by comprehensive restructuring of gut microbiota composition. Reduced maternal n-3 PUFA exposure led to significantly depleted Epsilonproteobacteria, Bacteroides, and Akkermansia and higher relative abundance of Clostridia. Interestingly, offspring metabolism and microbiota composition were more profoundly influenced by the maternal fatty acid profile during lactation than in utero. Furthermore, the maternal fatty acid profile appeared to have a long-lasting effect on offspring microbiota composition and function that persisted into adulthood after life-long high-fat diet feeding. Our data provide novel evidence that weight gain and metabolic dysfunction in adulthood is mediated by maternal fatty acid status through long-lasting restructuring of the gut microbiota. These results have important implications for understanding the interaction between modern Western diets, metabolic health, and the intestinal microbiome.

  19. WNT5A-JNK regulation of vascular insulin resistance in human obesity.

    PubMed

    Farb, Melissa G; Karki, Shakun; Park, Song-Young; Saggese, Samantha M; Carmine, Brian; Hess, Donald T; Apovian, Caroline; Fetterman, Jessica L; Bretón-Romero, Rosa; Hamburg, Naomi M; Fuster, José J; Zuriaga, María A; Walsh, Kenneth; Gokce, Noyan

    2016-12-01

    Obesity is associated with the development of vascular insulin resistance; however, pathophysiological mechanisms are poorly understood. We sought to investigate the role of WNT5A-JNK in the regulation of insulin-mediated vasodilator responses in human adipose tissue arterioles prone to endothelial dysfunction. In 43 severely obese (BMI 44±11 kg/m 2 ) and five metabolically normal non-obese (BMI 26±2 kg/m 2 ) subjects, we isolated arterioles from subcutaneous and visceral fat during planned surgeries. Using videomicroscopy, we examined insulin-mediated, endothelium-dependent vasodilator responses and characterized adipose tissue gene and protein expression using real-time polymerase chain reaction and Western blot analyses. Immunofluorescence was used to quantify endothelial nitric oxide synthase (eNOS) phosphorylation. Insulin-mediated vasodilation was markedly impaired in visceral compared to subcutaneous vessels from obese subjects (p<0.001), but preserved in non-obese individuals. Visceral adiposity was associated with increased JNK activation and elevated expression of WNT5A and its non-canonical receptors, which correlated negatively with insulin signaling. Pharmacological JNK antagonism with SP600125 markedly improved insulin-mediated vasodilation by sixfold (p<0.001), while endothelial cells exposed to recombinant WNT5A developed insulin resistance and impaired eNOS phosphorylation (p<0.05). We observed profound vascular insulin resistance in the visceral adipose tissue arterioles of obese subjects that was associated with up-regulated WNT5A-JNK signaling and impaired endothelial eNOS activation. Pharmacological JNK antagonism markedly improved vascular endothelial function, and may represent a potential therapeutic target in obesity-related vascular disease. © The Author(s) 2016.

  20. WNT5A-JNK regulation of vascular insulin resistance in human obesity

    PubMed Central

    Farb, Melissa G; Karki, Shakun; Park, Song-Young; Saggese, Samantha M; Carmine, Brian; Hess, Donald T; Apovian, Caroline; Fetterman, Jessica L; Bretón-Romero, Rosa; Hamburg, Naomi M; Fuster, José J; Zuriaga, María A; Walsh, Kenneth; Gokce, Noyan

    2017-01-01

    Obesity is associated with the development of vascular insulin resistance; however, pathophysiological mechanisms are poorly understood. We sought to investigate the role of WNT5A-JNK in the regulation of insulin-mediated vasodilator responses in human adipose tissue arterioles prone to endothelial dysfunction. In 43 severely obese (BMI 44±11 kg/m2) and five metabolically normal non-obese (BMI 26±2 kg/m2) subjects, we isolated arterioles from subcutaneous and visceral fat during planned surgeries. Using videomicroscopy, we examined insulin-mediated, endothelium-dependent vasodilator responses and characterized adipose tissue gene and protein expression using real-time polymerase chain reaction and Western blot analyses. Immunofluorescence was used to quantify endothelial nitric oxide synthase (eNOS) phosphorylation. Insulin-mediated vasodilation was markedly impaired in visceral compared to subcutaneous vessels from obese subjects (p<0.001), but preserved in non-obese individuals. Visceral adiposity was associated with increased JNK activation and elevated expression of WNT5A and its non-canonical receptors, which correlated negatively with insulin signaling. Pharmacological JNK antagonism with SP600125 markedly improved insulin-mediated vasodilation by sixfold (p<0.001), while endothelial cells exposed to recombinant WNT5A developed insulin resistance and impaired eNOS phosphorylation (p<0.05). We observed profound vascular insulin resistance in the visceral adipose tissue arterioles of obese subjects that was associated with up-regulated WNT5A-JNK signaling and impaired endothelial eNOS activation. Pharmacological JNK antagonism markedly improved vascular endothelial function, and may represent a potential therapeutic target in obesity-related vascular disease. PMID:27688298

  1. Maternal whole blood cell miRNA-340 is elevated in gestational diabetes and inversely regulated by glucose and insulin.

    PubMed

    Stirm, Laura; Huypens, Peter; Sass, Steffen; Batra, Richa; Fritsche, Louise; Brucker, Sara; Abele, Harald; Hennige, Anita M; Theis, Fabian; Beckers, Johannes; Hrabě de Angelis, Martin; Fritsche, Andreas; Häring, Hans-Ulrich; Staiger, Harald

    2018-01-22

    The number of pregnancies complicated by gestational diabetes (GDM) is increasing worldwide. To identify novel characteristics of GDM, we studied miRNA profiles of maternal and fetal whole blood cells (WBCs) from GDM and normal glucose tolerant (NGT) pregnant women matched for body mass index and maternal age. After adjustment for maternal weight gain and pregnancy week, we identified 29 mature micro-RNAs (miRNAs) up-regulated in GDM, one of which, i.e., miRNA-340, was validated by qPCR. mRNA and protein expression of PAIP1, a miRNA-340 target gene, was found down-regulated in GDM women, accordingly. In lymphocytes derived from the mothers' blood and treated in vitro, insulin increased and glucose reduced miRNA-340 expression. In fetal cord blood samples, no associations of miRNA-340 with maternal GDM were observed. Our results provide evidence for insulin-induced epigenetic, i.e., miRNA-dependent, programming of maternal WBCs in GDM.

  2. Maternal Obesity during Gestation Impairs Fatty Acid Oxidation and Mitochondrial SIRT3 Expression in Rat Offspring at Weaning

    PubMed Central

    Borengasser, Sarah J.; Lau, Franchesca; Kang, Ping; Blackburn, Michael L.; Ronis, Martin J. J.; Badger, Thomas M.; Shankar, Kartik

    2011-01-01

    In utero exposure to maternal obesity increases the offspring's risk of obesity in later life. We have also previously reported that offspring of obese rat dams develop hepatic steatosis, mild hyperinsulinemia, and a lipogenic gene signature in the liver at postnatal day (PND)21. In the current study, we examined systemic and hepatic adaptations in male Sprague-Dawley offspring from lean and obese dams at PND21. Indirect calorimetry revealed decreases in energy expenditure (p<0.001) and increases in RER values (p<0.001), which were further exacerbated by high fat diet (45% kcals from fat) consumption indicating an impaired ability to utilize fatty acids in offspring of obese dams as analyzed by PRCF. Mitochondrial function is known to be associated with fatty acid oxidation (FAO) in the liver. Several markers of hepatic mitochondrial function were reduced in offspring of obese dams. These included SIRT3 mRNA (p = 0.012) and mitochondrial protein content (p = 0.002), electron transport chain complexes (II, III, and ATPase), and fasting PGC-1α mRNA expression (p<0.001). Moreover, hepatic LCAD, a SIRT3 target, was not only reduced 2-fold (p<0.001) but was also hyperacetylated in offspring of obese dams (p<0.005) suggesting decreased hepatic FAO. In conclusion, exposure to maternal obesity contributes to early perturbations in whole body and liver energy metabolism. Mitochondrial dysfunction may be an underlying event that reduces hepatic fatty acid oxidation and precedes the development of detrimental obesity associated co-morbidities such as insulin resistance and NAFLD. PMID:21901160

  3. First trimester maternal adiposity is associated with infant body fat at age 2 weeks: A longitudinal follow-up study

    USDA-ARS?s Scientific Manuscript database

    Maternal obesity has been shown to be associated with childhood obesity risk in both experimental and epidemiological studies. However, longitudinal studies carefully evaluating other contributors to fetal and infant body fat accretion are lacking. The objective of this study was to evaluate the eff...

  4. Toddler parasympathetic regulation and fear: Links to maternal appraisal and behavior

    PubMed Central

    Cho, Sunghye; Buss, Kristin A.

    2017-01-01

    There is a growing recognition that parental socialization influences interact with young children’s emerging capacity for physiological regulation and shape children’s developmental trajectories. Nevertheless, the transactional processes linking parental socialization and physiological regulatory processes remain not well understood, particularly for fear-prone toddlers. To address this gap in the literature, the present study investigated the biopsychosocial processes that underlie toddlers’ fear regulation by examining the relations among toddler parasympathetic regulation, maternal appraisal, and parenting behaviors. Participants included 124 mothers and their toddlers (Mage = 24.43 months), who participated in a longitudinal study of temperament and socio-emotional development. Toddlers’ parasympathetic reactivity was found to moderate the links between maternal anticipatory appraisal of child fearfulness and (a) maternal provision of physical comfort and (b) preschool-age child inhibition. Additionally, maternal comforting behaviors during the low-threat task predicted preschool-age separation distress, specifically for toddlers demonstrating a low baseline RSA. PMID:27785806

  5. Toddler parasympathetic regulation and fear: Links to maternal appraisal and behavior.

    PubMed

    Cho, Sunghye; Buss, Kristin A

    2017-03-01

    There is a growing recognition that parental socialization influences interact with young children's emerging capacity for physiological regulation and shape children's developmental trajectories. Nevertheless, the transactional processes linking parental socialization and physiological regulatory processes remain not well understood, particularly for fear-prone toddlers. To address this gap in the literature, the present study investigated the biopsychosocial processes that underlie toddlers' fear regulation by examining the relations among toddler parasympathetic regulation, maternal appraisal, and parenting behaviors. Participants included 124 mothers and their toddlers (M age  = 24.43 months), who participated in a longitudinal study of temperament and socio-emotional development. Toddlers' parasympathetic reactivity was found to moderate the links between maternal anticipatory appraisal of child fearfulness and (a) maternal provision of physical comfort and (b) preschool-age child inhibition. Additionally, maternal comforting behaviors during the low-threat task predicted preschool-age separation distress, specifically for toddlers demonstrating a low baseline RSA. © 2016 Wiley Periodicals, Inc.

  6. Maternal regulation of sibling interactions in the preschool years: observational study in Japanese families.

    PubMed

    Kojima, Y

    2000-01-01

    Characteristics of three maternal regulating behaviors--(1) reference to one sibling's actions or emotional states toward the other sibling, (2) encouragement of sibling interactions, (3) distraction of one sibling's attention away from the other sibling-and their associations with children's positive and negative behaviors toward their siblings were investigated through semistructured home observations for 40 sibling pairs (1-4 years, 2-8 years) and their mothers in Japanese families. Maternal regulating behaviors were observed more frequently when the younger sibling was still in an early developmental stage in the preschool years, although the findings were modest. The older sibling's negative behaviors toward the younger sibling positively correlated with maternal distraction toward the younger; alternatively, the younger sibling's negative behaviors do not correlate with maternal distraction but do correlate with maternal encouragement directed toward the older sibling. Reliable associations were found between maternal regulating behaviors and prosocial exchanges between siblings; maternal reference to the younger sibling's actions or emotional states directed toward the older sibling was associated with the older sibling's positive behavior toward the younger sibling. Maternal regulating behaviors during mother-sibling triadic interactions were associated with the quality of sibling relationships.

  7. Maternal Rest/Nrsf Regulates Zebrafish Behavior through snap25a/b

    PubMed Central

    Moravec, Cara E.; Samuel, John; Weng, Wei; Wood, Ian C.

    2016-01-01

    During embryonic development, regulation of gene expression is key to creating the many subtypes of cells that an organism needs throughout its lifetime. Recent work has shown that maternal genetics and environmental factors have lifelong consequences on diverse processes ranging from immune function to stress responses. The RE1-silencing transcription factor (Rest) is a transcriptional repressor that interacts with chromatin-modifying complexes to repress transcription of neural-specific genes during early development. Here we show that in zebrafish, maternally supplied rest regulates expression of target genes during larval development and has lifelong impacts on behavior. Larvae deprived of maternal rest are hyperactive and show atypical spatial preferences. Adult male fish deprived of maternal rest present with atypical spatial preferences in a novel environment assay. Transcriptome sequencing revealed 158 genes that are repressed by maternal rest in blastula stage embryos. Furthermore, we found that maternal rest is required for target gene repression until at least 6 dpf. Importantly, disruption of the RE1 sites in either snap25a or snap25b resulted in behaviors that recapitulate the hyperactivity phenotype caused by absence of maternal rest. Both maternal rest mutants and snap25a RE1 site mutants have altered primary motor neuron architecture that may account for the enhanced locomotor activity. These results demonstrate that maternal rest represses snap25a/b to modulate larval behavior and that early Rest activity has lifelong behavioral impacts. SIGNIFICANCE STATEMENT Maternal factors deposited in the oocyte have well-established roles during embryonic development. We show that, in zebrafish, maternal rest (RE1-silencing transcription factor) regulates expression of target genes during larval development and has lifelong impacts on behavior. The Rest transcriptional repressor interacts with chromatin-modifying complexes to limit transcription of neural

  8. Maternal BMI and migration status as predictors of childhood obesity in Mexico

    PubMed Central

    Jiménez-Cruz, A.; Wojcicki, J. M.; Bacardí-Gascón, M.; Castellón-Zaragoza, A.; García-Gallardo, J. L.; Schwartz, N.; Heyman, M. B.

    2011-01-01

    Objective To assess the association of maternal migration to Baja California, body mass index (BMI) status, children’s perceived food insecurity, and childhood lifestyle behaviors with overweight (BMI > 85% ile), obesity (BMI > 95% ile) and abdominal obesity (Waist Circumference > 90% ile). Methods Convenience sampling methods were used to recruit a cross-sectional sample of 4th, 5th and 6th grade children and their parents at Tijuana and Tecate Public Schools. Children‘s and parents’ weights and heights were measured. Children were considered to have migrant parents if parents were not born in Baja California. Results One hundred and twenty-two children and their parents were recruited. The mean age of the children was 10.1 ± 1.0 years. Forty nine per cent of children were overweight or obese. Children with obese parents (BMI > 30) had greater odds of being obese, Odds Ratio (OR) 4.9 (95% Confidence Interval (CI), 1.2–19, p = 0.03). Children with migrant parents had greater odds of being obese, OR= 3.7 (95% CI, 1.6–8.3), p = 0.01) and of having abdominal obesity, OR = 3.2 (95% CI, 1.4–7.1, p = 0.01). Children from migrant parents have greater risk of higher consumption of potato chips, OR = 8.0 (95% CI, 2.1–29.1, p = 0.01). Children from non-migrant parents had greater odds of being at risk of hunger. Conclusions Parental obesity and migration are associated with increased risk of obesity among Mexican children. Children whose parents were born in Baja California have greater odds of being at risk of hunger. Further studies should evaluate the role of migration on risk for childhood obesity. PMID:21519746

  9. Parental work schedules and child overweight and obesity.

    PubMed

    Champion, S L; Rumbold, A R; Steele, E J; Giles, L C; Davies, M J; Moore, V M

    2012-04-01

    Studies in school-age children have consistently shown a positive association between maternal paid work hours and child obesity. However, there is conflicting evidence about the impact of maternal work hours scheduled at nonstandard times (for example, evenings, nights or weekends), and no previous examination of paternal work schedules and child weight. We examined the associations between maternal, paternal and combined parental paid work schedules and overweight/obesity in children at age 9 years. Data were analysed from the most recent follow-up of 9-year-old children (n=434) in an Australian birth cohort study. Children were measured and classified as overweight/obese using the International Obesity Taskforce body mass index cutoff points. Current working conditions of parents were obtained from a structured interview with the primary caregiver. Logistic regression analyses were used to investigate the effect of parental work schedules on child overweight/obesity with adjustment for a range of sociodemographic and household factors associated with parental employment and child weight. At 9 years of age, 99 children (22.8%) were overweight or obese. When parental work schedules were examined separately, child overweight/obesity was significantly associated with paternal nonstandard work schedules (adjusted odds ratio (OR) 1.97, 95% confidence interval (CI) 1.08-3.61). There was no association with any type of maternal work schedule. We also found an association between child overweight/obesity and circumstances in which both parents worked nonstandard schedules; however, this was of borderline statistical significance in the adjusted models (adjusted OR 2.26, 95% CI 0.99-5.16). Work hours scheduled at nonstandard times, when worked by the father or both parents, were associated with child overweight and obesity. These findings indicate the potential importance of fathers' paid work arrangements for child overweight/obesity, which until recently has largely

  10. Choline prevents fetal overgrowth and normalizes placental fatty acid and glucose metabolism in a mouse model of maternal obesity.

    PubMed

    Nam, Juha; Greenwald, Esther; Jack-Roberts, Chauntelle; Ajeeb, Tamara T; Malysheva, Olga V; Caudill, Marie A; Axen, Kathleen; Saxena, Anjana; Semernina, Ekaterina; Nanobashvili, Khatia; Jiang, Xinyin

    2017-11-01

    Maternal obesity increases placental transport of macronutrients, resulting in fetal overgrowth and obesity later in life. Choline participates in fatty acid metabolism, serves as a methyl donor and influences growth signaling, which may modify placental macronutrient homeostasis and affect fetal growth. Using a mouse model of maternal obesity, we assessed the effect of maternal choline supplementation on preventing fetal overgrowth and restoring placental macronutrient homeostasis. C57BL/6J mice were fed either a high-fat (HF, 60% kcal from fat) diet or a normal (NF, 10% kcal from fat) diet with a drinking supply of either 25 mM choline chloride or control purified water, respectively, beginning 4 weeks prior to mating until gestational day 12.5. Fetal and placental weight, metabolites and gene expression were measured. HF feeding significantly (P<.05) increased placental and fetal weight in the HF-control (HFCO) versus NF-control (NFCO) animals, whereas the HF choline-supplemented (HFCS) group effectively normalized placental and fetal weight to the levels of the NFCO group. Compared to HFCO, the HFCS group had lower (P<.05) glucose transporter 1 and fatty acid transport protein 1 expression as well as lower accumulation of glycogen in the placenta. The HFCS group also had lower (P<.05) placental 4E-binding protein 1 and ribosomal protein s6 phosphorylation, which are indicators of mechanistic target of rapamycin complex 1 activation favoring macronutrient anabolism. In summary, our results suggest that maternal choline supplementation prevented fetal overgrowth in obese mice at midgestation and improved biomarkers of placental macronutrient homeostasis. Copyright © 2017 Elsevier Inc. All rights reserved.

  11. Maternal lifestyle characteristics during pregnancy, and the risk of obesity in the offspring: a study of 5,125 children.

    PubMed

    Mourtakos, Stamatis P; Tambalis, Konstantinos D; Panagiotakos, Demosthenes B; Antonogeorgos, George; Arnaoutis, Giannis; Karteroliotis, Konstantinos; Sidossis, Labros S

    2015-03-21

    To investigate the association between gestational weight gain, maternal age and lifestyle habits (e.g., physical activity, smoking, and alcohol consumption) during pregnancy, with Body Mass Index of the offspring at the age of 8. Α random sample of 5,125 children was extracted from a national database and matched with their mothers. With the use of a standardised questionnaire, telephone interviews were carried out for the collection of information like: maternal age at pregnancy, gestational weight gain (GWG), exercise levels, smoking and alcohol consumption. The Body Mass Index (BMI) status of the offspring at the age of 8 was calculated from data retrieved from the national database (e.g., height and weight). The odds for being overweight/obese at the age of 8 for 1 kg GWG, for smoking, and for mild exercise during pregnancy compared to sedentary was 1.01 (95%CI: 1.00, 1.02), 1.23 (95%CI: 1.03, 1.47) and 0.77 (95%CI: 0.65, 0.91), respectively. Further analysis revealed that offspring of women who exceeded the Institute of Medicine (IOM) maternal weight gain recommendations were at an increased risk of obesity (OR: 1.45; 95%CI, 1.26, 1.67) compared with offspring of women with GWG within the recommended range. Maternal age and alcohol consumption were not associated with the outcome (p > 0.05). GWG, physical activity and smoking status during pregnancy were significantly associated with obesity for the offspring at the age of 8. Health care professionals should strongly advise women to not smoke and to perform moderate exercise during pregnancy to prevent obesity in the offspring in later life.

  12. Maternal Obesity, Overweight and Gestational Diabetes Affect the Offspring Neurodevelopment at 6 and 18 Months of Age--A Follow Up from the PREOBE Cohort.

    PubMed

    Torres-Espinola, Francisco J; Berglund, Staffan K; García-Valdés, Luz Ma; Segura, Ma Teresa; Jerez, Antonio; Campos, Daniel; Moreno-Torres, Rosario; Rueda, Ricardo; Catena, Andrés; Pérez-García, Miguel; Campoy, Cristina

    2015-01-01

    Brain development in fetal life and early infancy is critical to determine lifelong performance in various neuropsychological domains. Metabolic pathologies such as overweight, obesity, and gestational diabetes in pregnant women are prevalent and increasing risk factors that may adversely affect long-term brain development in their offspring. The objective of this research was to investigate the influence of maternal metabolic pathologies on the neurodevelopment of the offspring at 6 and 18 months of life. This was a prospective case-control study of 331 mother- and child pairs from Granada, Spain. The mothers were included during pregnancy into four groups according to their pre-gestational body mass index and their gestational diabetes status; overweight (n:56), obese (n:64), gestational diabetic (n:79), and healthy normal weight controls (n:132). At 6 months and 18 months we assessed the children with the Bayley III scales of neurodevelopment. At 6 months (n=215), we found significant group differences in cognition composite language, and expressive language. Post hoc test revealed unexpectedly higher scores in the obese group compared to the normal weight group and a similar trend in overweight and diabetic group. The effects on language remained significant after adjusting for confounders with an adjusted odds ratio for a value above median in composite language score of 3.3 (95% CI: 1.1, 10.0; p=0.035) for children of obese mothers. At 18 month (n=197), the offspring born to obese mothers had lost five points in language composite scores and the previous differences in language and cognition was replaced by a suggestive trend of lower gross motor scores in the overweight, obese, and diabetic groups. Infants of obese mothers had a temporary accelerated development of cognition and language, followed by a rapid deceleration until 18 months of age, particularly of language scores. This novel observation prompts further confirmative studies to explore possible

  13. Early Parturition: Is Young Maternal Age at First Birth Associated with Obesity?

    PubMed

    Patchen, Loral; Leoutsakos, Jeannie-Marie; Astone, Nan M

    2017-10-01

    Examine the association of age at first birth with body mass index (BMI), and explore the role of young maternal age and subsequent obesity. This study analyzed data from the Panel Study of Income Dynamics, a nationally representative longitudinal study of US families. Analyses were conducted using a mixed effects longitudinal linear regression with a random intercept to examine the effect of aging, age at first birth, and minority status using nested data. Study criteria yielded a final sample of 146 women with 707 observations. BMI. Age at first birth exhibited a significant association with BMI. The association of age at first birth with BMI was greatest for women age 21 and younger. Overall, women who experienced their first birth at age 21 or younger had a BMI 5 units greater than women who delayed childbearing until at least age 30 (point estimate, 5.02; P = .02; 95% confidence interval, 0.65-9.40). Young maternal age at first birth might be associated with increased BMI. Minority women also experience their first birth at younger ages compared with white women, suggesting possible linkages between the timing of reproductive events and obesity disparities. Copyright © 2016 North American Society for Pediatric and Adolescent Gynecology. Published by Elsevier Inc. All rights reserved.

  14. Maternal Obesity and Excessive Gestational Weight Gain Are Associated with Components of Child Cognition.

    PubMed

    Pugh, Sarah J; Richardson, Gale A; Hutcheon, Jennifer A; Himes, Katherine P; Brooks, Maria M; Day, Nancy L; Bodnar, Lisa M

    2015-11-01

    Maternal overweight and obesity affect two-thirds of women of childbearing age and may increase the risk of impaired child cognition. Our objective was to test the hypothesis that high/low gestational weight gain (GWG) and high/low prepregnancy BMI were associated with offspring intelligence quotient (IQ) and executive function at age 10. Mother-infant dyads (n = 763) enrolled in a birth cohort study were followed from early pregnancy to 10 y postpartum. IQ was assessed by trained examiners with the use of the Stanford Binet Intelligence Scale-4th edition. Executive function was assessed by the number of perseverative errors on the Wisconsin Card Sorting Test and time to complete Part B on the Trail Making Test. Self-reported total GWG was converted to gestational-age-standardized GWG z score. Multivariable linear regression and negative binomial regression were used to estimate independent and joint effects of GWG and BMI on outcomes while adjusting for covariates. At enrollment, the majority of women in the Maternal Health Practices and Child Development cohort were unmarried and unemployed, and more than one-half reported their race as black. The mean ± SD GWG z score was -0.5 ± 1.8, and 27% of women had a pregravid BMI ≥ 25. The median (IQR) number of perseverative errors was 23 (17, 29), the mean ± SD time on Part B was 103 ± 42.6 s, and 44% of children had a low average IQ (≤ 89). Maternal obesity was associated with 3.2 lower IQ points (95% CI: -5.6, -0.8) and a slower time to complete the executive function scale Part B (adjusted β: 12.7 s; 95% CI: 2.8, 23 s) compared with offspring of normal-weight mothers. Offspring of mothers whose GWG was >+1 SD, compared with -1 to +1 SD, performed 15 s slower on the executive function task (95% CI: 1.8, 28 s). There was no association between GWG z score and offspring composite IQ score (adjusted β: -0.32; 95% CI: -0.72, 0.10). Prepregnancy BMI did not modify these associations. Although GWG may be important

  15. Does Insulin Explain the Relation between Maternal Obesity and Poor Lactation Outcomes? An Overview of the Literature1234

    PubMed Central

    2016-01-01

    It is well established that obese women are at increased risk of delayed lactogenesis and short breastfeeding duration, but the underlying causal contributors remain unclear. This review summarizes the literature examining the role of insulin in lactation outcomes. Maternal obesity is a strong risk factor for insulin resistance and prediabetes, but until recently a direct role for insulin in milk production had not been elucidated. Over the past 6 y, studies in both animal models and humans have shown insulin-sensitive gene expression to be dramatically upregulated specifically during the lactation cycle. Insulin is now considered to play a direct role in lactation, including essential roles in secretory differentiation, secretory activation, and mature milk production. At the same time, emerging clinical research suggests an important association between suboptimal glucose tolerance and lactation difficulty. To develop effective interventions to support lactation success in obese women further research is needed to identify how, when, and for whom maternal insulin secretion and sensitivity affect lactation ability. PMID:26980825

  16. Sequential observation of infant regulated and dysregulated behavior following soothing and stimulating maternal behavior during feeding

    PubMed Central

    Brown, Lisa F.; Pridham, Karen A.; Brown, Roger

    2014-01-01

    Purpose To describe maternal behaviors occurring before infant regulated or dysregulated behavior at three times in early infancy and examine behavioral patterns over time with their prematurely born infants. Method & Design Video-recordings of 37 dyads were coded on infant regulated and dysregulated behaviors following maternal soothing and stimulating behaviors. Results At each time, infants showed more regulation after maternal soothing than after maternal stimulating. Further study is merited. Practice Implications Knowing infant regulation and dysregulation following categories of maternal behavior could help mothers anticipate infant regulatory or dysregulatory behavior in response to their own behavior and identify supportive caregiving strategies. PMID:24417766

  17. Maternal fat-soluble vitamins, brain development, and regulation of feeding behavior: an overview of research.

    PubMed

    Sánchez-Hernández, Diana; Anderson, G Harvey; Poon, Abraham N; Pannia, Emanuela; Cho, Clara E; Huot, Pedro S P; Kubant, Ruslan

    2016-10-01

    Recent research shows a link between vitamin intake during pregnancy and offspring health. Inadequate intakes of water-soluble vitamins during pregnancy lead to obesity and characteristics of the metabolic syndrome, concurrent with altered developments in food intake regulatory pathways. Few studies, however, have reported on the effects of fat-soluble vitamins (A, D, E, and K) on the development of food intake regulatory pathways. The majority of studies to date have focused on associations between inadequate and high intakes of folic acid and vitamin D and neurocognitive development of the offspring. Hence, the objective of this review is to present an evaluation of the role of maternal vitamins A, D, E, and K in brain development and function of neural pathways that regulate feeding behaviors. PubMed and Google Scholar were searched from 1975 through September, 2016. Most studies supporting a role for fat-soluble vitamins in regulating brain development and associated behaviors have been conducted in animal and cell models, leaving uncertain their relevance to neurocognitive development and function in humans. Nevertheless, although current research on defining the role of maternal fat-soluble vitamins in offspring's brain development is limited, it is sufficient to warrant further investigations on their impact when intake amounts during pregnancy are not only inadequate but also exceed requirements. Copyright © 2016 Elsevier Inc. All rights reserved.

  18. Warm and harsh parenting as mediators of the relation between maternal and adolescent emotion regulation.

    PubMed

    Sarıtaş, Dilek; Grusec, Joan E; Gençöz, Tülin

    2013-12-01

    Maternal hostility/rejection and warmth were considered as potential mediators of the relation between mothers' and adolescents' emotion regulation. Participants were first-year high school students living in Ankara, Turkey and their mothers (N = 365). Scales assessing emotion regulation difficulties and maternal hostility/rejection and warmth were administered to both the adolescents and their mothers. Maternal hostility/rejection, but not warmth, mediated the relation between maternal and adolescent emotion regulation. For girls there was, additionally, a direct effect of maternal emotion regulation. The different roles played by parental rejection and parental warmth in the development of adolescents' emotion regulation accord with arguments that socialization occurs in different domains and that rejection and warmth are not aspects of the same domain. Copyright © 2013 The Foundation for Professionals in Services for Adolescents. Published by Elsevier Ltd. All rights reserved.

  19. Does Insulin Explain the Relation between Maternal Obesity and Poor Lactation Outcomes? An Overview of the Literature.

    PubMed

    Nommsen-Rivers, Laurie A

    2016-03-01

    It is well established that obese women are at increased risk of delayed lactogenesis and short breastfeeding duration, but the underlying causal contributors remain unclear. This review summarizes the literature examining the role of insulin in lactation outcomes. Maternal obesity is a strong risk factor for insulin resistance and prediabetes, but until recently a direct role for insulin in milk production had not been elucidated. Over the past 6 y, studies in both animal models and humans have shown insulin-sensitive gene expression to be dramatically upregulated specifically during the lactation cycle. Insulin is now considered to play a direct role in lactation, including essential roles in secretory differentiation, secretory activation, and mature milk production. At the same time, emerging clinical research suggests an important association between suboptimal glucose tolerance and lactation difficulty. To develop effective interventions to support lactation success in obese women further research is needed to identify how, when, and for whom maternal insulin secretion and sensitivity affect lactation ability. © 2016 American Society for Nutrition.

  20. Maternal regulation of child affect in externalizing and typically-developing children.

    PubMed

    Lougheed, Jessica P; Hollenstein, Tom; Lichtwarck-Aschoff, Anna; Granic, Isabela

    2015-02-01

    Temporal contingencies between children's affect and maternal behavior play a role in the development of children's externalizing problems. The goal of the current study was to use a microsocial approach to compare dyads with externalizing dysregulation (N =191) to healthy controls (N = 54) on maternal supportive regulation of children's negative and positive affect. Children were between the ages of 8 and 12 years. Mother-child dyads participated in conflict and positive discussions, and child affect and maternal supportive affect regulation were coded in real time. First, no group differences on overall levels of mother supportive regulation or child affect were found. Second, three event history analyses in a 2-level Cox hazard regression framework were used to predict the hazard rate of (a) maternal supportiveness, and of children's transitions (b) out of negative affect and (c) into positive affect. The hazard rate of maternal supportiveness, regardless of child affect, was not different between groups. However, as expected, the likelihood of mothers' supportive responses to children's negative affect was lower in externalizing than comparison dyads. In addition, children with externalizing problems were significantly less likely than typically developing children to transition out of negative affect in response to maternal supportiveness. The likelihood of both typically developing children and children with externalizing problems transitioning into positive affect were not related to specific occurrences of maternal supportiveness. Results of the current study show the importance of temporal dynamics in mother-child interactions in the emergence of children's externalizing problems. PsycINFO Database Record (c) 2015 APA, all rights reserved.

  1. Maternal Attachment Style and Responses to Adolescents’ Negative Emotions: The Mediating Role of Maternal Emotion Regulation

    PubMed Central

    Jones, Jason D.; Brett, Bonnie E.; Ehrlich, Katherine B.; Lejuez, Carl W.; Cassidy, Jude

    2014-01-01

    SYNOPSIS Objective Previous research has examined the developmental consequences, particularly in early childhood, of parents’ supportive and unsupportive responses to children’s negative emotions. Much less is known about factors that explain why parents respond in ways that may support or undermine their children’s emotions, and even less is known about how these parenting processes unfold with adolescents. We examined the associations between mothers’ attachment styles and their distress, harsh, and supportive responses to their adolescents’ negative emotions two years later and whether these links were mediated by maternal emotion regulation difficulties. Design Mothers in a longitudinal study (n = 230) reported on their attachment style, difficulties regulating their emotions, and their hypothetical responses to their adolescents’ negative emotions, respectively, at consecutive laboratory visits one year apart. Results Mothers who reported greater attachment-related avoidance and anxiety reported having greater difficulties with emotion regulation one year later. Emotion dysregulation, in turn, predicted more distressed, harsher, and less supportive maternal responses to adolescents’ negative emotions the following year. In addition, greater avoidance directly predicted harsher maternal responses two years later. Conclusions These findings extend previous research by identifying maternal attachment style as a predictor of responses to adolescent distress and by documenting the underlying role of emotion dysregulation in the link between adult attachment style and parenting. PMID:25568638

  2. Maternal emotion regulation during child distress, child anxiety accommodation, and links between maternal and child anxiety.

    PubMed

    Kerns, Caroline E; Pincus, Donna B; McLaughlin, Katie A; Comer, Jonathan S

    2017-08-01

    Environmental contributions are thought to play a primary role in the familial aggregation of anxiety, but parenting influences remain poorly understood. We examined dynamic relations between maternal anxiety, maternal emotion regulation (ER) during child distress, maternal accommodation of child distress, and child anxiety. Mothers (N=45) of youth ages 3-8 years (M=4.8) participated in an experimental task during which they listened to a standardized audio recording of a child in anxious distress pleading for parental intervention. Measures of maternal and child anxiety, mothers' affective states, mothers' ER strategies during the child distress, and maternal accommodation of child anxiety were collected. Mothers' resting respiratory sinus arrhythmia (RSA) reactivity during the recording was also acquired. Higher maternal negative affect and greater maternal ER switching (i.e., using multiple ER strategies in a short time without positive regulatory results) during child distress were associated with child anxiety. Sequential mediation modeling showed that maternal anxiety predicted ineffective maternal ER during child distress exposure, which in turn predicted greater maternal accommodation, which in turn predicted higher child anxiety. Findings support the mediating roles of maternal ER and accommodation in linking maternal and child anxiety, and suggest that ineffective maternal ER and subsequent attempts to accommodate child distress may act as mechanisms underlying the familial aggregation of anxiety. Copyright © 2017 Elsevier Ltd. All rights reserved.

  3. Maternal Work and Children’s Diet, Activity, and Obesity

    PubMed Central

    Datar, Ashlesha; Nicosia, Nancy; Shier, Victoria

    2014-01-01

    Mothers’ work hours are likely to affect their time allocation towards activities related to children’s diet, activity and well-being. For example, mothers who work more may be more reliant on processed foods, foods prepared away from home and school meal programs for their children’s meals. A greater number of work hours may also lead to more unsupervised time for children that may, in turn, allow for an increase in unhealthy behaviors among their children such as snacking and sedentary activities such as TV watching. Using data on a national cohort of children, we examine the relationship between mothers’ average weekly work hours during their children’s school years on children’s dietary and activity behaviors, BMI and obesity in 5th and 8th grade. Our results are consistent with findings from the literature that maternal work hours are positively associated with children’s BMI and obesity especially among children with higher socioeconomic status. Unlike previous papers, our detailed data on children’s behaviors allow us to speak directly to affected behaviors that may contribute to the increased BMI. We show that children whose mothers work more consume more unhealthy foods (e.g. soda, fast food) and less healthy foods (e.g. fruits, vegetables, milk) and watch more television. Although they report being slightly more physically active, likely due to organized physical activities, the BMI and obesity results suggest that the deterioration in diet and increase in sedentary behaviors dominate. PMID:24491828

  4. Meta-review of protein network regulating obesity between validated obesity candidate genes in the white adipose tissue of high-fat diet-induced obese C57BL/6J mice.

    PubMed

    Kim, Eunjung; Kim, Eun Jung; Seo, Seung-Won; Hur, Cheol-Goo; McGregor, Robin A; Choi, Myung-Sook

    2014-01-01

    Worldwide obesity and related comorbidities are increasing, but identifying new therapeutic targets remains a challenge. A plethora of microarray studies in diet-induced obesity models has provided large datasets of obesity associated genes. In this review, we describe an approach to examine the underlying molecular network regulating obesity, and we discuss interactions between obesity candidate genes. We conducted network analysis on functional protein-protein interactions associated with 25 obesity candidate genes identified in a literature-driven approach based on published microarray studies of diet-induced obesity. The obesity candidate genes were closely associated with lipid metabolism and inflammation. Peroxisome proliferator activated receptor gamma (Pparg) appeared to be a core obesity gene, and obesity candidate genes were highly interconnected, suggesting a coordinately regulated molecular network in adipose tissue. In conclusion, the current network analysis approach may help elucidate the underlying molecular network regulating obesity and identify anti-obesity targets for therapeutic intervention.

  5. Origins in the Womb: Potential Role of the Physical Therapist in Modulating the Deleterious Effects of Obesity on Maternal and Offspring Health Through Movement Promotion and Prescription During Pregnancy.

    PubMed

    Tinius, Rachel A; Cahill, Alison G; Cade, W Todd

    2017-01-01

    Maternal obesity and associated metabolic disease contribute to adverse outcomes in women and their offspring, and many of these outcomes have significant acute and chronic implications for both mother and neonate. Targeted movement (ie, physical activity or exercise training) during pregnancy has been shown to be safe and effective for improving many of these outcomes in women at a healthy weight and women who are obese. However, movement prescription and advice during pregnancy are often not addressed by health care providers; this situation creates a unique opportunity for physical therapists to use their expertise in movement with patients who are pregnant. The objective of this article is to briefly review the adverse maternal and neonatal outcomes associated with maternal obesity, the benefits of intentional maternal movement during pregnancy for women who are obese, the evidence-based guidelines for prescribing intentional movement during pregnancy for women who are obese, and the potential for physical therapists to become the driving force behind a necessary increase in movement levels in women who are pregnant. Physical therapists can play a significant role in encouraging movement in women who are healthy and women who have metabolic challenges during pregnancy and thus assist in combating the vicious cycle of obesity by improving maternal and offspring health. © 2017 American Physical Therapy Association.

  6. Cardiac parasympathetic regulation in obese women with binge eating disorder.

    PubMed

    Friederich, H-C; Schild, S; Schellberg, D; Quenter, A; Bode, C; Herzog, W; Zipfel, S

    2006-03-01

    Obese individuals with a binge eating disorder (BED) differ from obese non-binge eaters (NBED) with respect to (a) eating behaviour, (b) psychiatric comorbidity and (c) level of psychosocial distress. The aim of the study was to explore whether these three factors have an influence on cardiac parasympathetic function, that is independent of obesity: as alterations in cardiac parasympathetic function may have a role in the higher cardiovascular mortality that is present in obese individuals. In total, 38 obese women (BMI>30 kg/m(2)), with a BED and 34 age and BMI matched healthy controls (NBED) completed a laboratory stress protocol that incorporated a baseline resting period, Head-up Tilt Testing (HUT) and two challenging mental tasks. Heart rate and blood pressure were measured continuously during the protocol. Parasympathetic cardiac regulation was assessed as the high frequency component of heart rate variability (HRV-HF). Mental challenge led to an augmented reduction of HRV-HF in obese binge eaters, which was linked to the binge eating frequency and hunger perception, but not to psychiatric comorbidity. During baseline conditions and HUT, no significant differences in parasympathetic measures were observed between the two subject groups. Subjects with a BED showed greater reduction in parasympathetic cardiac control (HRV-HF) during mental stress, suggesting higher stress vulnerability in women with a BED. Longitudinal investigations are necessary to evaluate whether this is associated with an increased cardiovascular mortality.

  7. Maternal obesity upregulates fatty acid and glucose transporters and increases expression of enzymes mediating fatty acid biosynthesis in fetal adipose tissue depots.

    PubMed

    Long, N M; Rule, D C; Zhu, M J; Nathanielsz, P W; Ford, S P

    2012-07-01

    Maternal nutrient restriction leads to alteration in fetal adipose tissue, and offspring from obese mothers have an increased risk of developing obesity. We hypothesized that maternal obesity increases fetal adipogenesis. Multiparous ewes (Columbia/Rambouillet cross 3 to 5 yr of age) carrying twins were assigned to a diet of 100% (Control; CON; n = 4) or 150% (Obese; OB, n = 7) of NRC maintenance requirements from 60 d before conception until necropsy on d 135 of gestation. Maternal and fetal plasma were collected and stored at -80°C for glucose and hormone analyses. Fetal measurements were made at necropsy, and perirenal, pericardial, and subcutaneous adipose tissues were collected from 7 male twin fetuses per group and snap frozen at -80°C. Protein and mRNA expression of fatty acid translocase [cluster of differentiation (CD) 36], fatty acid transport proteins (FATP) 1 and 4, insulin-sensitive glucose transporter (GLUT-4), fatty acid synthase (FASN), and acetyl-coA carboxylase (ACC) was evaluated. Fetal weight was similar, but fetal carcass weight (FCW) was reduced (P < 0.05) in OB versus CON fetuses. Pericardial and perirenal adipose tissue weights were increased (P < 0.05) as a percentage of FCW in OB versus CON fetuses, as was subcutaneous fat thickness (P < 0.001). Average adipocyte diameter was greater (P < 0.01) in the perirenal fat and the pericardial fat (P = 0.06) in OB fetuses compared with CON fetuses. Maternal plasma showed no difference (P > 0.05) in glucose or other hormones, fetal plasma glucose was similar (P = 0.42), and cortisol, IGF-1, and thyroxine were reduced (P ≤ 0.05) in OB fetuses compared with CON fetuses. Protein and mRNA expression of CD 36, FATP 1 and 4, and GLUT-4 were increased (P ≤ 0.05) in all fetal adipose depots in OB versus CON fetuses. The mRNA expression of FASN and ACC was increased (P < 0.05) in OB vs. CON fetuses in all 3 fetal adipose tissue depots. Fatty acid concentrations were increased (P = 0.01) in the

  8. The maternal womb: a novel target for cancer prevention in the era of the obesity pandemic?

    PubMed Central

    Simmen, Frank A.; Simmen, Rosalia C.M.

    2011-01-01

    The dramatic rise in worldwide prevalence of obesity has necessitated the search for more efficacious anti-obesity strategies to counter the increased cancer risks in overweight and obese individuals. The mechanistic pathways linking obesity status with adult chronic diseases such as cancer remain incompletely understood. A growing body of evidence suggests that novel approaches and interventional agents to disrupt the feed-forward cycle of maternal to offspring obesity transfer that is initiated in utero, will be important for stemming both the obesity pandemic and the associated increase in cancer incidence. The convergence of multiple research areas including those encompassing the insulin and insulin-like growth factor (IGF) systems, epigenetics, and stem cell biology is providing insights into the potential for cancer prevention in adult offspring previously exposed to the intrauterine environment of overweight/obese mothers. Here, we review the current state of this nascent research field, with a focus on three major cancers namely breast, colorectal and liver, and suggest some possible future directions to optimize its impact for the health of future generations. PMID:21701386

  9. A Study on Mediation by Offspring BMI in the Association between Maternal Obesity and Child Respiratory Outcomes in the Amsterdam Born and Their Development Study Cohort.

    PubMed

    Harskamp-van Ginkel, Margreet W; London, Stephanie J; Magnus, Maria C; Gademan, Maaike G; Vrijkotte, Tanja G

    2015-01-01

    A causal relationship between maternal obesity and offspring asthma is hypothesized to begin during early development, but no underlying mechanism for the found association is identified. We quantitatively examined mediation by offspring body mass index (BMI) in the association of maternal pre-pregnancy BMI on risk of asthma and wheezing during the first 7-8 years of life in a large Amsterdam born birth cohort. For 3185 mother-child pairs, mothers reported maternal pre-pregnancy BMI and offspring outcomes "ever being diagnosed with asthma" and "wheezing in the past 12 months" on questionnaires. We measured offspring height and weight at age 5-6 years. We performed a multivariate log linear regression comparing outcomes in offspring of mothers with different BMI categories. For each category we quantified and tested mediation by offspring BMI and also investigated interaction by parental asthma. At the age of 7-8 years, 8% of the offspring ever had asthma and 7% had current wheezing. Maternal pre-pregnancy obesity was associated with higher risks of asthma (adjusted RR 2.32 (95% CI: 1.49-3.61) and wheezing (adjusted RR 2.16 (95% CI: 1.28-3.64). Offspring BMI was a mediator in the association between maternal BMI and offspring wheezing, but not for asthma. There was no interaction by parental asthma. Maternal pre-pregnancy obesity was associated with higher risks of offspring asthma and wheezing. The association between maternal obesity and offspring wheezing was both direct and indirect (mediated) through the child's own BMI.

  10. A Qualitative Study of the Maternity Care Experiences of Women with Obesity: "More than Just a Number on the Scale".

    PubMed

    DeJoy, Sharon Bernecki; Bittner, Krystle; Mandel, Deborah

    2016-01-01

    The prevalence of obesity among pregnant women in the United States is high. Obesity can have long-term health consequences for both women and their offspring, so high-quality perinatal care for women with obesity is essential. However, stigmatizing encounters with health care professionals can decrease quality and promote avoidance of care. The purpose of this study was to explore the experiences of women with obesity in the maternity care system in the United States. In-depth telephone interviews were conducted with 16 women with a body mass index of 30 or greater. The authors used an inductive analytical process to translate women's experiences into themes. Women with obesity reported diverse maternity care experiences, with some reporting appropriate and satisfactory care, while most reported at least one negative encounter over the course of perinatal care. Three major themes emerged from the analysis: personalized care, depersonalized care, and setting the tone. Interactions with providers during pregnancy had psychological and emotional effects on women with obesity and influenced the content and perceived quality of their care. Further research is required to explore this phenomenon and its implications for care of women during pregnancy and birth outcomes. In the meantime, providers may wish to consider greater sensitivity to the needs of women with obesity during the perinatal period. © 2016 by the American College of Nurse-Midwives.

  11. Metabolic syndrome in Spanish adolescents and its association with birth weight, breastfeeding duration, maternal smoking, and maternal obesity: a cross-sectional study.

    PubMed

    González-Jiménez, Emilio; Montero-Alonso, Miguel A; Schmidt-RioValle, Jacqueline; García-García, Carmen J; Padez, Cristina

    2015-06-01

    The metabolic syndrome (MetS) in adolescents is a growing problem. The objectives were to verify the association among early predictors such as birth weight, breastfeeding, maternal weight status, smoking during pregnancy, and the development of MetS. A cross-sectional study was performed of 976 children and adolescents, 10-15 years of age, at schools in the provinces of Granada and Almeria (Spain). For this purpose, we analyzed the physical characteristics as well as the biochemical markers of the participants with a view to ascertaining the prevalence of the MetS. Relevant data were also extracted from the clinical histories of their mothers. It was found that 3.85% of the female subjects and 5.38% of the male subjects in the sample population suffered from MetS. In both sexes, there was an association between birth weight and positive MetS diagnosis (OR 1.27). For both males and females, there was an inverse association between the length of time that they had been breastfed and positive MetS diagnosis (OR1-3 months 3.16; OR4-6 months 1.70; OR(>6 months) 0.13). There was also a significant association between maternal weight (OR(overweight )30.79; OR(obesity) 49.36) and cigarette consumption during pregnancy (OR 1.47) and the subsequent development of MetS in the children of these mothers. Those subjects born with a higher than average birth weight had a greater risk of developing MetS in childhood and adolescence. Breastfeeding children for longer than 6 months protected them from MetS in their early years as well as in their teens. Other risk factors for MetS were maternal smoking during pregnancy as well as maternal overweight and obesity.

  12. Associations of maternal employment and three-generation families with pre-school children's overweight and obesity in Japan.

    PubMed

    Watanabe, E; Lee, J S; Kawakubo, K

    2011-07-01

    Maternal employment has been shown to be associated with childhood overweight and obesity (Ow/Ob), but the presence of family members who care for children in place of the mothers might influence children's Ow/Ob and lifestyles. The influence of maternal employment on children's Ow/Ob should be examined together with the presence of caregivers such as grandparents. The effects of maternal employment and the presence of grandparents on lifestyles and Ow/Ob in Japanese pre-school children were investigated. Cross-sectional study on 2114 children aged 3-6 years who attended all childcare facilities in a city and primary caregivers was conducted. Children's weight and height, family environments (family members, maternal employment, single parent, number of siblings and parental Ow/Ob) and lifestyles (dietary, physical activity and sleeping habits) were surveyed using a self-administered questionnaire. Ow/Ob was defined by the International Obesity Task Force cut-offs. The eligible participants were 1765 children. The prevalence of Ow/Ob was 8.4% in boys and 9.9% in girls. Maternal employment was associated positively with irregular mealtimes, unfixed snacking times, bedtime after 10 p.m. and nighttime sleep duration of less than 10 h, whereas three-generation families were associated negatively with irregular mealtimes after adjustment for children's characteristics and family environments. Irregular mealtimes (OR (95% CI); 2.03 (1.36, 3.06)) and nighttime sleep duration of less than 10 h (1.96 (1.28, 3.01)) were associated with increased risks of being Ow/Ob. Both maternal employment and three-generation families were significantly associated with children's Ow/Ob. However, three-generation families maintained a significant association (1.59 (1.08, 2.35)) after adjustment for maternal employment. These study results suggest that the grandparents who care for pre-school children in place of mothers are more likely to contribute to childhood Ow/Ob than maternal

  13. Experimental Models of Maternal Obesity and Neuroendocrine Programming of Metabolic Disorders in Offspring.

    PubMed

    Reynolds, Clare M; Segovia, Stephanie A; Vickers, Mark H

    2017-01-01

    Evidence from epidemiological, clinical, and experimental studies have clearly shown that disease risk in later life is increased following a poor early life environment, a process preferentially termed developmental programming. In particular, this work clearly highlights the importance of the nutritional environment during early development with alterations in maternal nutrition, including both under- and overnutrition, increasing the risk for a range of cardiometabolic and neurobehavioral disorders in adult offspring characterized by both adipokine resistance and obesity. Although the mechanistic basis for such developmental programming is not yet fully defined, a common feature derived from experimental animal models is that of alterations in the wiring of the neuroendocrine pathways that control energy balance and appetite regulation during early stages of developmental plasticity. The adipokine leptin has also received significant attention with clear experimental evidence that normal regulation of leptin levels during the early life period is critical for the normal development of tissues and related signaling pathways that are involved in metabolic and cardiovascular homeostasis. There is also increasing evidence that alterations in the epigenome and other underlying mechanisms including an altered gut-brain axis may contribute to lasting cardiometabolic dysfunction in offspring. Ongoing studies that further define the mechanisms between these associations will allow for identification of early risk markers and implementation of strategies around interventions that will have obvious beneficial implications in breaking a programmed transgenerational cycle of metabolic disorders.

  14. Linking Maternal Warmth and Responsiveness to Children's Self-Regulation

    ERIC Educational Resources Information Center

    von Suchodoletz, Antje; Trommsdorff, Gisela; Heikamp, Tobias

    2011-01-01

    The present study demonstrated that a more differentiated view of positive parenting practices is necessary in the study of children's acquisition of self-regulation. Here, the unique contributions of maternal warmth and responsiveness to distress to children's self-regulation were tested in a sample of 102 German mothers and their kindergarten…

  15. Carry-over of self-regulation for physical activity to self-regulating eating in women with morbid obesity.

    PubMed

    Annesi, James J; Porter, Kandice J; Johnson, Ping H

    2015-01-01

    Poor outcomes from behavioral treatments of severe obesity have led to a dependence on invasive medical interventions, including surgery for morbidly obese individuals. Improved methods to self-regulate eating will be required to reduce obesity. The use of self-regulation methods for completing physical activity may carry over to increased self-regulation for eating through improved feelings of competence (self-efficacy) and mood. The study recruited women (Meanage = 43 years) with morbid obesity (MeanBMI = 44 kg/m(2)) to participate in 26 weeks of cognitive-behavioral support of physical activity paired with either nutrition education (n = 51) or cognitive-behavioral nutrition (n = 51) methods. Data collected were from 2011 and 2012. Significant improvements in self-regulation for physical activity, self-regulation for eating, overall mood, and self-efficacy for eating, with greater improvement in self-regulation for eating, were observed in the cognitive-behavioral nutrition group. Changes in mood and self-efficacy for eating significantly mediated the relationship between changes in self-regulation for physical activity and self-regulation for eating. When subscales of overall mood and self-efficacy were entered into separate regression equations as mediators, the only significant mediators were vigor, and controlling eating when socially pressured and when increased cues to overeat were present.

  16. Maternal obesity increases insulin resistance, low-grade inflammation and osteochondrosis lesions in foals and yearlings until 18 months of age

    PubMed Central

    Nouveau, E.; Gautier, C.; Mendoza, L.; Dubois, C.; Dahirel, M.; Lagofun, B.; Aubrière, M-C; Lejeune, J-P; Caudron, I.; Guenon, I.; Viguié, C.; Wimel, L.; Bouraima-Lelong, H.; Serteyn, D.; Couturier-Tarrade, A.; Chavatte-Palmer, P.

    2018-01-01

    Introduction Obesity is a growing concern in horses. The effects of maternal obesity on maternal metabolism and low-grade inflammation during pregnancy, as well as offspring growth, metabolism, low-grade inflammation, testicular maturation and osteochondrotic lesions until 18 months of age were investigated. Material and methods Twenty-four mares were used and separated into two groups at insemination according to body condition score (BCS): Normal (N, n = 10, BCS ≤4) and Obese (O, n = 14, BCS ≥4.25). BCS and plasma glucose, insulin, triglyceride, urea, non-esterified fatty acid, serum amyloid A (SAA), leptin and adiponectin concentrations were monitored throughout gestation. At 300 days of gestation, a Frequently Sampled Intravenous Glucose Tolerance Test (FSIGT) was performed. After parturition, foals’ weight and size were monitored until 18 months of age with plasma SAA, leptin, adiponectin, triiodothyronine (T3), thyroxine (T4) and cortisol concentrations measured at regular intervals. At 6, 12 and 18 months of age, FSIGT and osteoarticular examinations were performed. Males were gelded at one year and expression of genes involved in testicular maturation analysed by RT-qPCR. Results Throughout the experiment, maternal BCS was higher in O versus N mares. During gestation, plasma urea and adiponectin were decreased and SAA and leptin increased in O versus N mares. O mares were also more insulin resistant than N mares with a higher glucose effectiveness. Postnatally, there was no difference in offspring growth between groups. Nevertheless, plasma SAA concentrations were increased in O versus N foals until 6 months, with O foals being consistently more insulin resistant with a higher glucose effectiveness. At 12 months of age, O foals were significantly more affected by osteochondrosis than N foals. All other parameters were not different between groups. Conclusion In conclusion, maternal obesity altered metabolism and increased low-grade inflammation in

  17. Obesity prevention: the role of policies, laws and regulations.

    PubMed

    Swinburn, Boyd A

    2008-06-05

    The commercial drivers of the obesity epidemic are so influential that obesity can be considered a robust sign of commercial success - consumers are buying more food, more cars and more energy-saving machines. It is unlikely that these powerful economic forces will change sufficiently in response to consumer desires to eat less and move more or corporate desires to be more socially responsible. When the free market creates substantial population detriments and health inequalities, government policies are needed to change the ground rules in favour of population benefits.Concerted action is needed from governments in four broad areas: provide leadership to set the agenda and show the way; advocate for a multi-sector response and establish the mechanisms for all sectors to engage and enhance action; develop and implement policies (including laws and regulations) to create healthier food and activity environments, and; secure increased and continued funding to reduce obesogenic environments and promote healthy eating and physical activity.Policies, laws and regulations are often needed to drive the environmental and social changes that, eventually, will have a sustainable impact on reducing obesity. An 'obesity impact assessment' on legislation such as public liability, urban planning, transport, food safety, agriculture, and trade may identify 'rules' which contribute to obesogenic environments. In other areas, such as marketing to children, school food, and taxes/levies, there may be opportunities for regulations to actively support obesity prevention. Legislation in other areas such as to reduce climate change may also contribute to obesity prevention ('stealth interventions'). A political willingness to use policy instruments to drive change will probably be an early hallmark of successful obesity prevention.

  18. PACSIN2 accelerates nephrin trafficking and is up-regulated in diabetic kidney disease

    PubMed Central

    Dumont, Vincent; Tolvanen, Tuomas A.; Kuusela, Sara; Wang, Hong; Nyman, Tuula A.; Lindfors, Sonja; Tienari, Jukka; Nisen, Harry; Suetsugu, Shiro; Plomann, Markus; Kawachi, Hiroshi; Lehtonen, Sanna

    2017-01-01

    Nephrin is a core component of podocyte (glomerular epithelial cell) slit diaphragm and is required for kidney ultrafiltration. Down-regulation or mislocalization of nephrin has been observed in diabetic kidney disease (DKD), characterized by albuminuria. Here, we investigate the role of protein kinase C and casein kinase 2 substrate in neurons 2 (PACSIN2), a regulator of endocytosis and recycling, in the trafficking of nephrin and development of DKD. We observe that PACSIN2 is up-regulated and nephrin mislocalized in podocytes of obese Zucker diabetic fatty (ZDF) rats that have altered renal function. In cultured podocytes, PACSIN2 and nephrin colocalize and interact. We show that nephrin is endocytosed in PACSIN2-positive membrane regions and that PACSIN2 overexpression increases both nephrin endocytosis and recycling. We identify rabenosyn-5, which is involved in early endosome maturation and endosomal sorting, as a novel interaction partner of PACSIN2. Interestingly, rabenosyn-5 expression is increased in podocytes in obese ZDF rats, and, in vitro, its overexpression enhances the association of PACSIN2 and nephrin. We also show that palmitate, which is elevated in diabetes, enhances this association. Collectively, PACSIN2 is up-regulated and nephrin is abnormally localized in podocytes of diabetic ZDF rats. In vitro, PACSIN2 enhances nephrin turnover apparently via a mechanism involving rabenosyn-5. The data suggest that elevated PACSIN2 expression accelerates nephrin trafficking and associates with albuminuria.—Dumont, V., Tolvanen, T. A., Kuusela, S., Wang, H., Nyman, T. A., Lindfors, S., Tienari, J., Nisen, H., Suetsugu, S., Plomann, M., Kawachi, H., Lehtonen, S. PACSIN2 accelerates nephrin trafficking and is up-regulated in diabetic kidney disease. PMID:28550045

  19. Regulation of food intake and obesity.

    PubMed

    Mayer, J; Thomas, D W

    1967-04-21

    This is not the place to consider the medical significance of obesity in terms of conditions such as heart disease and hypertension, diabetes, and arthritis. These very complex interrelationships have been dealt with elsewhere (69). We hope that enough evidence has been presented to demonstrate that energy balance is normally maintained by a precise and reliable physiologic mechanism, and that the energy surplus represented by obesity may reflect direct failure of this mechanism or some combination from a variety of neurological, endocrine, enzymatic, and psychological disorders. Environmental conditions as well as genetic and traumatic factors may contribute to the development of obesity. If increasing mechanization brings tus below the level of energy expenditure at which food intake is properly regulated, appropriate habits of exercise will have to be established and maintained.

  20. A DRD4 Gene by Maternal Sensitivity Interaction Predicts Risk for Overweight or Obesity in Two Independent Cohorts of Preschool Children

    ERIC Educational Resources Information Center

    Levitan, Robert D.; Jansen, Pauline; Wendland, Barbara; Tiemeier, Henning; Jaddoe, Vincent W.; Silveira, Patricia P.; Kennedy, James L.; Atkinson, Leslie; Fleming, Alison; Sokolowski, Marla; Gaudreau, Helene; Steiner, Meir; Dubé, Laurette; Hamilton, Jill; Moss, Ellen; Wazana, Ashley; Meaney, Michael

    2017-01-01

    Background: Recent evidence suggests that early exposure to low maternal sensitivity is a risk factor for obesity in children and adolescents. A separate line of study shows that the seven-repeat (7R) allele of the dopamine-4 receptor gene (DRD4) increases susceptibility to environmental factors including maternal sensitivity. The current study…

  1. Maternal obesity increases the risk of metabolic disease and impacts renal health in offspring

    PubMed Central

    Glastras, Sarah J.; Chen, Hui; Pollock, Carol A.; Saad, Sonia

    2018-01-01

    Obesity, together with insulin resistance, promotes multiple metabolic abnormalities and is strongly associated with an increased risk of chronic disease including type 2 diabetes (T2D), hypertension, cardiovascular disease, non-alcoholic fatty liver disease (NAFLD) and chronic kidney disease (CKD). The incidence of obesity continues to rise in astronomical proportions throughout the world and affects all the different stages of the lifespan. Importantly, the proportion of women of reproductive age who are overweight or obese is increasing at an alarming rate and has potential ramifications for offspring health and disease risk. Evidence suggests a strong link between the intrauterine environment and disease programming. The current review will describe the importance of the intrauterine environment in the development of metabolic disease, including kidney disease. It will detail the known mechanisms of fetal programming, including the role of epigenetic modulation. The evidence for the role of maternal obesity in the developmental programming of CKD is derived mostly from our rodent models which will be described. The clinical implication of such findings will also be discussed. PMID:29483369

  2. Maternal ratings of child health and child obesity, variations by mother's race/ethnicity and nativity.

    PubMed

    Baker, Elizabeth H; Altman, Claire E

    2015-05-01

    We examined whether indicators of child health, focusing on obesity, are associated with maternal ratings of child health (MRCH) and its variation by mother's ethnicity/nativity, focusing on Hispanics. The early childhood longitudinal study, kindergarten cohort kindergarten-eighth grade waves (n = 48,814) and nested general linear mixed modeling are used to examine excellent MRCH. The only indicator of child health that varies by mother's ethnicity/nativity for MRCH is child obesity. Child obesity did not influence MRCH for foreign-born Hispanic mothers, especially among less acculturated mothers, though significant differences among immigrants by acculturation were not found. However, among native-born white, black, and Hispanic mothers child obesity was associated with a lower likelihood of excellent MRCH even after controls for socioeconomic characteristics, family characteristics, and other indicators of child health are included. MRCH reflect not only child's actual health, but also the mother's perception of what contributes to poor child health. Our findings suggest that less acculturated foreign-born Hispanic mothers are less likely to associate child obesity with poor child health. Cultural orientations that prefer heavier children or are unlikely to associate child obesity with poor child health may contribute to the higher levels of obesity found among their children.

  3. MATERNAL TRAUMA AFFECTS PRENATAL MENTAL HEALTH AND INFANT STRESS REGULATION AMONG PALESTINIAN DYADS.

    PubMed

    Isosävi, Sanna; Diab, Safwat Y; Kangaslampi, Samuli; Qouta, Samir; Kankaanpää, Saija; Puura, Kaija; Punamäki, Raija-Leena

    2017-09-01

    We examined how diverse and cumulated traumatic experiences predicted maternal prenatal mental health and infant stress regulation in war conditions and whether maternal mental health mediated the association between trauma and infant stress regulation. Participants were 511 Palestinian mothers from the Gaza Strip who reported exposure to current war trauma (WT), past childhood emotional (CEA) and physical abuse, socioeconomic status (SES), prenatal mental health problems (posttraumatic stress disorder and depression symptoms), and perceived stress during their secondtrimester of pregnancy as well as infant stress regulation at 4 months. While all trauma types were associated with high levels of prenatal symptoms, CEA had the most wide-ranging effects and was uniquely associated with depression symptoms. Concerning infant stress regulation, mothers' CEA predicted negative affectivity, but only among mothers with low WT. Against hypothesis, the effects of maternal trauma on infant stress regulation were not mediated by mental health symptoms. Mothers' higher SES was associated with better infant stress regulation whereas infant prematurity and male sex predisposed for difficulties. Our findings suggest that maternal childhood abuse, especially CEA, should be a central treatment target among war-exposed families. Cumulated psychosocial stressors might increase the risk for transgenerational problems. © 2017 Michigan Association for Infant Mental Health.

  4. Maternal gestational smoking, diabetes, alcohol drinking, pre-pregnancy obesity and the risk of cryptorchidism: a systematic review and meta-analysis of observational studies.

    PubMed

    Zhang, Lin; Wang, Xing-Huan; Zheng, Xin-Min; Liu, Tong-Zu; Zhang, Wei-Bin; Zheng, Hang; Chen, Mi-Feng

    2015-01-01

    Maternal gestational smoking, diabetes, alcohol drinking, and pre-pregnancy obesity are thought to increase the risk of cryptorchidism in newborn males, but the evidence is inconsistent. We conducted a systematic review and meta-analysis of studies on the association between maternal gestational smoking, diabetes, alcohol drinking, and pre-pregnancy obesity and the risk of cryptorchidism. Articles were retrieved by searching PubMed and ScienceDirect, and the meta-analysis was conducted using Stata/SE 12.0 software. Sensitivity analysis was used to evaluate the influence of confounding variables. We selected 32 articles, including 12 case-control, five nested case-control, and 15 cohort studies. The meta-analysis showed that maternal smoking (OR = 1.17, 95% CI: 1.11-1.23) or diabetes (OR = 1.21, 95%CI: 1.00-1.46) during pregnancy were associated with increased risk of cryptorchidism. Overall, the association between maternal alcohol drinking (OR = 0.97, 95% CI: 0.87-1.07), pre-pregnancy body mass index (OR = 1.02, 95% CI: 0.95-1.09) and risk of cryptorchidism were not statistically significant. Additional analysis showed reduced risk (OR = 0.89, 95% CI: 0.82-0.96) of cryptorchidism with moderate alcohol drinking during pregnancy. No dose-response relationship was observed for increments in body mass index in the risk of cryptorchidism. Sensitivity analysis revealed an unstable result for the association between maternal diabetes, alcohol drinking and cryptorchidism. Moderate heterogeneity was detected in studies of the effect of maternal alcohol drinking and diabetes. No publication bias was detected. Maternal gestational smoking, but not maternal pre-pregnancy overweight or obesity, was associated with increased cryptorchidism risk in the offspring. Moderate alcohol drinking may reduce the risk of cryptorchidism while gestational diabetes may be a risk factor, but further studies are needed to verify this.

  5. Maternal correlates of maternal child feeding practices: a systematic review.

    PubMed

    McPhie, Skye; Skouteris, Helen; Daniels, Lynne; Jansen, Elena

    2014-01-01

    Establishing healthy eating habits early in life is one important strategy to combat childhood obesity. Given that early maternal child feeding practices have been linked to child food intake and weight, identifying the maternal correlates of maternal child feeding practices is important in order to understand the determinants of childhood obesity; this was the overall aim of the current review. Academic databases were searched for studies examining the relationship between maternal child feeding practices and parenting, personal characteristics and psychopathology of mothers with preschoolers. Papers were limited to those published in English, between January 2000 and June 2012. Only studies with mothers of normally developing children between the ages of 2 and 6 years were included. There were no restrictions regarding the inclusion of maternal nationality or socioeconomic status (SES). Seventeen eligible studies were sourced. Information on the aim, sample, measures and findings of these was summarised into tables. The findings of this review support a relationship between maternal controlling parenting, general and eating psychopathology, and SES and maternal child feeding practices. The main methodological issues of the studies reviewed included inconsistency in measures of maternal variables across studies and cross-sectional designs. We conclude that the maternal correlates associated with maternal child feeding practices are complex, and the pathways by which maternal correlates impact these feeding practices require further investigation. © 2012 John Wiley & Sons Ltd.

  6. Maternal obesity characterized by gestational diabetes increases the susceptibility of rat offspring to hepatic steatosis via a disrupted liver metabolome

    PubMed Central

    Pereira, Troy J; Fonseca, Mario A; Campbell, Kristyn E; Moyce, Brittany L; Cole, Laura K; Hatch, Grant M; Doucette, Christine A; Klein, Julianne; Aliani, Michel; Dolinsky, Vernon W

    2015-01-01

    Maternal obesity is associated with a high risk for gestational diabetes mellitus (GDM), which is a common complication of pregnancy. The influence of maternal obesity and GDM on the metabolic health of the offspring is poorly understood. We hypothesize that GDM associated with maternal obesity will cause obesity, insulin resistance and hepatic steatosis in the offspring. Female Sprague-Dawley rats were fed a high-fat (45%) and sucrose (HFS) diet to cause maternal obesity and GDM. Lean control pregnant rats received low-fat (LF; 10%) diets. To investigate the interaction between the prenatal environment and postnatal diets, rat offspring were assigned to LF or HFS diets for 12 weeks, and insulin sensitivity and hepatic steatosis were evaluated. Pregnant GDM dams exhibited excessive gestational weight gain, hyperinsulinaemia and hyperglycaemia. Offspring of GDM dams gained more weight than the offspring of lean dams due to excess adiposity. The offspring of GDM dams also developed hepatic steatosis and insulin resistance. The postnatal consumption of a LF diet did not protect offspring of GDM dams against these metabolic disorders. Analysis of the hepatic metabolome revealed increased diacylglycerol and reduced phosphatidylethanolamine in the offspring of GDM dams compared to offspring of lean dams. Consistent with altered lipid metabolism, the expression of CTP:phosphoethanolamine cytidylyltransferase, and peroxisomal proliferator activated receptor-α mRNA was reduced in the livers of GDM offspring. GDM exposure programs gene expression and hepatic metabolite levels and drives the development of hepatic steatosis and insulin resistance in young adult rat offspring. Key points Gestational diabetes mellitus is a common complication of pregnancy, but its effects on the offspring are poorly understood. We developed a rat model of diet-induced gestational diabetes mellitus that recapitulates many of the clinical features of the disease, including excessive gestational

  7. Controlling the Messenger: Regulated Translation of Maternal mRNAs in Xenopus laevis Development

    PubMed Central

    Fox, Catherine A.; Dowdle, Megan E.; Blaser, Susanne Imboden; Chung, Andy; Park, Sookhee

    2017-01-01

    The selective translation of maternal mRNAs encoding cell-fate determinants drives the earliest decisions of embryogenesis that establish the vertebrate body plan. This chapter will discuss studies in Xenopus laevis that provide insights into mechanisms underlying this translational control. Xenopus has been a powerful model organism for many discoveries relevant to the translational control of maternal mRNAs because of the large size of its oocytes and eggs that allow for microinjection of molecules and the relative ease of manipulating the oocyte to egg transition (maturation) and fertilization in culture. Consequently, many key studies have focused on the expression of maternal mRNAs during the oocyte to egg transition (the meiotic cell cycle) and the rapid cell divisions immediately following fertilization. This research has made seminal contributions to our understanding of translational regulatory mechanisms, but while some of the mRNAs under consideration at these stages encode cell-fate determinants, many encode cell cycle regulatory proteins that drive these early cell cycles. In contrast, while maternal mRNAs encoding key developmental (i.e., cell-fate) regulators that function after the first cleavage stages may exploit aspects of these foundational mechanisms, studies reveal that these mRNAs must also rely on distinct and, as of yet, incompletely understood mechanisms. These findings are logical because the functions of such developmental regulatory proteins have requirements distinct from cell cycle regulators, including becoming relevant only after fertilization and then only in specific cells of the embryo. Indeed, key maternal cell-fate determinants must be made available in exquisitely precise amounts (usually low), only at specific times and in specific cells during embryogenesis. To provide an appreciation for the regulation of maternal cell-fate determinant expression, an overview of the maternal phase of Xenopus embryogenesis will be presented

  8. Oxytocin in the medial prefrontal cortex regulates maternal care, maternal aggression and anxiety during the postpartum period

    PubMed Central

    Sabihi, Sara; Dong, Shirley M.; Durosko, Nicole E.; Leuner, Benedetta

    2014-01-01

    The neuropeptide oxytocin (OT) acts on a widespread network of brain regions to regulate numerous behavioral adaptations during the postpartum period including maternal care, maternal aggression, and anxiety. In the present study, we examined whether this network also includes the medial prefrontal cortex (mPFC). We found that bilateral infusion of a highly specific oxytocin receptor antagonist (OTR-A) into the prelimbic (PL) region of the mPFC increased anxiety-like behavior in postpartum, but not virgin, females. In addition, OTR blockade in the postpartum mPFC impaired maternal care behaviors and enhanced maternal aggression. Overall, these results suggest that OT in the mPFC modulates maternal care and aggression, as well as anxiety-like behavior, during the postpartum period. Although the relationship among these behaviors is complicated and further investigation is required to refine our understanding of OT actions in the maternal mPFC, these data nonetheless provide new insights into neural circuitry of OT-mediated postpartum behaviors. PMID:25147513

  9. Alkbh4 and Atrn Act Maternally to Regulate Zebrafish Epiboly

    PubMed Central

    Sun, Qingrui; Liu, Xingfeng; Gong, Bo; Wu, Di; Meng, Anming; Jia, Shunji

    2017-01-01

    During embryonic gastrulation, coordinated cell movements occur to bring cells to their correct position. Among them, epiboly produces the first distinct morphological changes, which is essential for the early development of zebrafish. Despite its fundamental importance, little is known to understand the underlying molecular mechanisms. By generating maternal mutant lines with CRISPR/Cas9 technology and using morpholino knockdown strategy, we showed that maternal Alkbh4 depletion leads to severe epiboly defects in zebrafish. Immunofluorescence assays revealed that Alkbh4 promotes zebrafish embryonic epiboly through regulating actomyosin contractile ring formation, which is composed of Actin and non-muscular myosin II (NMII). To further investigate this process, yeast two hybridization assay was performed and Atrn was identified as a binding partner of Alkbh4. Combining with the functional results of Alkbh4, we found that maternal Atrn plays a similar role in zebrafish embryonic morphogenesis by regulating actomyosin formation. On the molecular level, our data revealed that Atrn prefers to interact with the active form of Alkbh4 and functions together with it to regulate the demethylation of Actin, the actomyosin formation, and subsequently the embryonic epiboly. PMID:28924386

  10. Improving Self-Regulation for Obesity Prevention in Head Start: A Randomized Controlled Trial.

    PubMed

    Lumeng, Julie C; Miller, Alison L; Horodynski, Mildred A; Brophy-Herb, Holly E; Contreras, Dawn; Lee, Hannah; Sturza, Julie; Kaciroti, Niko; Peterson, Karen E

    2017-05-01

    To determine the effect of an intervention to improve emotional and behavioral self-regulation in combination with an obesity-prevention program on the prevalence of obesity and obesity-related behaviors in preschoolers. This was a cluster-randomized intervention trial in Head Start (HS) classrooms conducted in each of 4 academic years from 2011 to 2015. Participants (697 children; 49% boys; mean age: 4.1 ± 0.5 years; 48% white, 30% African American, 12% Hispanic) were randomly assigned by classroom to 1 of 3 intervention arms: (1) HS + Preschool Obesity Prevention Series (POPS) + Incredible Years Series (IYS) (HS enhanced by the POPS [program targeting evidence-based obesity-prevention behaviors] and the IYS [program to improve children's self-regulation]), (2) HS+POPS, or (3) HS. Primary outcomes were changes in prevalence of obesity, overweight/obesity, BMI z score, and teacher-reported child emotional and behavioral self-regulation; secondary outcomes were dietary intake, outdoor play, screen time, and parent nutrition knowledge and nutrition self-efficacy. HS+POPS+IYS improved teacher-reported self-regulation compared with HS+POPS ( P < .001) and HS ( P < .001), but there was no effect on the prevalence of obesity (16.4% preintervention to 14.3% postintervention in HS+POPS+IYS versus 17.3% to 14.4% in HS+POPS [ P = .54] versus 12.2% to 13.0% in HS [ P = .33]). There was no effect of HS+POPS compared with HS alone ( P = .16). There was no effect on other outcomes except for sugar-sweetened beverage intake (HS+POPS+IYS resulted in a greater decline than HS; P = .005). An intervention for parents and children to improve HS preschoolers' emotional and behavioral self-regulation in combination with an obesity-prevention curriculum did not reduce obesity prevalence or most obesity-related behaviors. Copyright © 2017 by the American Academy of Pediatrics.

  11. Obesity, voracity, and short stature: the impact of glutamate on the regulation of appetite.

    PubMed

    Hermanussen, M; García, A P; Sunder, M; Voigt, M; Salazar, V; Tresguerres, J A F

    2006-01-01

    World-wide obesity has risen to alarming levels. We present experimental support for a new and very challenging hypothesis linking obesity, voracity, and growth hormone (GH) deficiency, to the consumption of elevated amounts of the amino-acid glutamate (GLU). Supraphysiological doses of GLU are toxic for neuronal cells. Human data were obtained from 807,592 German conscripts born between 1974 and 1978, and from 1,432,368 women of the German birth statistics (deutsche Perinatalerhebung) 1995-1997. The effects of orally administered monosodium glutamate (MSG) were investigated in 30 pregnant Wistar rats and their offspring. Pregnant animals either received no extra MSG, or 2.5 g MSG, or 5 g MSG per day, up to the end of the weaning period. In all, 2.5 g, respectively 5 g, MSG accounted for some 10%, respectively 20%, of dry weight of the average daily food ration. After weaning, MSG feeding was continued in the offspring. Morbid obesity associates with short stature. Average stature of conscripts progressively declines when body mass index increases above 38 kg/m2. Also morbidly obese young women are shorter than average though to a lesser extent than conscripts. Oral administration of MSG to pregnant rats affects birth weight of the offspring. Maternal feeding with 5 g MSG per day results in severe birth weight reduction (P<0.01). Weight increments remain subnormal when MSG feeding to the mothers is maintained during weaning (P < 0.01). GH serum levels are affected in animals that received MSG during prenatal life via maternal feeding. Animals that are kept on high MSG diet (5 g MSG per day) continue to show serum GH levels that are as low or even lower than those of MSG injected animals (P < 0.05), both at day 30 and at day 90 of life. Animals that were kept on medium MSG diet (2.5 g MSG per day) showed low serum GH levels at day 30 of life (P < 0.01), but seemed to partially recover before day 90. Almost identical results were observed in IGF-1 serum levels. Oral

  12. Obesity and Sex Interact in the Regulation of Alzheimer’s Disease

    PubMed Central

    Moser, V. Alexandra; Pike, Christian J.

    2015-01-01

    Alzheimer’s disease (AD) is a progressive neurodegenerative disorder, for which a number of genetic, environmental, and lifestyle risk factors have been identified. A significant modifiable risk factor is obesity in mid-life. Interestingly, both obesity and AD exhibit sex differences and are regulated by sex steroid hormones. Accumulating evidence suggests interactions between obesity and sex in regulation of AD risk, although the pathways underlying this relationship are unclear. Inflammation and the E4 allele of apolipoprotein E have been identified as independent risk factors for AD and both interact with obesity and sex steroid hormones. We review the individual and cooperative effects of obesity and sex on development of AD and examine the potential contributions of apolipoprotein E, inflammation, and their interactions to this relationship. PMID:26708713

  13. Breast-Feeding and Risk for Childhood Obesity

    PubMed Central

    Mayer-Davis, Elizabeth J.; Rifas-Shiman, Sheryl L.; Zhou, Li; Hu, Frank B.; Colditz, Graham A.; Gillman, Matthew W.

    2011-01-01

    OBJECTIVE We sought to evaluate whether maternal diabetes or weight status attenuates a previously reported beneficial effect of breast-feeding on childhood obesity. RESEARCH DESIGN AND METHODS Growing Up Today Study (GUTS) participants were offspring of women who participated in the Nurses’ Health Study II. In the present study, 15,253 girls and boys (aged 9–14 years in 1996) were included. Maternal diabetes and weight status and infant feeding were obtained by maternal self-report. We defined maternal overweight as BMI ≥25 kg/m2. Childhood obesity, from self-reported height and weight, was based on the Centers for Disease Control and Prevention definitions as normal, at risk for overweight, or overweight. Maternal status categories were nondiabetes/normal weight, nondiabetes/overweight, or diabetes. Logistic regression models used generalized estimating equations to account for nonindependence between siblings. RESULTS For all subjects combined, breast-feeding was associated with reduced overweight (compared with normal weight) in childhood. Compared with exclusive use of formula, the odds ratio (OR) for exclusive breast-feeding was 0.66 (95% CI 0.53– 0.82), adjusted for age, sex, and Tanner stage. Results did not differ according to maternal status (nondiabetes/normal weight OR 0.73 [95% CI 0.49 –1.09]; nondiabetes/overweight 0.75 [0.57– 0.99]; and diabetes 0.62 [0.24 –1.60]). Further adjustment for potential confounders attenuated results, but results remained consistent across strata of maternal status (P value for interaction was 0.50). CONCLUSIONS Breast-feeding was inversely associated with childhood obesity regardless of maternal diabetes status or weight status. These data provide support for all mothers to breast-feed their infants to reduce the risk for childhood overweight. PMID:17003298

  14. Saponins from stems and leaves of Panax ginseng prevent obesity via regulating thermogenesis, lipogenesis and lipolysis in high-fat diet-induced obese C57BL/6 mice.

    PubMed

    Chen, Guilin; Li, Haijun; Zhao, Yan; Zhu, Hongyan; Cai, Enbo; Gao, Yugang; Liu, Shuangli; Yang, He; Zhang, Lianxue

    2017-08-01

    In this study, high-fat diet (HFD)-induced obesity in mouse model was used to evaluate the dietary effect of saponins from stems and leaves of Panax ginseng (SLG), and to explore its mechanism of action in producing anti-obesity effects. The results indicate that SLG showed significant anti-obesity effects in diet-induced obese mice, represented by decreased serum levels of free fatty acids (FFA), total cholesterol (TC), triglycerides (TG), low-density lipoprotein (LDL)-cholesterol, glucose, leptin and insulin, as well as a reduction in overall body and liver weight, epididymal adipose tissue weight, and food efficiency, and inhibition of abnormal increases in acyl carnitine levels normally caused by an HFD. Additionally, the down-regulated expression of PPARγ, FAS, CD36, FATP2 and up-regulated expression of CPT-1, UCP-2, PPARα, HSL, and ATGL in liver tissue was induced by SLG. In addition, the SLG groups showed decreased PPARγ, aP2 and leptin mRNA levels and increased expression of PPARα, PGC-1α, UCP-1 and UCP-3 genes in adipose tissues, compared with the HFD group. In short, SLG may play a key role in producing anti-obesity effects in mice fed an HFD, and its mechanism may be related to regulation of thermogenesis, lipogenesis and lipolysis. Copyright © 2017 Elsevier Ltd. All rights reserved.

  15. Increased deficits in emotion recognition and regulation in children and adolescents with exogenous obesity.

    PubMed

    Percinel, Ipek; Ozbaran, Burcu; Kose, Sezen; Simsek, Damla Goksen; Darcan, Sukran

    2018-03-01

    In this study we aimed to evaluate emotion recognition and emotion regulation skills of children with exogenous obesity between the ages of 11 and 18 years and compare them with healthy controls. The Schedule for Affective Disorders and Schizophrenia for School Aged Children was used for psychiatric evaluations. Emotion recognition skills were evaluated using Faces Test and Reading the Mind in the Eyes Test. The Difficulties in Emotions Regulation Scale was used for evaluating skills of emotion regulation. Children with obesity had lower scores on Faces Test and Reading the Mind in the Eyes Test, and experienced greater difficulty in emotional regulation skills. Improved understanding of emotional recognition and emotion regulation in young people with obesity may improve their social adaptation and help in the treatment of their disorder. To the best of our knowledge, this is the first study to evaluate both emotional recognition and emotion regulation functions in obese children and obese adolescents between 11 and 18 years of age.

  16. Pre-pregnancy obesity and maternal nutritional biomarker status during pregnancy: a factor analysis.

    PubMed

    Tomedi, Laura E; Chang, Chung-Chou H; Newby, P K; Evans, Rhobert W; Luther, James F; Wisner, Katherine L; Bodnar, Lisa M

    2013-08-01

    Pre-pregnancy obesity has been associated with adverse birth outcomes. Poor essential fatty acid (EFA) and micronutrient status during pregnancy may contribute to these associations. We assessed the associations between pre-pregnancy BMI and nutritional patterns of maternal micronutrient and EFA status during mid-pregnancy. A cross-sectional analysis from a prospective cohort study. Women provided non-fasting blood samples at ≥ 20 weeks’ gestation that were assayed for red cell EFA; plasma folate, homocysteine and ascorbic acid; and serum retinol, 25-hydroxyvitamin D, a-tocopherol, soluble transferrin receptors and carotenoids. These nutritional biomarkers were employed in a factor analysis and three patterns were derived: EFA, Micronutrients and Carotenoids. The Antidepressant Use During Pregnancy Study, Pittsburgh, PA, USA. Pregnant women (n 129). After adjustment for parity, race/ethnicity and age, obese pregnant women were 3.0 (95% CI 1.1, 7.7) times more likely to be in the lowest tertile of the EFA pattern and 4.5 (95% CI 1.7, 12.3) times more likely to be in the lowest tertile of the Carotenoid pattern compared with their lean counterparts. We found no association between pre-pregnancy obesity and the Micronutrient pattern after confounder adjustment. Our results suggest that obese pregnant women have diminished EFA and carotenoid concentrations.

  17. Maternal Regulation of Estrogen Receptor α Methylation

    PubMed Central

    Champagne, Frances A.; Curley, James P.

    2008-01-01

    Summary Advances in molecular biology have provided tools for studying the epigenetic factors which modulate gene expression. DNA methylation is an epigenetic modification which can have sustained effects on transcription and is associated with long-term gene silencing. In this review, we focus on the regulation of estrogen receptor alpha (ERα) expression by hormonal and environmental cues, the consequences of these cues for female maternal and sexual behavior and recent studies which explore the role of DNA methylation in mediating these developmental effects, with particular focus on the mediating role of maternal care. The methylation status of ERα has implications for reproductive behavior, cancer susceptibility and recovery from ischemic injury suggesting an epigenetic basis for risk and resilience across the life span. PMID:18644464

  18. Teratology Public Affairs Committee position paper: maternal obesity and pregnancy.

    PubMed

    Scialli, Anthony R

    2006-02-01

    Compared to normal-weight women, obese women have an increased risk of infertility and pregnancy complications. The most consistently described pregnancy complications are hypertensive disorders, gestational diabetes mellitus, thromboembolic events, and cesarean section. Fetal and neonatal complications may include congenital malformations, macrosomia, and shoulder dystocia. The literature suggests that women with a body mass index (BMI) >or=30 have approximately double the risk of having a child with a neural tube defect (NTD) compared to normal-weight women, and the increased risk associated with higher maternal body weight does not appear to be modified by folic acid supplementation. The Public Affairs Committee of the Teratology Society supports the public health initiatives identified by the U.S. Food and Drug Administration in 2004 and the research initiatives identified by the National Institutes of Health in 2004. The Public Affairs Committee recommends that clinicians counsel women about appropriate caloric intake and exercise and that health-care providers educate parents about appropriate childhood nutrition. Breast-feeding should be encouraged based on evidence of a protective effect against childhood obesity, as well as other health advantages. Birth Defects Research (Part A), 2006. (c) 2006 Wiley-Liss, Inc.

  19. Maternal obesity and malnourishment exacerbate perinatal oxidative stress resulting in diabetogenic programming in F1 offspring.

    PubMed

    Saad, M I; Abdelkhalek, T M; Haiba, M M; Saleh, M M; Hanafi, M Y; Tawfik, S H; Kamel, M A

    2016-06-01

    The effect of in-utero environment on fetal health and survival is long-lasting, and this is known as the fetal origin hypothesis. The oxidative stress state during gestation could play a pivotal role in fetal programming and development of diseases such as diabetes. In this study, we investigated the effect of intra-uterine obesity and malnutrition on oxidative stress markers in pancreatic and peripheral tissues of F1 offspring both prenatally and postnatally. Furthermore, the effect of postnatal diet on oxidative stress profile was evaluated. The results indicated that intra-uterine obesity and malnourishment significantly increased oxidative stress in F1 offspring. Moreover, the programming effect of obesity was more pronounced and protracted than malnutrition. The obesity-induced programming of offspring tissues was independent of high-caloric environment that the offspring endured; however, high-caloric diet potentiated its effect. In addition, pancreas and liver were the most affected tissues by fetal reprogramming both prenatally and postnatally. In conclusion, maternal obesity and malnutrition-induced oxidative stress could predispose offspring to insulin resistance and diabetes.

  20. Endoplasmic reticulum chaperone GRP78 regulates macrophage function and insulin resistance in diet-induced obesity.

    PubMed

    Kim, Jong Hun; Lee, Eunjung; Friedline, Randall H; Suk, Sujin; Jung, Dae Young; Dagdeviren, Sezin; Hu, Xiaodi; Inashima, Kunikazu; Noh, Hye Lim; Kwon, Jung Yeon; Nambu, Aya; Huh, Jun R; Han, Myoung Sook; Davis, Roger J; Lee, Amy S; Lee, Ki Won; Kim, Jason K

    2018-04-01

    Obesity-mediated inflammation is a major cause of insulin resistance, and macrophages play an important role in this process. The 78-kDa glucose-regulated protein (GRP78) is a major endoplasmic reticulum chaperone that modulates unfolded protein response (UPR), and mice with GRP78 heterozygosity were resistant to diet-induced obesity. Here, we show that mice with macrophage-selective ablation of GRP78 (Lyz- GRP78 -/- ) are protected from skeletal muscle insulin resistance without changes in obesity compared with wild-type mice after 9 wk of high-fat diet. GRP78-deficient macrophages demonstrated adapted UPR with up-regulation of activating transcription factor (ATF)-4 and M2-polarization markers. Diet-induced adipose tissue inflammation was reduced, and bone marrow-derived macrophages from Lyz- GRP78 -/- mice demonstrated a selective increase in IL-6 expression. Serum IL-13 levels were elevated by >4-fold in Lyz- GRP78 -/- mice, and IL-6 stimulated the myocyte expression of IL-13 and IL-13 receptor. Lastly, recombinant IL-13 acutely increased glucose metabolism in Lyz- GRP78 -/- mice. Taken together, our data indicate that GRP78 deficiency activates UPR by increasing ATF-4, and promotes M2-polarization of macrophages with a selective increase in IL-6 secretion. Macrophage-derived IL-6 stimulates the myocyte expression of IL-13 and regulates muscle glucose metabolism in a paracrine manner. Thus, our findings identify a novel crosstalk between macrophages and skeletal muscle in the modulation of obesity-mediated insulin resistance.-Kim, J. H., Lee, E., Friedline, R. H., Suk, S., Jung, D. Y., Dagdeviren, S., Hu, X., Inashima, K., Noh, H. L., Kwon, J. Y., Nambu, A., Huh, J. R., Han, M. S., Davis, R. J., Lee, A. S., Lee, K. W., Kim, J. K. Endoplasmic reticulum chaperone GRP78 regulates macrophage function and insulin resistance in diet-induced obesity.

  1. Maternal Weight Gain in Pregnancy and Risk of Obesity among Offspring: A Systematic Review

    PubMed Central

    Lau, Erica Y.; Liu, Junxiu; McDonald, Samantha M.

    2014-01-01

    Objectives. To systematically review the evidence from prospective and retrospective cohort studies on the association between gestational weight gain (GWG) and offspring's body weight. Methods. Electronic databases PubMed, Web of Science, CINAHL, and Academic Search Premiere were searched from inception through March 18, 2013. Included studies (n = 23) were English articles that examined the independent associations of GWG with body mass index (BMI) and/or overweight status in the offspring aged 2 to 18.9 years. Two authors independently extracted the data and assessed methodological quality of the included studies. Results. Evidence from cohort studies supports that total GWG and exceeding the Institute of Medicine maternal weight gain recommendation were associated with higher BMI z-score and elevated risk of overweight or obesity in offspring. The evidence of high rate of GWG during early- and mid-pregnancy is suggestive. Additionally, the evidence on inadequate GWG and net GWG in relation to body weight outcomes in offspring is insufficient to draw conclusions. Conclusions. These findings suggest that GWG is a potential risk factor for childhood obesity. However, findings should be interpreted with caution due to measurement issues of GWG and potential confounding effects of shared familial characteristics (i.e., genetics and maternal and child's lifestyle factors). PMID:25371815

  2. The Role of Placental Nutrient Sensing in Maternal-Fetal Resource Allocation1

    PubMed Central

    Díaz, Paula; Powell, Theresa L.; Jansson, Thomas

    2014-01-01

    ABSTRACT The placenta mediates maternal-fetal exchange and has historically been regarded as a passive conduit for nutrients. However, emerging evidence suggests that the placenta actively responds to nutritional and metabolic signals from the mother and the fetus. We propose that the placenta integrates a multitude of maternal and fetal nutritional cues with information from intrinsic nutrient-sensing signaling pathways to match fetal demand with maternal supply by regulating maternal physiology, placental growth, and nutrient transport. This process, which we have called placental nutrient sensing, ensures optimal allocation of resources between the mother and the fetus to maximize the chances for propagation of parental genes without jeopardizing maternal health. We suggest that these mechanisms have evolved because of the evolutionary pressures of maternal undernutrition, which result in decreased placental growth and down-regulation of nutrient transporters, thereby limiting fetal growth to ensure maternal survival. These regulatory loops may also function in response to maternal overnutrition, leading to increased placental growth and nutrient transport in cases of maternal obesity or gestational diabetes. Thus, placental nutrient sensing modulates maternal-fetal resource allocation to increase the likelihood of reproductive success. This model implies that the placenta plays a critical role in mediating fetal programming and determining lifelong health. PMID:25122064

  3. Obesity, fast food manufacture, and regulation: revisiting opportunities for reform.

    PubMed

    Ahmed, Haitham M

    2009-01-01

    Regulations have historically been able to shape public behavior in various ways. As poor dietary practices and obesity continue to pose major health and economic threats to society, attention will continue to be directed towards the ethical and legal responsibilities of fast food manufacturers as potential contributors to these problems. In light of these considerations, several opportunities emerge that may impact dietary behavior and obesity through regulation of the fast food industry. This article addresses the health consequences of fast food consumption, as well as the historical and legal contexts of fast food regulation in the United States.

  4. The interplay of maternal sensitivity and toddler engagement of mother in predicting self-regulation.

    PubMed

    Ispa, Jean M; Su-Russell, Chang; Palermo, Francisco; Carlo, Gustavo

    2017-03-01

    Using data from the Early Head Start Research and Evaluation Project, a cross-lag mediation model was tested to examine longitudinal relations among low-income mothers' sensitivity; toddlers' engagement of their mothers; and toddler's self-regulation at ages 1, 2, and 3 years (N = 2,958). Age 1 maternal sensitivity predicted self-regulation at ages 2 and 3 years, and age 2 engagement of mother mediated the relation between age 1 maternal sensitivity and age 3 self-regulation. Lagged relations from toddler self-regulation at ages 1 and 2 years to later maternal sensitivity were not significant, suggesting stronger influence from mother to toddler than vice versa. Model fit was similar regardless of child gender and depth of family poverty. (PsycINFO Database Record (c) 2017 APA, all rights reserved).

  5. Relationship Between Breastfeeding and Early Childhood Obesity: Results of a Prospective Longitudinal Study from Birth to 4 Years.

    PubMed

    Wallby, Thomas; Lagerberg, Dagmar; Magnusson, Margaretha

    To study a potential link between breastfeeding in infancy and obesity at age 4. A total of 30,508 infants born during 2002-2007 from the databases of the Preventive Child Health Services in two Swedish counties and from national registers were studied. The outcome variable was obesity at age 4. Analyses were conducted by logistic regression models using the methodology of generalized estimating equations. Analyses were adjusted for child sex and maternal anthropometric and sociodemographic variables. In unadjusted analyses, any breastfeeding up to 9 months was linked to successively decreasing odds ratios (ORs) for obesity at age 4 (ORs 0.78-0.33), however, not significantly for 1 week and 2 months of breastfeeding. In adjusted analyses, the same pattern remained statistically significant for breastfeeding for 4 (OR 0.51), 6 (OR 0.55), and 9 (OR 0.47) months. Child sex, maternal education, maternal body mass index, and maternal smoking additionally influenced child obesity. Breastfeeding duration for at least 4 months may contribute independently to a reduced risk for childhood obesity at 4 years.

  6. Microbial transmission from mothers with obesity or diabetes to infants: an innovative opportunity to interrupt a vicious cycle

    PubMed Central

    Soderborg, Taylor K.; Borengasser, Sarah J.; Barbour, Linda A.; Friedman, Jacob E.

    2016-01-01

    Maternal obesity and diabetes dramatically increase the long-term risk for obesity in the next generation, and pregnancy and lactation may be critical periods at which to aim primary prevention to break the obesity cycle. It is becoming increasingly clear that the gut microbiome in newborns and infants plays a significant role in gut health and therefore child development. Alteration of the early infant gut microbiome has been correlated with the development of childhood obesity and autoimmune conditions, including asthma, allergies and, more recently, type 1 diabetes. This is likely to be due to complex interactions between mode of delivery, antibiotic use, maternal diet, components of breastfeeding and a network of regulatory events involving both the innate and adaptive immune systems within the infant host. Each of these factors are critical for informing microbiome development and can affect immune signalling, toxin release and metabolic signals, including short-chain fatty acids and bile acids, that regulate appetite, metabolism and inflammation. In several randomised controlled trials, probiotics have been administered with the aim of targeting the microbiome during pregnancy to improve maternal and infant health but the findings have often been confounded by mode of delivery, antibiotic use, ethnicity, infant sex, maternal health and length of exposure. Understanding how nutritional exposure, including breast milk, affects the assembly and development of both maternal and infant microbial communities may help to identify targeted interventions during pregnancy and in infants born to mothers with obesity or diabetes to slow the transmission of obesity risk to the next generation. The aim of this review is to discuss influences on infant microbiota colonisation and the mechanism(s) underlying how alterations due to maternal obesity and diabetes may lead to increased risk of childhood obesity. PMID:26843076

  7. Microbial transmission from mothers with obesity or diabetes to infants: an innovative opportunity to interrupt a vicious cycle.

    PubMed

    Soderborg, Taylor K; Borengasser, Sarah J; Barbour, Linda A; Friedman, Jacob E

    2016-05-01

    Maternal obesity and diabetes dramatically increase the long-term risk for obesity in the next generation, and pregnancy and lactation may be critical periods at which to aim primary prevention to break the obesity cycle. It is becoming increasingly clear that the gut microbiome in newborns and infants plays a significant role in gut health and therefore child development. Alteration of the early infant gut microbiome has been correlated with the development of childhood obesity and autoimmune conditions, including asthma, allergies and, more recently, type 1 diabetes. This is likely to be due to complex interactions between mode of delivery, antibiotic use, maternal diet, components of breastfeeding and a network of regulatory events involving both the innate and adaptive immune systems within the infant host. Each of these factors are critical for informing microbiome development and can affect immune signalling, toxin release and metabolic signals, including short-chain fatty acids and bile acids, that regulate appetite, metabolism and inflammation. In several randomised controlled trials, probiotics have been administered with the aim of targeting the microbiome during pregnancy to improve maternal and infant health but the findings have often been confounded by mode of delivery, antibiotic use, ethnicity, infant sex, maternal health and length of exposure. Understanding how nutritional exposure, including breast milk, affects the assembly and development of both maternal and infant microbial communities may help to identify targeted interventions during pregnancy and in infants born to mothers with obesity or diabetes to slow the transmission of obesity risk to the next generation. The aim of this review is to discuss influences on infant microbiota colonisation and the mechanism(s) underlying how alterations due to maternal obesity and diabetes may lead to increased risk of childhood obesity.

  8. Effect of maternal behavior on regulation during feeding in healthy infants and infants with transposition

    PubMed Central

    Harrison, Tondi M.

    2010-01-01

    Objective To compare physiologic regulation and the effect of maternal sensitive caregiving during feeding on physiologic regulation in healthy infants and in infants with transposition of the great arteries (TGA). Design Descriptive, two group, repeated measures. Setting Three children's hospitals in the Midwest. Participants A convenience sample of 15 infants with TGA matched with 16 healthy infants. Methods Measures of physiologic regulation before, during, and after feeding and quality of maternal affect and behavior during feeding were collected post-operatively at two weeks and two months of age. Results At two weeks, infants with TGA demonstrated impaired physiologic regulation with feedings when compared with healthy infants. Healthy infants of more sensitive mothers were more likely to demonstrate a physiologically adaptive response during feeding. Maternal effect on physiologic regulation was not observed in infants with TGA. No differences between groups were found at two months. Conclusions For infants with TGA, effects of surgical recovery and limited contact with their mothers relative to healthy infants may have outweighed the supportive effect of maternal sensitivity during feeding in the early weeks of life. Further research is needed to identify ways of enhancing the regulatory effect of maternal behavior on infants with heart defects. PMID:19614886

  9. Children's Self-Regulation and School Achievement in Cultural Contexts: The Role of Maternal Restrictive Control

    PubMed Central

    Weis, Mirjam; Trommsdorff, Gisela; Muñoz, Lorena

    2016-01-01

    Self-regulation can be developed through parent-child interactions and has been related to developmental outcomes, e.g., such as educational achievement. This study examined cross-cultural differences and similarities in maternal restrictive control, self-regulation (i.e., behavior and emotion regulation) and school achievement and relations among these variables in Germany and Chile. Seventy-six German and 167 Chilean fourth graders, their mothers, and their teachers participated. Mothers and teachers rated children's behavior regulation with a subscale of the Strengths and Difficulties Questionnaire. Children reported their use of emotion regulation strategies on the Questionnaire for the Measurement of Stress and Coping. Mothers rated maternal restrictive control by answering the Parenting Practice Questionnaire. School achievement was assessed by grades for language and mathematics. Results showed higher behavior regulation of German children in comparison to Chilean children and a higher preference of restrictive parental control in Chilean mothers than in German mothers. Regression analyses revealed positive relations between children's behavior regulation and school achievement in Germany and in Chile. Further, in both cultural contexts, maternal restrictive control was related negatively to behavior regulation and positively to anger-oriented emotion regulation. In sum, the study showed the central function of behavior regulation for school achievement underlining negative relations of maternal restrictive control with children's self-regulation and school achievement in diverse cultural contexts. Culturally adapted interventions related to parenting practices to promote children's behavior regulation may assist in also promoting children's school achievement. PMID:27303318

  10. Severe maternal stress exposure due to bereavement before, during and after pregnancy and risk of overweight and obesity in young adult men: a Danish National Cohort Study.

    PubMed

    Hohwü, Lena; Li, Jiong; Olsen, Jørn; Sørensen, Thorkild I A; Obel, Carsten

    2014-01-01

    Perinatal stress may programme overweight and obesity. We examined whether maternal pre- and post-natal bereavement was associated with overweight and obesity in young men. A cohort study was conducted including 119,908 men born from 1976 to 1993 and examined for military service between 2006 and 2011. Among them, 4,813 conscripts were born to mothers bereaved by death of a close relative from 12 months preconception to birth of the child (exposed group). Median body mass index (BMI) and prevalence of overweight and obesity were estimated. Odds ratio of overweight (BMI≥25 kg/m2) and obesity (BMI≥30 kg/m2) were estimated by logistic regression analysis adjusted for maternal educational level. Median BMI was similar in the exposed and the unexposed group but the prevalence of overweight (33.3% versus 30.4%, p = 0.02) and obesity (9.8% versus 8.5%, p = 0.06) was higher in the exposed group. Conscripts exposed 6 to 0 months before conception and during pregnancy had a higher risk of overweight (odds ratio 1.15, 95% confidence interval (CI): 1.03; 1.27 and odds ratio 1.13, 95% CI: 1.03; 1.25, respectively). Conscripts born to mothers who experienced death of the child's biological father before child birth had a two-fold risk of obesity (odds ratio 2.00, 95% CI: 0.93; 4.31). There was no elevated risk in those who experienced maternal bereavement postnatally. Maternal bereavement during the prenatal period was associated with increased risk of overweight or obesity in a group of young male conscripts, and this may possibly be reflected to severe stress exposure early in life. However, not all associations were clear, and further studies are warranted.

  11. The childhood obesity epidemic as a result of nongenetic evolution: the maternal resources hypothesis.

    PubMed

    Archer, Edward

    2015-01-01

    Over the past century, socioenvironmental evolution (eg, reduced pathogenic load, decreased physical activity, and improved nutrition) led to cumulative increments in maternal energy resources (ie, body mass and adiposity) and decrements in energy expenditure and metabolic control. These decrements reduced the competition between maternal and fetal energy demands and increased the availability of energy substrates to the intrauterine milieu. This perturbation of mother-conceptus energy partitioning stimulated fetal pancreatic β-cell and adipocyte hyperplasia, thereby inducing an enduring competitive dominance of adipocytes over other tissues in the acquisition and sequestering of nutrient energy via intensified insulin secretion and hyperplastic adiposity. At menarche, the competitive dominance of adipocytes was further amplified via hormone-induced adipocyte hyperplasia and weight-induced decrements in physical activity. These metabolic and behavioral effects were propagated progressively when obese, inactive, metabolically compromised women produced progressively larger, more inactive, metabolically compromised children. Consequently, the evolution of human energy metabolism was markedly altered. This phenotypic evolution was exacerbated by increments in the use of cesarean sections, which allowed both the larger fetuses and the metabolically compromised mothers who produced them to survive and reproduce. Thus, natural selection was iatrogenically rendered artificial selection, and the frequency of obese, inactive, metabolically compromised phenotypes increased in the global population. By the late 20th century, a metabolic tipping point was reached at which the postprandial insulin response was so intense, the relative number of adipocytes so large, and inactivity so pervasive that the competitive dominance of adipocytes in the sequestering of nutrient energy was inevitable and obesity was unavoidable. Copyright © 2015 Mayo Foundation for Medical Education and

  12. Influence of maternal adiposity, preterm birth and birth weight centiles on early childhood obesity in an Indigenous Australian pregnancy-through-to-early-childhood cohort study.

    PubMed

    Pringle, K G; Lee, Y Q; Weatherall, L; Keogh, L; Diehm, C; Roberts, C T; Eades, S; Brown, A; Smith, R; Lumbers, E R; Brown, L J; Collins, C E; Rae, K M

    2018-05-16

    Childhood obesity rates are higher among Indigenous compared with non-Indigenous Australian children. It has been hypothesized that early-life influences beginning with the intrauterine environment predict the development of obesity in the offspring. The aim of this paper was to assess, in 227 mother-child dyads from the Gomeroi gaaynggal cohort, associations between prematurity, Gestation Related-Optimal Weight (GROW) centiles, maternal adiposity (percentage body fat, visceral fat area), maternal non-fasting plasma glucose levels (measured at mean gestational age of 23.1 weeks) and offspring BMI and adiposity (abdominal circumference, subscapular skinfold thickness) in early childhood (mean age 23.4 months). Maternal non-fasting plasma glucose concentrations were positively associated with infant birth weight (P=0.005) and GROW customized birth weight centiles (P=0.008). There was a significant association between maternal percentage body fat (P=0.02) and visceral fat area (P=0.00) with infant body weight in early childhood. Body mass index (BMI) in early childhood was significantly higher in offspring born preterm compared with those born at term (P=0.03). GROW customized birth weight centiles was significantly associated with body weight (P=0.01), BMI (P=0.007) and abdominal circumference (P=0.039) at early childhood. Our findings suggest that being born preterm, large for gestational age or exposed to an obesogenic intrauterine environment and higher maternal non-fasting plasma glucose concentrations are associated with increased obesity risk in early childhood. Future strategies should aim to reduce the prevalence of overweight/obesity in women of child-bearing age and emphasize the importance of optimal glycemia during pregnancy, particularly in Indigenous women.

  13. Maternal underweight and obesity and risk of orofacial clefts in a large international consortium of population-based studies.

    PubMed

    Kutbi, Hebah; Wehby, George L; Moreno Uribe, Lina M; Romitti, Paul A; Carmichael, Suzan; Shaw, Gary M; Olshan, Andrew F; DeRoo, Lisa; Rasmussen, Sonja A; Murray, Jeffrey C; Wilcox, Allen; Lie, Rolv T; Munger, Ronald G

    2017-02-01

    Evidence on association of maternal pre-pregnancy weight with risk of orofacial clefts is inconsistent. Six large case-control studies of orofacial clefts from Northern Europe and the USA were included in analyses pooling individual-level data. Cases included 4943 mothers of children with orofacial clefts (cleft lip only: 1135, cleft palate with cleft lip: 2081, cleft palate only: 1727) and controls included 10 592 mothers of unaffected children. Association of orofacial cleft risk with pre-pregnancy maternal weight classified by level of body mass index (BMI, kg/m 2 ) was evaluated using logistic regression adjusting for multiple covariates. Cleft palate, both alone and with cleft lip (CP+/-CL), was associated with maternal class II+ pre-pregnancy obesity (≥ 35)compared with normal weight [adjusted odds ratio (aOR) = 1.36; 95% confidence interval (CI) = 1.16, 1.58]. CP+/-CL was marginally associated with maternal underweight (aOR = 1.16; 95% CI = 0.98, 1.36). Cleft lip alone was not associated with BMI. In this largest population-based study to date, we found an increased risk of cleft palate, with or without cleft lip, in class II+ obese mothers compared with normal-weight mothers; underweight mothers may also have an increased risk, but this requires further study. These results also suggest that extremes of weight may have a specific effect on palatal development. © The Author 2016; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association

  14. Infant adiposity following a randomised controlled trial of a behavioural intervention in obese pregnancy

    PubMed Central

    Patel, Nashita; Godfrey, Keith M.; Pasupathy, Dharmintra; Levin, Julia; Flynn, Angela C; Hayes, Louise; Briley, Annette L; Bell, Ruth; Lawlor, Debbie A; Oteng-Ntim, Eugene; Nelson, Scott M.; Robson, Stephen C.; Sattar, Naveed; Singh, Claire; Wardle, Jane; White, Sara; Seed, Paul T; Poston, Lucilla

    2017-01-01

    Objective Randomised controlled trials are required to address causality in the reported associations between maternal influences and offspring adiposity. The aim of this study was to determine whether an antenatal lifestyle intervention in obese pregnant women associated with improved maternal diet and reduced gestational weight gain leads to a reduction in infant adiposity and sustained improvements in maternal lifestyle behaviours at 6 months postpartum. Subjects and Methods We conducted a planned postnatal follow up of a randomised controlled trial (UPBEAT) of a complex behavioural intervention targeting maternal diet (glycemic load and saturated fat intake) and physical activity in 1555 obese pregnant women. The main outcome measure was infant adiposity, assessed by subscapular and triceps skinfold thicknesses. Maternal diet and physical activity, indices of the familial lifestyle environment, were assessed by questionnaire. Results 698 (45.9%) infants (342 intervention, 356 standard antenatal care) were followed up at mean age 5.92 months. There was no difference in triceps skinfold thickness z-scores between the intervention vs. standard care arms (difference -0.14 SD, 95% CI -0.38 to 0.10, p=0.246), but subscapular skinfold thickness z-score was 0.26 SD (-0.49 to -0.02; p=0.03) lower in the intervention arm. Maternal dietary glycemic load (-35.34; -48.0 to -22.67; p<0.001) and saturated fat intake (-1.93% energy; -2.64 to -1.22; p<0.001) were reduced in the intervention arm at 6 months postpartum. Causal mediation analysis suggested that lower infant subscapular skinfold thickness was mediated by changes in antenatal maternal diet and gestational weight gain rather than postnatal diet. Conclusion This study provides evidence from follow-up of a randomised controlled trial that a maternal behavioural intervention in obese pregnant women has the potential to reduce infant adiposity and to produce a sustained improvement in maternal diet at 6 months postpartum

  15. Birth mode-dependent association between pre-pregnancy maternal weight status and the neonatal intestinal microbiome.

    PubMed

    Mueller, Noel T; Shin, Hakdong; Pizoni, Aline; Werlang, Isabel C; Matte, Ursula; Goldani, Marcelo Z; Goldani, Helena A S; Dominguez-Bello, Maria Gloria

    2016-04-01

    The intestinal microbiome is a unique ecosystem that influences metabolism in humans. Experimental evidence indicates that intestinal microbiota can transfer an obese phenotype from humans to mice. Since mothers transmit intestinal microbiota to their offspring during labor, we hypothesized that among vaginal deliveries, maternal body mass index is associated with neonatal gut microbiota composition. We report the association of maternal pre-pregnancy body mass index on stool microbiota from 74 neonates, 18 born vaginally (5 to overweight or obese mothers) and 56 by elective C-section (26 to overweight or obese mothers). Compared to neonates delivered vaginally to normal weight mothers, neonates born to overweight or obese mothers had a distinct gut microbiota community structure (weighted UniFrac distance PERMANOVA, p < 0.001), enriched in Bacteroides and depleted in Enterococcus, Acinetobacter, Pseudomonas, and Hydrogenophilus. We show that these microbial signatures are predicted to result in functional differences in metabolic signaling and energy regulation. In contrast, among elective Cesarean deliveries, maternal body mass index was not associated with neonatal gut microbiota community structure (weighted UniFrac distance PERMANOVA, p = 0.628). Our findings indicate that excess maternal pre-pregnancy weight is associated with differences in neonatal acquisition of microbiota during vaginal delivery, but not Cesarean delivery. These differences may translate to altered maintenance of metabolic health in the offspring.

  16. Birth mode-dependent association between pre-pregnancy maternal weight status and the neonatal intestinal microbiome

    PubMed Central

    Mueller, Noel T.; Shin, Hakdong; Pizoni, Aline; Werlang, Isabel C.; Matte, Ursula; Goldani, Marcelo Z.; Goldani, Helena A. S.; Dominguez-Bello, Maria Gloria

    2016-01-01

    The intestinal microbiome is a unique ecosystem that influences metabolism in humans. Experimental evidence indicates that intestinal microbiota can transfer an obese phenotype from humans to mice. Since mothers transmit intestinal microbiota to their offspring during labor, we hypothesized that among vaginal deliveries, maternal body mass index is associated with neonatal gut microbiota composition. We report the association of maternal pre-pregnancy body mass index on stool microbiota from 74 neonates, 18 born vaginally (5 to overweight or obese mothers) and 56 by elective C-section (26 to overweight or obese mothers). Compared to neonates delivered vaginally to normal weight mothers, neonates born to overweight or obese mothers had a distinct gut microbiota community structure (weighted UniFrac distance PERMANOVA, p < 0.001), enriched in Bacteroides and depleted in Enterococcus, Acinetobacter, Pseudomonas, and Hydrogenophilus. We show that these microbial signatures are predicted to result in functional differences in metabolic signaling and energy regulation. In contrast, among elective Cesarean deliveries, maternal body mass index was not associated with neonatal gut microbiota community structure (weighted UniFrac distance PERMANOVA, p = 0.628). Our findings indicate that excess maternal pre-pregnancy weight is associated with differences in neonatal acquisition of microbiota during vaginal delivery, but not Cesarean delivery. These differences may translate to altered maintenance of metabolic health in the offspring. PMID:27033998

  17. A maternal 'junk food' diet in pregnancy and lactation promotes an exacerbated taste for 'junk food' and a greater propensity for obesity in rat offspring.

    PubMed

    Bayol, Stéphanie A; Farrington, Samantha J; Stickland, Neil C

    2007-10-01

    Obesity is generally associated with high intake of junk foods rich in energy, fat, sugar and salt combined with a dysfunctional control of appetite and lack of exercise. There is some evidence to suggest that appetite and body mass can be influenced by maternal food intake during the fetal and suckling life of an individual. However, the influence of a maternal junk food diet during pregnancy and lactation on the feeding behaviour and weight gain of the offspring remains largely uncharacterised. In this study, six groups of rats were fed either rodent chow alone or with a junk food diet during gestation, lactation and/or post-weaning. The daily food intakes and body mass were measured in forty-two pregnant and lactating mothers as well as in 216 offspring from weaning up to 10 weeks of age. Results showed that 10 week-old rats born to mothers fed the junk food diet during gestation and lactation developed an exacerbated preference for fatty, sugary and salty foods at the expense of protein-rich foods when compared with offspring fed a balanced chow diet prior to weaning or during lactation alone. Male and female offspring exposed to the junk food diet throughout the study also exhibited increased body weight and BMI compared with all other offspring. This study shows that a maternal junk food diet during pregnancy and lactation may be an important contributing factor in the development of obesity.

  18. Maternal obesity and physical activity and exercise levels as pregnancy advances: an observational study.

    PubMed

    Daly, N; Mitchell, C; Farren, M; Kennelly, M M; Hussey, J; Turner, M J

    2016-05-01

    Increases in clinical complications associated with maternal obesity have generated interest in increasing physical activity (PA) and exercise levels as an intervention to improve pregnancy outcomes. The objective of this study was to examine the relationship between BMI categorisation and PA and exercise levels as pregnancy advances. This was an observational study in a large university maternity hospital. Women were recruited at their convenience before they left hospital after delivering a baby weighing 500 g or more. They completed a detailed customised physical activity and exercise questionnaire. BMI categorisation was based on the measurement of weight and height in early pregnancy. Of the 155 women recruited, 42.5 % (n = 66) were primigravidas and 10.3 % (n = 16) were smokers. Mean Body Mass Index (BMI) was 24.6 kg/m(2) and 14.2 % (n = 22) were obese, based on a BMI >29.9 kg/m(2). Overall, women decreased their exercise from an average 194 min (range 0-650 min) per week pre-pregnancy to 98 min antenatally (range 0-420 min) (p < 0.0001). Obese women exercised least pre-pregnancy and antenatally at 187.5 and 75 min per week, respectively, compared with 193.2 and 95.5 min per week in the normal BMI group and 239.3 and 106.7 min per week in the overweight group. The mean gestation at which all women reduced their activity levels was 29 weeks. We found that women decreased their PA  and exercise levels significantly in the third trimester and, thus, in the absence of a medical contra-indication there is considerable scope for an exercise intervention to improve activity  and exercise levels as pregnancy advances. However, an increase in PA levels in obese women needs further studies to determine whether it will improve the clinical outcomes for the woman and her offspring.

  19. The ubiquitin ligase Siah2 regulates obesity-induced adipose tissue inflammation.

    PubMed

    Kilroy, Gail; Carter, Lauren E; Newman, Susan; Burk, David H; Manuel, Justin; Möller, Andreas; Bowtell, David D; Mynatt, Randall L; Ghosh, Sujoy; Floyd, Z Elizabeth

    2015-11-01

    Chronic, low-grade adipose tissue inflammation associated with adipocyte hypertrophy is an important link in the relationship between obesity and insulin resistance. Although ubiquitin ligases regulate inflammatory processes, the role of these enzymes in metabolically driven adipose tissue inflammation is relatively unexplored. Herein, the effect of the ubiquitin ligase Siah2 on obesity-related adipose tissue inflammation was examined. Wild-type and Siah2KO mice were fed a low- or high-fat diet for 16 weeks. Indirect calorimetry, body composition, and glucose and insulin tolerance were assayed along with glucose and insulin levels. Gene and protein expression, immunohistochemistry, adipocyte size distribution, and lipolysis were also analyzed. Enlarged adipocytes in obese Siah2KO mice were not associated with obesity-induced insulin resistance. Proinflammatory gene expression, stress kinase signaling, fibrosis, and crown-like structures were reduced in the Siah2KO adipose tissue, and Siah2KO adipocytes were more responsive to insulin-dependent inhibition of lipolysis. Loss of Siah2 increased expression of PPARγ target genes involved in lipid metabolism and decreased expression of proinflammatory adipokines regulated by PPARγ. Siah2 links adipocyte hypertrophy with adipocyte dysfunction and recruitment of proinflammatory immune cells to adipose tissue. Selective regulation of PPARγ activity is a Siah2-mediated mechanism contributing to obesity-induced adipose tissue inflammation. © 2015 The Obesity Society.

  20. Association Between Maternal Prepregnancy Body Mass Index and Plasma Folate Concentrations With Child Metabolic Health.

    PubMed

    Wang, Guoying; Hu, Frank B; Mistry, Kamila B; Zhang, Cuilin; Ren, Fazheng; Huo, Yong; Paige, David; Bartell, Tami; Hong, Xiumei; Caruso, Deanna; Ji, Zhicheng; Chen, Zhu; Ji, Yuelong; Pearson, Colleen; Ji, Hongkai; Zuckerman, Barry; Cheng, Tina L; Wang, Xiaobin

    2016-08-01

    Previous reports have linked maternal prepregnancy obesity with low folate concentrations and child overweight or obesity (OWO) in separate studies. To our knowledge, the role of maternal folate concentrations, alone or in combination with maternal OWO, in child metabolic health has not been examined in a prospective birth cohort. To test the hypotheses that maternal folate concentrations can significantly affect child metabolic health and that sufficient maternal folate concentrations can mitigate prepregnancy obesity-induced child metabolic risk. This prospective birth cohort study was conducted at the Boston Medical Center, Boston, Massachusetts. It included 1517 mother-child dyads recruited at birth from 1998 to 2012 and followed up prospectively up to 9 years from 2003 to 2014. Child body mass index z score calculated according to US reference data, OWO defined as a body mass index in the 85th percentile or greater for age and sex, and metabolic biomarkers (leptin, insulin, and adiponectin). The mean (SD) age was 28.6 (6.5) years for mothers and 6.2 (2.4) years for the children. An L-shaped association between maternal folate concentrations and child OWO was observed: the risk for OWO was higher among those in the lowest quartile (Q1) as compared with those in Q2 through Q4, with an odds ratio of 1.45 (95% CI, 1.13-1.87). The highest risk for child OWO was found among children of obese mothers with low folate concentrations (odds ratio, 3.05; 95% CI, 1.91-4.86) compared with children of normal-weight mothers with folate concentrations in Q2 through Q4 after accounting for multiple covariables. Among children of obese mothers, their risk for OWO was associated with a 43% reduction (odds ratio, 0.57; 95% CI, 0.34-0.95) if their mothers had folate concentrations in Q2 through Q4 compared with Q1. Similar patterns were observed for child metabolic biomarkers. In this urban low-income prospective birth cohort, we demonstrated an L-shaped association between

  1. Profiles of disruptive behavior across early childhood: Contributions of frustration reactivity, physiological regulation, and maternal behavior

    PubMed Central

    Degnan, Kathryn A.; Calkins, Susan D.; Keane, Susan P.; Hill-Soderlund, Ashley L.

    2010-01-01

    Disruptive behavior, including aggression, defiance, and temper tantrums, typically peaks in early toddlerhood and decreases by school entry; however, some children do not show this normative decline. The current study examined disruptive behavior in 318 boys and girls at 2, 4, and 5 years of age and frustration reactivity, physiological regulation, and maternal behavior in the laboratory at 2 years of age. A latent profile analysis (LPA) resulted in 4 longitudinal profiles of disruptive behavior, which were differentiated by interactions between reactivity, regulation, and maternal behavior. A high profile was associated with high reactivity combined with high maternal control or low regulation combined with low maternal control. Results are discussed from a developmental psychopathology perspective. PMID:18826530

  2. The Childhood Obesity Epidemic As a Result of Non-Genetic Evolution: the Maternal Resources Hypothesis

    PubMed Central

    Archer, Edward

    2014-01-01

    Over the past century, socio-environmental evolution (e.g., reduced pathogenic load, decreased physical activity [PA], improved nutrition) led to cumulative increments in maternal energy resources (i.e., body mass, adiposity) and decrements in energy expenditure and metabolic control. These decrements reduced the competition between maternal and fetal energy demands and increased the availability of energy substrates to the intrauterine milieu. This perturbation of mother-conceptus energy partitioning stimulated fetal pancreatic beta-cell and adipocyte hyperplasia, thereby inducing an enduring competitive advantage of adipocytes over other tissues in the acquisition and sequestering of nutrient-energy via intensified insulin secretion and hyperplastic adiposity. At menarche, the competitive dominance of adipocytes was further amplified via hormone-induced adipocyte hyperplasia and weight-induced decrements in PA. These metabolic and behavioral effects were propagated progressively when obese, inactive, metabolically compromised women produced progressively larger, more inactive and metabolically compromised children. Consequently, the evolution of human energy metabolism was significantly altered. This phenotypic evolution was exacerbated by increments in the use of Caesarian sections that allowed both the larger fetuses and the metabolically compromised mothers who produced them to survive and reproduce. Thus, natural selection was iatrogenically rendered artificial selection, and the frequency of obese, inactive, metabolically compromised phenotypes increased in the global population. By the late 20th century, a metabolic tipping point was reached in which the post-prandial insulin response was so intense, the relative number of adipocytes so magnified, and inactivity so pervasive that the competitive dominance of adipocytes in the sequestering of nutrient-energy was inevitable, and obesity was unavoidable. PMID:25440888

  3. Postpartum maternal fat distribution and its association with offspring body fat through the first year of life

    USDA-ARS?s Scientific Manuscript database

    Maternal obesity is known to increase the risk of offspring obesity. Despite the evidence supporting the impact of maternal obesity on infant health, there are no studies examining the effects of maternal fat distribution on the programming of offspring obesity. We hypothesized that increased matern...

  4. Beneficial effects of exercise on offspring obesity and insulin resistance are reduced by maternal high-fat diet

    PubMed Central

    Schreiber, Saskia; Klaus, Susanne; Kanzleiter, Isabel

    2017-01-01

    Scope We investigated the long-term effects of maternal high-fat consumption and post-weaning exercise on offspring obesity susceptibility and insulin resistance. Methods C57BL/6J dams were fed either a high-fat (HFD, 40% kcal fat) or low-fat (LFD, 10% kcal fat) semi-synthetic diet during pregnancy and lactation. After weaning, male offspring of both maternal diet groups (mLFD; mHFD) received a LFD. At week 7, half of the mice got access to a running wheel (+RW) as voluntary exercise training. To induce obesity, all offspring groups (mLFD +/-RW and mHFD +/-RW) received HFD from week 15 until week 25. Results Compared to mLFD, mHFD offspring were more prone to HFD-induced body fat gain and exhibited an increased liver mass which was not due to increased hepatic triglyceride levels. RW improved the endurance capacity in mLFD, but not in mHFD offspring. Additionally, mHFD offspring +RW exhibited higher plasma insulin levels during glucose tolerance test and an elevated basal pancreatic insulin production compared to mLFD offspring. Conclusion Taken together, maternal HFD reduced offspring responsiveness to the beneficial effects of voluntary exercise training regarding the improvement of endurance capacity, reduction of fat mass gain, and amelioration of HFD-induced insulin resistance. PMID:28235071

  5. Offspring predisposition to obesity due to maternal-diet-induced obesity in rats is preventable by dietary normalization before mating.

    PubMed

    Castro, Heriberto; Pomar, Catalina Amadora; Palou, Andreu; Picó, Catalina; Sánchez, Juana

    2017-03-01

    We studied in rats whether the expected detrimental effects in offspring associated to maternal dietary obesity may be reverted by obesogenic diet removal 1 month before mating. Female rats were fed a cafeteria diet (CD) from days 10 to 100 and then a standard diet (SD) (postcafeteria rats). One month after CD removal, postcafeteria rats and a group of SD-fed female rats (controls) were mated with males. At weaning, offspring were fed SD and followed until 4 months old. CD was effective at inducing obesity in dams. Its removal led to a reduction in body weight, although, after 30 days, rats retained excess body weight and fat than controls. During lactation, postcafeteria dams showed greater body fat, and higher leptin and adiponectin levels in milk than controls. From 2 months of life, offspring of postcafeteria dams displayed lower body weight than controls, with no differences in the percentage of fat, homeostatic model assessment for insulin resistance, or circulating parameters. Removal of CD in obese rats before gestation, although without complete reversion of body weight excess, may prevent the expected detrimental effects in offspring associated to an excess fat accumulation in adulthood and the related metabolic disturbances. © 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

  6. Obesity and industry self-regulation of food and beverage marketing: a literature review.

    PubMed

    Ronit, K; Jensen, J D

    2014-07-01

    Obesity is a growing concern at national and international levels, and it is increasingly recognised that the industry has a role in and hence needs to be involved in halting the obesity epidemic. The objective of this study is to describe, analyse and evaluate research on industry self-regulation regarding food and beverage marketing and nutrition labelling. Five databases were searched for combinations of the search terms-obesity, nutrition, food, beverages, industry, self-regulation, labelling, advertising and marketing-and papers were selected on the basis of paper titles and, subsequently, on the basis of abstracts. Of the 4978 identified publications, 22 were included in the final review. The studies show that commitments in industry self-regulation schemes tend to be relatively vague and permissive, that the measurable effects of the self-regulations tend to be relatively small and that some extent of public regulation may catalyse the effectiveness of industry self-regulation. Although the reviewed studies vary in terms of analytic units and methods applied, they generally stress an ineffectiveness of existing self-regulation schemes. Food industry self-regulation in relation to obesity prevention is an emerging field of research, and further research is needed in such schemes' definitions of regulatory standards, their monitoring and sanctioning mechanisms, and their interactions with public regulation, if industry self-regulation of marketing behaviour is to become an effective and credible approach.

  7. Quality of Early Maternal–Child Relationship and Risk of Adolescent Obesity

    PubMed Central

    Gooze, Rachel A.; Lemeshow, Stanley; Whitaker, Robert C.

    2012-01-01

    Objectives: The goal of this study was to determine whether obesity in adolescence is related to the quality of the early maternal–child relationship. Methods: We analyzed data from 977 of 1364 participants in the Study of Early Child Care and Youth Development. Child attachment security and maternal sensitivity were assessed by observing mother–child interaction at 15, 24, and 36 months of age. A maternal–child relationship quality score was constructed as the number of times across the 3 ages that the child was either insecurely attached or experienced low maternal sensitivity. Adolescent obesity was defined as a measured BMI ≥95th percentile at age 15 years. Results: Poor-quality maternal–child relationships (score: ≥3) were experienced by 24.7% of children compared with 22.0% who, at all 3 ages, were neither insecurely attached nor exposed to low maternal sensitivity (score: 0). The prevalence of adolescent obesity was 26.1%, 15.5%, 12.1%, and 13.0% for those with risk scores of ≥3, 2, 1, and 0, respectively. After adjustment for gender and birth weight, the odds (95% confidence interval) of adolescent obesity was 2.45 (1.49–4.04) times higher in those with the poorest quality early maternal–child relationships (score: ≥3) compared with those with the highest quality (score: 0). Low maternal sensitivity was more strongly associated with obesity than insecure attachment. Conclusions: Poor quality of the early maternal–child relationship was associated with a higher prevalence of adolescent obesity. Interventions aimed at improving the quality of maternal–child interactions should consider assessing effects on children’s weight and examining potential mechanisms involving stress response and emotion regulation. PMID:22201144

  8. Review: Adiponectin – The Missing Link between Maternal Adiposity, Placental Transport and Fetal Growth?

    PubMed Central

    Aye, Irving L. M. H.; Powell, Theresa L.; Jansson, Thomas

    2012-01-01

    Adiponectin has well-established insulin-sensitizing effects in non-pregnant individuals. Pregnant women who are obese or have gestational diabetes typically have low circulating levels of adiponectin, which is associated with increased fetal growth. Lean women, on the other hand, have high circulating levels of adiponectin. As a result, maternal serum adiponectin is inversely correlated to fetal growth across the full range of birth weights, suggesting that maternal adiponectin may limit fetal growth. In the mother, adiponectin is predicted to promote insulin sensitivity and stimulate glucose uptake in maternal skeletal muscle thereby reducing nutrient availability for placental transfer. Adiponectin prevents insulin-stimulated amino acid uptake in cultured primary human trophoblast cells by modulating insulin receptor substrate phosphorylation. Furthermore, chronic administration of adiponectin to pregnant mice inhibits placental insulin and mammalian target of rapamycin complex 1 (mTORC1) signaling, down-regulates the activity and expression of key placental nutrient transporters and decreases fetal growth. Preliminary findings indicate that adiponectin binds to the adiponectin receptor-2 on the trophoblast cell and activates p38 MAPK and PPAR-α, which inhibits the insulin/IGF-1 signaling pathway. In contrast to maternal adiponectin, recent reports suggest that fetal adiponectin may promote expansion of adipose tissue and stimulate fetal growth. Regulation of placental function by adiponectin constitutes a novel physiological mechanism by which the endocrine functions of maternal adipose tissue influence fetal growth. These findings may help us better understand the factors determining birth weight in normal pregnancies and in pregnancy complications associated with altered maternal adiponectin levels such as obesity and gestational diabetes. PMID:23245987

  9. Maternity Leave Policies

    PubMed Central

    Strang, Lucy; Broeks, Miriam

    2017-01-01

    Abstract Over recent years many European Union countries have made changes to the design of the maternity leave provision. These policy developments reflect calls for greater gender equality in the workforce and more equal share of childcare responsibilities. However, while research shows that long period of leave can have negative effects on women's labour market attachment and career advancements, early return to work can be seen as a factor preventing exclusive breastfeeding, and therefore, potentially having negative health impacts for babies. Indeed, the World Health Organisation recommends exclusive breastfeeding up to 6 months of age to provide babies with the nutrition for healthy growth and brain development, protection from life-threatening ailments, obesity and non-communicable diseases such as asthma and diabetes. Therefore, labour market demands on women may be at odds with the health benefits for children gained by longer periods of maternity leave. The aim of this article is to examine the relationship between leave provision and health benefits for children. We examine maternity and parental leave provision across European countries and its potential impact on the breastfeeding of very young babies (up to 6-months of age). We also consider economic factors of potential extension of maternity leave provision to 6 months, such as costs to businesses, effects on the female labour market attachment, and wider consequences (benefits and costs) for individuals, families, employers and the wider society. PMID:28983432

  10. Cross Talk between Adipose Tissue and Placenta in Obese and Gestational Diabetes Mellitus Pregnancies via Exosomes.

    PubMed

    Jayabalan, Nanthini; Nair, Soumyalekshmi; Nuzhat, Zarin; Rice, Gregory E; Zuñiga, Felipe A; Sobrevia, Luis; Leiva, Andrea; Sanhueza, Carlos; Gutiérrez, Jaime Agustín; Lappas, Martha; Freeman, Dilys Jane; Salomon, Carlos

    2017-01-01

    Obesity is an important public health issue worldwide, where it is commonly associated with the development of metabolic disorders, especially insulin resistance (IR). Maternal obesity is associated with an increased risk of pregnancy complications, especially gestational diabetes mellitus (GDM). Metabolism is a vital process for energy production and the maintenance of essential cellular functions. Excess energy storage is predominantly regulated by the adipose tissue. Primarily made up of adipocytes, adipose tissue acts as the body's major energy reservoir. The role of adipose tissue, however, is not restricted to a "bag of fat." The adipose tissue is an endocrine organ, secreting various adipokines, enzymes, growth factors, and hormones that take part in glucose and lipid metabolism. In obesity, the greater portion of the adipose tissue comprises fat, and there is increased pro-inflammatory cytokine secretion, macrophage infiltration, and reduced insulin sensitivity. Obesity contributes to systemic IR and its associated metabolic complications. Similar to adipose tissue, the placenta is also an endocrine organ. During pregnancy, the placenta secretes various molecules to maintain pregnancy physiology. In addition, the placenta plays an important role in metabolism and exchange of nutrients between mother and fetus. Inflammation at the placenta may contribute to the severity of maternal IR and her likelihood of developing GDM and may also mediate the adverse consequences of obesity and GDM on the fetus. Interestingly, studies on maternal insulin sensitivity and secretion of placental hormones have not shown a positive correlation between these phenomena. Recently, a great interest in the field of extracellular vesicles (EVs) has been observed in the literature. EVs are produced by a wide range of cells and are present in all biological fluids. EVs are involved in cell-to-cell communication. Recent evidence points to an association between adipose tissue

  11. Cross Talk between Adipose Tissue and Placenta in Obese and Gestational Diabetes Mellitus Pregnancies via Exosomes

    PubMed Central

    Jayabalan, Nanthini; Nair, Soumyalekshmi; Nuzhat, Zarin; Rice, Gregory E.; Zuñiga, Felipe A.; Sobrevia, Luis; Leiva, Andrea; Sanhueza, Carlos; Gutiérrez, Jaime Agustín; Lappas, Martha; Freeman, Dilys Jane; Salomon, Carlos

    2017-01-01

    Obesity is an important public health issue worldwide, where it is commonly associated with the development of metabolic disorders, especially insulin resistance (IR). Maternal obesity is associated with an increased risk of pregnancy complications, especially gestational diabetes mellitus (GDM). Metabolism is a vital process for energy production and the maintenance of essential cellular functions. Excess energy storage is predominantly regulated by the adipose tissue. Primarily made up of adipocytes, adipose tissue acts as the body’s major energy reservoir. The role of adipose tissue, however, is not restricted to a “bag of fat.” The adipose tissue is an endocrine organ, secreting various adipokines, enzymes, growth factors, and hormones that take part in glucose and lipid metabolism. In obesity, the greater portion of the adipose tissue comprises fat, and there is increased pro-inflammatory cytokine secretion, macrophage infiltration, and reduced insulin sensitivity. Obesity contributes to systemic IR and its associated metabolic complications. Similar to adipose tissue, the placenta is also an endocrine organ. During pregnancy, the placenta secretes various molecules to maintain pregnancy physiology. In addition, the placenta plays an important role in metabolism and exchange of nutrients between mother and fetus. Inflammation at the placenta may contribute to the severity of maternal IR and her likelihood of developing GDM and may also mediate the adverse consequences of obesity and GDM on the fetus. Interestingly, studies on maternal insulin sensitivity and secretion of placental hormones have not shown a positive correlation between these phenomena. Recently, a great interest in the field of extracellular vesicles (EVs) has been observed in the literature. EVs are produced by a wide range of cells and are present in all biological fluids. EVs are involved in cell-to-cell communication. Recent evidence points to an association between adipose tissue

  12. Maternal obesity reduces milk lipid production in lactating mice by inhibiting acetyl-CoA carboxylase and impairing fatty acid synthesis.

    PubMed

    Saben, Jessica L; Bales, Elise S; Jackman, Matthew R; Orlicky, David; MacLean, Paul S; McManaman, James L

    2014-01-01

    Maternal metabolic and nutrient trafficking adaptations to lactation differ among lean and obese mice fed a high fat (HF) diet. Obesity is thought to impair milk lipid production, in part, by decreasing trafficking of dietary and de novo synthesized lipids to the mammary gland. Here, we report that de novo lipogenesis regulatory mechanisms are disrupted in mammary glands of lactating HF-fed obese (HF-Ob) mice. HF feeding decreased the total levels of acetyl-CoA carboxylase-1 (ACC), and this effect was exacerbated in obese mice. The relative levels of phosphorylated (inactive) ACC, were elevated in the epithelium, and decreased in the adipose stroma, of mammary tissue from HF-Ob mice compared to those of HF-fed lean (HF-Ln) mice. Mammary gland levels of AMP-activated protein kinase (AMPK), which catalyzes formation of inactive ACC, were also selectively elevated in mammary glands of HF-Ob relative to HF-Ln dams or to low fat fed dams. These responses correlated with evidence of increased lipid retention in mammary adipose, and decreased lipid levels in mammary epithelial cells, of HF-Ob dams. Collectively, our data suggests that maternal obesity impairs milk lipid production, in part, by disrupting the balance of de novo lipid synthesis in the epithelial and adipose stromal compartments of mammary tissue through processes that appear to be related to increased mammary gland AMPK activity, ACC inhibition, and decreased fatty acid synthesis.

  13. Maternal Obesity Reduces Milk Lipid Production in Lactating Mice by Inhibiting Acetyl-CoA Carboxylase and Impairing Fatty Acid Synthesis

    PubMed Central

    Saben, Jessica L.; Bales, Elise S.; Jackman, Matthew R.; Orlicky, David; MacLean, Paul S.; McManaman, James L.

    2014-01-01

    Maternal metabolic and nutrient trafficking adaptations to lactation differ among lean and obese mice fed a high fat (HF) diet. Obesity is thought to impair milk lipid production, in part, by decreasing trafficking of dietary and de novo synthesized lipids to the mammary gland. Here, we report that de novo lipogenesis regulatory mechanisms are disrupted in mammary glands of lactating HF-fed obese (HF-Ob) mice. HF feeding decreased the total levels of acetyl-CoA carboxylase-1 (ACC), and this effect was exacerbated in obese mice. The relative levels of phosphorylated (inactive) ACC, were elevated in the epithelium, and decreased in the adipose stroma, of mammary tissue from HF-Ob mice compared to those of HF-fed lean (HF-Ln) mice. Mammary gland levels of AMP-activated protein kinase (AMPK), which catalyzes formation of inactive ACC, were also selectively elevated in mammary glands of HF-Ob relative to HF-Ln dams or to low fat fed dams. These responses correlated with evidence of increased lipid retention in mammary adipose, and decreased lipid levels in mammary epithelial cells, of HF-Ob dams. Collectively, our data suggests that maternal obesity impairs milk lipid production, in part, by disrupting the balance of de novo lipid synthesis in the epithelial and adipose stromal compartments of mammary tissue through processes that appear to be related to increased mammary gland AMPK activity, ACC inhibition, and decreased fatty acid synthesis. PMID:24849657

  14. Hypothalamic circuits regulating appetite and energy homeostasis: pathways to obesity

    PubMed Central

    Timper, Katharina; Brüning, Jens C.

    2017-01-01

    ABSTRACT The ‘obesity epidemic’ represents a major global socioeconomic burden that urgently calls for a better understanding of the underlying causes of increased weight gain and its associated metabolic comorbidities, such as type 2 diabetes mellitus and cardiovascular diseases. Improving our understanding of the cellular basis of obesity could set the stage for the development of new therapeutic strategies. The CNS plays a pivotal role in the regulation of energy and glucose homeostasis. Distinct neuronal cell populations, particularly within the arcuate nucleus of the hypothalamus, sense the nutrient status of the organism and integrate signals from peripheral hormones including pancreas-derived insulin and adipocyte-derived leptin to regulate calorie intake, glucose metabolism and energy expenditure. The arcuate neurons are tightly connected to other specialized neuronal subpopulations within the hypothalamus, but also to various extrahypothalamic brain regions, allowing a coordinated behavioral response. This At a Glance article gives an overview of the recent knowledge, mainly derived from rodent models, regarding the CNS-dependent regulation of energy and glucose homeostasis, and illustrates how dysregulation of the neuronal networks involved can lead to overnutrition and obesity. The potential impact of recent research findings in the field on therapeutic treatment strategies for human obesity is also discussed. PMID:28592656

  15. Hypothalamic circuits regulating appetite and energy homeostasis: pathways to obesity.

    PubMed

    Timper, Katharina; Brüning, Jens C

    2017-06-01

    The 'obesity epidemic' represents a major global socioeconomic burden that urgently calls for a better understanding of the underlying causes of increased weight gain and its associated metabolic comorbidities, such as type 2 diabetes mellitus and cardiovascular diseases. Improving our understanding of the cellular basis of obesity could set the stage for the development of new therapeutic strategies. The CNS plays a pivotal role in the regulation of energy and glucose homeostasis. Distinct neuronal cell populations, particularly within the arcuate nucleus of the hypothalamus, sense the nutrient status of the organism and integrate signals from peripheral hormones including pancreas-derived insulin and adipocyte-derived leptin to regulate calorie intake, glucose metabolism and energy expenditure. The arcuate neurons are tightly connected to other specialized neuronal subpopulations within the hypothalamus, but also to various extrahypothalamic brain regions, allowing a coordinated behavioral response. This At a Glance article gives an overview of the recent knowledge, mainly derived from rodent models, regarding the CNS-dependent regulation of energy and glucose homeostasis, and illustrates how dysregulation of the neuronal networks involved can lead to overnutrition and obesity. The potential impact of recent research findings in the field on therapeutic treatment strategies for human obesity is also discussed. © 2017. Published by The Company of Biologists Ltd.

  16. Maternal obesity and diabetes induces latent metabolic defects and widespread epigenetic changes in isogenic mice

    PubMed Central

    Li, Cheryl C.Y.; Young, Paul E.; Maloney, Christopher A.; Eaton, Sally A.; Cowley, Mark J.; Buckland, Michael E; Preiss, Thomas; Henstridge, Darren C.; Cooney, Gregory J.; Febbraio, Mark A.; Martin, David I.K.; Cropley, Jennifer E.; Suter, Catherine M.

    2013-01-01

    Intrauterine nutrition can program metabolism, creating stable changes in physiology that may have significant health consequences. The mechanism underlying these changes is widely assumed to involve epigenetic changes to the expression of metabolic genes, but evidence supporting this idea is limited. Here we have performed the first study of the epigenomic consequences of exposure to maternal obesity and diabetes. We used a mouse model of natural-onset obesity that allows comparison of genetically identical mice whose mothers were either obese and diabetic or lean with a normal metabolism. We find that the offspring of obese mothers have a latent metabolic phenotype that is unmasked by exposure to a Western-style diet, resulting in glucose intolerance, insulin resistance and hepatic steatosis. The offspring show changes in hepatic gene expression and widespread but subtle alterations in cytosine methylation. Contrary to expectation, these molecular changes do not point to metabolic pathways but instead reside in broadly developmental ontologies. We propose that, rather than being adaptive, these changes may simply produce an inappropriate response to suboptimal environments; maladaptive phenotypes may be avoidable if postnatal nutrition is carefully controlled. PMID:23764993

  17. Understanding of Self and Maternal Warmth Predict Later Self-Regulation in Toddlers

    ERIC Educational Resources Information Center

    Jennings, Kay D.; Sandberg, Ian; Kelley, Sue A.; Valdes, Lourdes; Yaggi, Kirsten; Abrew, Amy; Macey-Kalcevic, Melody

    2008-01-01

    Research on the development of self-regulation has focused primarily on the roles of maternal behavior and attention, but cognitive understanding of the self is also likely to contribute, as is exposure to maternal depression. In this study toddlers' understanding of self-as-object and understanding of agency were assessed behaviorally at both 20…

  18. Effect of maternal body mass index on hormones in breast milk: a systematic review.

    PubMed

    Andreas, Nicholas J; Hyde, Matthew J; Gale, Chris; Parkinson, James R C; Jeffries, Suzan; Holmes, Elaine; Modi, Neena

    2014-01-01

    Maternal Body Mass Index (BMI) is positively associated with infant obesity risk. Breast milk contains a number of hormones that may influence infant metabolism during the neonatal period; these may have additional downstream effects on infant appetite regulatory pathways, thereby influencing propensity towards obesity in later life. To conduct a systematic review of studies examining the association between maternal BMI and the concentration of appetite-regulating hormones in breast milk. Pubmed was searched for studies reporting the association between maternal BMI and leptin, adiponectin, insulin, ghrelin, resistin, obestatin, Peptide YY and Glucagon-Like Peptide 1 in breast milk. Twenty six studies were identified and included in the systematic review. There was a high degree of variability between studies with regard to collection, preparation and analysis of breast milk samples. Eleven of fifteen studies reporting breast milk leptin found a positive association between maternal BMI and milk leptin concentration. Two of nine studies investigating adiponectin found an association between maternal BMI and breast milk adiponectin concentration; however significance was lost in one study following adjustment for time post-partum. No association was seen between maternal BMI and milk adiponectin in the other seven studies identified. Evidence for an association between other appetite regulating hormones and maternal BMI was either inconclusive, or lacking. A positive association between maternal BMI and breast milk leptin concentration is consistently found in most studies, despite variable methodology. Evidence for such an association with breast milk adiponectin concentration, however, is lacking with additional research needed for other hormones including insulin, ghrelin, resistin, obestatin, peptide YY and glucagon-like peptide-1. As most current studies have been conducted with small sample sizes, future studies should ensure adequate sample sizes and

  19. Maternal medical conditions during pregnancy and gross motor development up to age 24 months in the Upstate KIDS Study

    PubMed Central

    Ghassabian, Akhgar; Sundaram, Rajeshwari; Wylie, Amanda; Bell, Erin; Bello, Scott C.; Yeung, Edwina

    2015-01-01

    Aims We examined whether children of mothers with a medical condition diagnosed before or during pregnancy took longer to achieve gross motor milestones up to age 24 months. Methods We obtained information on medical conditions using self-reports, birth certificates, and hospital records in 4909 mothers participating in Upstate KIDS, a population-based birth cohort. Mothers reported on their children’s motor milestone achievement at 4, 8, 12, 18, and 24 months of age. Results After adjustment for covariates (including prepregnancy body mass index), children of mothers with gestational diabetes took longer to achieve sitting without support [Hazard Ratio (HR)=0.84, 95%CI:0.75-0.93), walking with assistance (HR=0.88, 95%CI:0.77-0.98) and walking alone (HR=0.88, 95%CI:0.77-0.99) than children of women with no gestational diabetes. Similar findings emerged for maternal diabetes. Gestational hypertension was associated with a longer time to achieve walking with assistance. These associations did not change after adjustment for gestational age or birth weight. Severe hypertensive disorders of pregnancy were related to a longer time to achieve milestones, but not after adjustment for perinatal factors. Interpretation Children exposed to maternal diabetes, gestational or pre-gestational, may take longer to achieve motor milestones than non-exposed children, independent of maternal obesity. PMID:26502927

  20. Maternal obesity and fetal deaths: results from the Brazilian cross-sectional Demographic Health Survey, 2006.

    PubMed

    Felisbino-Mendes, Mariana Santos; Matozinhos, Fernanda Penido; Miranda, J Jaime; Villamor, Eduardo; Velasquez-Melendez, Gustavo

    2014-01-07

    Obesity is highly related to negative reproductive health outcomes, but its relationship with spontaneous abortion and stillbirth remains to be understood, especially in transitioning economies. This study aimed to examine the relationship between obesity and spontaneous abortions and stillbirths in a representative sample of the Brazilian population. Cross-sectional study using secondary data of Brazilian women of reproductive age (15-45 years old) from the National Demographic and Health Survey in 2006. Obesity was measured by body mass index (BMI), waist circumference (WC) and waist-to-height ratio (WHR). Logistic regression modeling of the survey data was used to evaluate the relationship between obesity and the study outcomes. The three obesity markers used were found to be strongly and positively associated with spontaneous abortion and stillbirth occurrence. In the adjusted models, there was strong evidence that for each unit increase in BMI (OR = 1.05; 95%CI: 1.02-1.08) and WHR (OR = 1.32; 95%CI: 1.03-1.69), the odds of having a spontaneous abortion was higher. In addition, compared to those of optimal weight, obese women were more likely to have negative outcomes. Maternal age, parity, skin color, educational level and household income were important covariates for adjustment. A sensitivity analysis among women who had only one pregnancy was also performed and showed similar results. Obesity is potentially associated with an increased risk of spontaneous abortion and stillbirth in a representative sample of the Brazilian population. These findings are in accordance with previous studies and thus reinforce the need for obstetric care providers to counsel obese reproductive-age women regarding the risks, complications and importance of weight loss and weight control prior to pregnancy.

  1. Infant nutrition and maternal obesity influence the risk of non-alcoholic fatty liver disease in adolescents.

    PubMed

    Ayonrinde, Oyekoya T; Oddy, Wendy H; Adams, Leon A; Mori, Trevor A; Beilin, Lawrence J; de Klerk, Nicholas; Olynyk, John K

    2017-09-01

    The pathway to non-alcoholic fatty liver disease (NAFLD) in adolescents may have its origins in adiposity gains, nutrition and sedentary lifestyle established during childhood. There is inadequate knowledge regarding the associations between infant nutrition and subsequent NAFLD. We examined the association of maternal factors and infant nutrition, with the subsequent diagnosis of NAFLD in adolescents. Adolescents aged 17years in the Western Australian Pregnancy (Raine) Cohort study had fatty liver assessment using liver ultrasound. Prospectively recorded data on maternal pregnancy and infant feeding were examined against a NAFLD outcome during late adolescence. NAFLD was diagnosed in 15.2% of the 1,170 adolescents examined. Ninety-four percent had been breastfed as infants. The duration of breastfeeding before starting supplementary milk was ⩾4months in 54.4% and ⩾6months in 40.6%. Breastfeeding without supplementary milk ⩾6months (adjusted odds ratio [OR]: 0.64; 95% confidence interval [CI]: 0.43-0.94, p=0.02), maternal pre-pregnancy obesity (adjusted OR: 2.29; 95% CI: 1.21-4.32, p=0.01) and adolescent obesity (adjusted OR: 9.08; 95% CI: 6.26-13.17, p<0.001) were associated with NAFLD independent of a Western dietary pattern at 17years of age. Adolescents with NAFLD who had been breastfed for ⩾6months had a less adverse metabolic profile compared with adolescents breastfed for <6months. Supplementary milk intake starting before 6months was associated with a higher prevalence and ultrasound severity of NAFLD compared with intake starting after 6months (17.7% vs. 11.2%, p=0.003 and 7.8% vs. 3.4%, p=0.005 respectively). Though NAFLD is generally mediated through adiposity gains, breastfeeding for at least 6months, avoidance of early supplementary formula milk feeding, and normal maternal pre-pregnancy BMI may reduce the odds of a NAFLD diagnosis during adolescence. Non-alcoholic fatty liver disease (NAFLD) is a common liver disorder in which there is too

  2. Maternal Socialization and Child Temperament as Predictors of Emotion Regulation in Turkish Preschoolers

    ERIC Educational Resources Information Center

    Yagmurlu, Bilge; Altan, Ozge

    2010-01-01

    This study investigated the role of maternal socialization and temperament in Turkish preschool children's emotion regulation. Participants consisted of 145 preschoolers (79 boys, 69 girls; M[subscript age]= 62 months), their mothers, and daycare teachers from middle-high socioeconomic suburbs of Istanbul. Maternal child-rearing practices and…

  3. Regulating migrant maternity: nursing and midwifery's emancipatory aims and assimilatory practices.

    PubMed

    DeSouza, Ruth

    2013-12-01

    In contemporary Western societies, birthing is framed as transformative for mothers; however, it is also a site for the regulation of women and the exercise of power relations by health professionals. Nursing scholarship often frames migrant mothers as a problem, yet nurses are imbricated within systems of scrutiny and regulation that are unevenly imposed on 'other' mothers. Discourses deployed by New Zealand Plunket nurses (who provide a universal 'well child' health service) to frame their understandings of migrant mothers were analysed using discourse analysis and concepts of power drawn from the work of French philosopher Michel Foucault, read through a postcolonial feminist perspective. This research shows how Plunket nurses draw on liberal feminist discourses, which have emancipatory aims but reflect assimilatory practices, paradoxically disempowering women who do not subscribe to ideals of individual autonomy. Consequently, the migrant mother, her family and new baby are brought into a neoliberal project of maternal improvement through surveillance. This project--enacted differentially but consistently among nurses--attempts to alter maternal and familial relationships by 'improving' mothering. Feminist critiques of patriarchy in maternity must be supplemented by a critique of the implicitly western subject of maternity to make empowerment a possibility for all mothers. © 2013 John Wiley & Sons Ltd.

  4. Maternal high-fat diet modulates brown adipose tissue response to B-adrenergic agonist

    USDA-ARS?s Scientific Manuscript database

    Maternal obesity increases offspring risk for several metabolic diseases. We previously showed that offspring of obese dams are predisposed to obesity, liver and adipose tissue anomalies. However, the effect of maternal obesity on developmental programing brown adipose tissue (BAT) is poorly underst...

  5. Volitional regulation of brain responses to food stimuli in overweight and obese subjects: A real-time fMRI feedback study.

    PubMed

    Spetter, Maartje S; Malekshahi, Rahim; Birbaumer, Niels; Lührs, Michael; van der Veer, Albert H; Scheffler, Klaus; Spuckti, Sophia; Preissl, Hubert; Veit, Ralf; Hallschmid, Manfred

    2017-05-01

    Obese subjects who achieve weight loss show increased functional connectivity between dorsolateral prefrontal cortex (dlPFC) and ventromedial prefrontal cortex (vmPFC), key areas of executive control and reward processing. We investigated the potential of real-time functional magnetic resonance imaging (rt-fMRI) neurofeedback training to achieve healthier food choices by enhancing self-control of the interplay between these brain areas. We trained eight male individuals with overweight or obesity (age: 31.8 ± 4.4 years, BMI: 29.4 ± 1.4 kg/m 2 ) to up-regulate functional connectivity between the dlPFC and the vmPFC by means of a four-day rt-fMRI neurofeedback protocol including, on each day, three training runs comprised of six up-regulation and six passive viewing trials. During the up-regulation runs of the four training days, participants successfully learned to increase functional connectivity between dlPFC and vmPFC. In addition, a trend towards less high-calorie food choices emerged from before to after training, which however was associated with a trend towards increased covertly assessed snack intake. Findings of this proof-of-concept study indicate that overweight and obese participants can increase functional connectivity between brain areas that orchestrate the top-down control of appetite for high-calorie foods. Neurofeedback training might therefore be a useful tool in achieving and maintaining weight loss. Copyright © 2017 Elsevier Ltd. All rights reserved.

  6. To Assess the Effect of Maternal BMI on Obstetrical Outcome

    NASA Astrophysics Data System (ADS)

    Lakhanpal, Shuchi; Aggarwal, Asha; Kaur, Gurcharan

    2012-06-01

    AIMS: To assess the effect of maternal BMI on complications in pregnancy, mode of delivery, complications of labour and delivery.METHODS:A crossectional study was carried out in the Obst and Gynae department, Kasturba Hospital, Delhi. The study enrolled 100 pregnant women. They were divided into 2 groups based on their BMI, more than or equal to 30.0 kg/m2 were categorized as obese and less than 30 kg/m2 as non obese respectively. Maternal complications in both types of patients were studied.RESULTS:CONCLUSION: As the obstetrical outcome is significantly altered due to obesity, we can improve maternal outcome by overcoming obesity. As obesity is a modifiable risk factor, preconception counseling creating awareness regarding health risk associated with obesity should be encouraged and obstetrical complications reduced.

  7. Maternal obesity in the agouti viable yellow (Avy) mouse produces defective secretory activation that is associated with mammary inflammation and activation of adrenocorticosteroid-dependent gene expression

    USDA-ARS?s Scientific Manuscript database

    Maternal obesity is known to interfere with normal lactation in women, rodents, and dairy animals. Obesity is also correlated with profound changes in an array of endocrine factors and is causally linked with inflammation and insulin resistance. Recent work suggests that elevated aldosterone actin...

  8. Polysome Profiling in Liver Identifies Dynamic Regulation of Endoplasmic Reticulum Translatome by Obesity and Fasting

    PubMed Central

    Fu, Suneng; Fan, Jason; Blanco, Joshua; Gimenez-Cassina, Alfredo; Danial, Nika N.; Watkins, Steve M.; Hotamisligil, Gökhan S.

    2012-01-01

    Obesity-associated metabolic complications are generally considered to emerge from abnormalities in carbohydrate and lipid metabolism, whereas the status of protein metabolism is not well studied. Here, we performed comparative polysome and associated transcriptional profiling analyses to study the dynamics and functional implications of endoplasmic reticulum (ER)–associated protein synthesis in the mouse liver under conditions of obesity and nutrient deprivation. We discovered that ER from livers of obese mice exhibits a general reduction in protein synthesis, and comprehensive analysis of polysome-bound transcripts revealed extensive down-regulation of protein synthesis machinery, mitochondrial components, and bile acid metabolism in the obese translatome. Nutrient availability also plays an important but distinct role in remodeling the hepatic ER translatome in lean and obese mice. Fasting in obese mice partially reversed the overall translatomic differences between lean and obese nonfasted controls, whereas fasting of the lean mice mimicked many of the translatomic changes induced by the development of obesity. The strongest examples of such regulations were the reduction in Cyp7b1 and Slco1a1, molecules involved in bile acid metabolism. Exogenous expression of either gene significantly lowered plasma glucose levels, improved hepatic steatosis, but also caused cholestasis, indicating the fine balance bile acids play in regulating metabolism and health. Together, our work defines dynamic regulation of the liver translatome by obesity and nutrient availability, and it identifies a novel role for bile acid metabolism in the pathogenesis of metabolic abnormalities associated with obesity. PMID:22927828

  9. Polysome profiling in liver identifies dynamic regulation of endoplasmic reticulum translatome by obesity and fasting.

    PubMed

    Fu, Suneng; Fan, Jason; Blanco, Joshua; Gimenez-Cassina, Alfredo; Danial, Nika N; Watkins, Steve M; Hotamisligil, Gökhan S

    2012-08-01

    Obesity-associated metabolic complications are generally considered to emerge from abnormalities in carbohydrate and lipid metabolism, whereas the status of protein metabolism is not well studied. Here, we performed comparative polysome and associated transcriptional profiling analyses to study the dynamics and functional implications of endoplasmic reticulum (ER)-associated protein synthesis in the mouse liver under conditions of obesity and nutrient deprivation. We discovered that ER from livers of obese mice exhibits a general reduction in protein synthesis, and comprehensive analysis of polysome-bound transcripts revealed extensive down-regulation of protein synthesis machinery, mitochondrial components, and bile acid metabolism in the obese translatome. Nutrient availability also plays an important but distinct role in remodeling the hepatic ER translatome in lean and obese mice. Fasting in obese mice partially reversed the overall translatomic differences between lean and obese nonfasted controls, whereas fasting of the lean mice mimicked many of the translatomic changes induced by the development of obesity. The strongest examples of such regulations were the reduction in Cyp7b1 and Slco1a1, molecules involved in bile acid metabolism. Exogenous expression of either gene significantly lowered plasma glucose levels, improved hepatic steatosis, but also caused cholestasis, indicating the fine balance bile acids play in regulating metabolism and health. Together, our work defines dynamic regulation of the liver translatome by obesity and nutrient availability, and it identifies a novel role for bile acid metabolism in the pathogenesis of metabolic abnormalities associated with obesity.

  10. Maternal obesity accelerates fetal pancreatic beta-cell but not alpha-cell development in sheep: prenatal consequences.

    PubMed

    Ford, Stephen P; Zhang, Liren; Zhu, Meijun; Miller, Myrna M; Smith, Derek T; Hess, Bret W; Moss, Gary E; Nathanielsz, Peter W; Nijland, Mark J

    2009-09-01

    Maternal obesity affects offspring weight, body composition, and organ function, increasing diabetes and metabolic syndrome risk. We determined effects of maternal obesity and a high-energy diet on fetal pancreatic development. Sixty days prior to breeding, ewes were assigned to control [100% of National Research Council (NRC) recommendations] or obesogenic (OB; 150% NRC) diets. At 75 days gestation, OB ewes exhibited elevated insulin-to-glucose ratios at rest and during a glucose tolerance test, demonstrating insulin resistance compared with control ewes. In fetal studies, ewes ate their respective diets from 60 days before to 75 days after conception when animals were euthanized under general anesthesia. OB and control ewes increased in body weight by approximately 43% and approximately 6%, respectively, from diet initiation until necropsy. Although all organs were heavier in fetuses from OB ewes, only pancreatic weight increased as a percentage of fetal weight. Blood glucose, insulin, and cortisol were elevated in OB ewes and fetuses on day 75. Insulin-positive cells per unit pancreatic area were 50% greater in fetuses from OB ewes as a result of increased beta-cell mitoses rather than decreased programmed cell death. Lambs of OB ewes were born earlier but weighed the same as control lambs; however, their crown-to-rump length was reduced, and their fat mass was increased. We conclude that increased systemic insulin in fetuses from OB ewes results from increased glucose exposure and/or cortisol-induced accelerated fetal beta-cell maturation and may contribute to premature beta-cell function loss and predisposition to obesity and metabolic disease in offspring.

  11. Maternal obesity accelerates fetal pancreatic β-cell but not α-cell development in sheep: prenatal consequences

    PubMed Central

    Ford, Stephen P.; Zhang, Liren; Zhu, Meijun; Miller, Myrna M.; Smith, Derek T.; Hess, Bret W.; Moss, Gary E.; Nathanielsz, Peter W.; Nijland, Mark J.

    2009-01-01

    Maternal obesity affects offspring weight, body composition, and organ function, increasing diabetes and metabolic syndrome risk. We determined effects of maternal obesity and a high-energy diet on fetal pancreatic development. Sixty days prior to breeding, ewes were assigned to control [100% of National Research Council (NRC) recommendations] or obesogenic (OB; 150% NRC) diets. At 75 days gestation, OB ewes exhibited elevated insulin-to-glucose ratios at rest and during a glucose tolerance test, demonstrating insulin resistance compared with control ewes. In fetal studies, ewes ate their respective diets from 60 days before to 75 days after conception when animals were euthanized under general anesthesia. OB and control ewes increased in body weight by ∼43% and ∼6%, respectively, from diet initiation until necropsy. Although all organs were heavier in fetuses from OB ewes, only pancreatic weight increased as a percentage of fetal weight. Blood glucose, insulin, and cortisol were elevated in OB ewes and fetuses on day 75. Insulin-positive cells per unit pancreatic area were 50% greater in fetuses from OB ewes as a result of increased β-cell mitoses rather than decreased programmed cell death. Lambs of OB ewes were born earlier but weighed the same as control lambs; however, their crown-to-rump length was reduced, and their fat mass was increased. We conclude that increased systemic insulin in fetuses from OB ewes results from increased glucose exposure and/or cortisol-induced accelerated fetal β-cell maturation and may contribute to premature β-cell function loss and predisposition to obesity and metabolic disease in offspring. PMID:19605766

  12. Dietary patterns are associated with child, maternal and household-level characteristics and overweight/obesity among young Samoan children.

    PubMed

    Choy, Courtney C; Wang, Dongqing; Baylin, Ana; Soti-Ulberg, Christina; Naseri, Take; Reupena, Muagututia S; Thompson, Avery A; Duckham, Rachel L; Hawley, Nicola L

    2018-05-01

    Among young Samoan children, diet may not be optimal: in 2015, 16·1 % of 24-59-month-olds were overweight/obese, 20·3 % stunted and 34·1 % anaemic. The present study aimed to identify dietary patterns among 24-59-month-old Samoan children and evaluate their association with: (i) child, maternal and household characteristics; and (ii) nutritional status indicators (stunting, overweight/obesity, anaemia). A community-based, cross-sectional study. Principal component analysis on 117 FFQ items was used to identify empirical dietary patterns. Distributions of child, maternal and household characteristics were examined by factor score quintiles. The regression of nutritional status indicators v. these quintiles was performed using logistic regression models. Ten villages on the Samoan island of Upolu. A convenience sample of mother-child pairs (n 305). Two dietary patterns, modern and neo-traditional, emerged. The modern pattern was loaded with 'westernized' foods (red meat, condiments and snacks). The neo-traditional pattern included vegetables, local starches, coconuts, fish and poultry. Following the modern diet was associated with urban residence, greater maternal educational attainment, higher socio-economic status, lower vitamin C intake and higher sugar intake. Following the neo-traditional diet was associated with rural residence, lower socio-economic status, higher vitamin C intake and lower sugar intake. While dietary patterns were not related to stunting or anaemia, following the neo-traditional pattern was positively associated with child overweight/obesity (adjusted OR=4·23, 95 % CI 1·26, 14·17, for the highest quintile, P-trend=0·06). Further longitudinal monitoring and evaluation of early childhood growth and development are needed to understand the influences of early diet on child health in Samoa.

  13. Factors associated with abdominal obesity in children

    PubMed Central

    Melzer, Matheus Ribeiro Theodósio Fernandes; Magrini, Isabella Mastrangi; Domene, Semíramis Martins Álvares; Martins, Paula Andrea

    2015-01-01

    Objective: To identify the association of dietary, socioeconomic factors, sedentary behaviors and maternal nutritional status with abdominal obesity in children. Methods: A cross-sectional study with household-based survey, in 36 randomly selected census tracts in the city of Santos, SP. 357 families were interviewed and questionnaires and anthropometric measurements were applied in mothers and their 3-10 years-old children. Assessment of abdominal obesity was made by maternal and child's waist circumference measurement; for classification used cut-off points proposed by World Health Organization (1998) and Taylor et al. (2000) were applied. The association between variables was performed by multiple logistic regression analysis. Results: 30.5% of children had abdominal obesity. Associations with children's and maternal nutritional status and high socioeconomic status were shown in the univariate analysis. In the regression model, children's body mass index for age (OR=93.7; 95%CI 39.3-223.3), female gender (OR=4.1; 95%CI 1.8-9.3) and maternal abdominal obesity (OR=2.7; 95%CI 1.2-6.0) were significantly associated with children's abdominal obesity, regardless of the socioeconomic status. Conclusions: Abdominal obesity in children seems to be associated with maternal nutritional status, other indicators of their own nutritional status and female gender. Intervention programs for control of childhood obesity and prevention of metabolic syndrome should consider the interaction of the nutritional status of mothers and their children. PMID:26298655

  14. [Factors associated with abdominal obesity in children].

    PubMed

    Melzer, Matheus Ribeiro Theodósio Fernandes; Magrini, Isabella Mastrangi; Domene, Semíramis Martins Álvares; Martins, Paula Andrea

    2015-12-01

    To identify the association of dietary, socioeconomic factors, sedentary behaviors and maternal nutritional status with abdominal obesity in children. A cross-sectional study with household-based survey, in 36 randomly selected census tracts in the city of Santos/SP. 357 families were interviewed and questionnaires and anthropometric measurements were applied in mothers and their 3-0 years-old children. Assessment of abdominal obesity was made by maternal and child's waist circumference measurement; for classification used cut-off points proposed by World Health Organization (1998) and Taylor et al. (2000) were applied. The association between variables was performed by multiple logistic regression analysis. 30.5% of children had abdominal obesity. Associations with children's and maternal nutritional status and high socioeconomic status were shown in the univariate analysis. In the regression model, children's body mass index for age (OR=93.7; 95%CI 39.3-223.3), female gender (OR=4.1; 95%CI 1.8-9.3) and maternal abdominal obesity (OR=2.7; 95%CI 1.2-6.0) were significantly associated with children's abdominal obesity, regardless of the socioeconomic status. Abdominal obesity in children seems to be associated with maternal nutritional status, other indicators of their own nutritional status and female gender. Intervention programs for control of childhood obesity and prevention of metabolic syndrome should consider the interaction of the nutritional status of mothers and their children. Copyright © 2015 Sociedade de Pediatria de São Paulo. Publicado por Elsevier Editora Ltda. All rights reserved.

  15. Programming of the appetite-regulating neural network: a link between maternal overnutrition and the programming of obesity?

    PubMed

    Mühlhäusler, B S

    2007-01-01

    The concept of a functional foetal "appetite regulatory neural network" is a new and potentially critical one. There is a growing body of evidence showing that the nutritional environment to which the foetus is exposed during prenatal and perinatal development has long-term consequences for the function of the appetite-regulating neural network and therefore the way in which an individual regulates energy balance throughout later life. This is of particular importance in the context of evidence obtained from a wide range of epidemiological studies, which have shown that individuals exposed to an elevated nutrient supply before birth have an increased risk of becoming obese as children and adults. This review summarises the key pieces of experimental evidence, by our group and others, that have contributed to our current understanding of the programming of appetite, and highlights the important questions that are yet to be answered. It is clear that this area of research has the potential to generate, within the next few years, interventions that could begin to alleviate the adverse long-term consequences of being exposed to an elevated nutrient supply before birth.

  16. Obesity, Gynecological Factors, and Abnormal Mammography Follow-Up in Minority and Medically Underserved Women

    PubMed Central

    Wujcik, Debra; Lin, Jin-Mann S.; Grau, Ana; Wilson, Veronica; Champion, Victoria; Zheng, Wei; Egan, Kathleen M.

    2009-01-01

    Abstract Background The relationship between obesity and screening mammography adherence has been examined previously, yet few studies have investigated obesity as a potential mediator of timely follow-up of abnormal (Breast Imaging Reporting and Data System [BIRADS-0]) mammography results in minority and medically underserved patients. Methods We conducted a retrospective cohort study of 35 women who did not return for follow-up >6 months from index abnormal mammography and 41 who returned for follow-up ≤6 months in Nashville, Tennessee. Patients with a BIRADS-0 mammography event in 2003–2004 were identified by chart review. Breast cancer risk factors were collected by telephone interview. Multivariate logistic regression was performed on selected factors with return for diagnostic follow-up. Results Obesity and gynecological history were significant predictors of abnormal mammography resolution. A significantly higher frequency of obese women delayed return for mammography resolution compared with nonobese women (64.7% vs. 35.3%). A greater number of hysterectomized women returned for diagnostic follow-up compared with their counterparts without a hysterectomy (77.8% vs. 22.2%). Obese patients were more likely to delay follow-up >6 months (adjusted OR 4.09, p = 0.02). Conversely, hysterectomized women were significantly more likely to return for timely mammography follow-up ≤6 months (adjusted OR 7.95, p = 0.007). Conclusions Study results suggest that weight status and gynecological history influence patients' decisions to participate in mammography follow-up studies. Strategies are necessary to reduce weight-related barriers to mammography follow-up in the healthcare system including provider training related to mammography screening of obese women. PMID:19558307

  17. Lymphotoxin Regulates Commensal Responses to Enable Diet-Induced Obesity

    PubMed Central

    Upadhyay, Vaibhav; Poroyko, Valeriy; Kim, Tae-jin; Devkota, Suzanne; Fu, Sherry; Liu, Donald; Tumanov, Alexei V.; Koroleva, Ekaterina P.; Deng, Liufu; Nagler, Cathryn; Chang, Eugene; Tang, Hong; Fu, Yang-Xin

    2013-01-01

    The microbiota plays a critical, weight-promoting role in diet-induced obesity (DIO), but the pathways that cause the microbiota to induce weight gain are unknown. We report that mice deficient in lymphotoxin (LT), a key molecule in gut immunity, were resistant to DIO. Ltbr−/− mice differed in microbial community composition compared to their heterozygous littermates, including an overgrowth of segmented filamentous bacteria (SFB). Furthermore, cecal transplantation conferred leanness to germ-free recipients. Housing Ltbr−/− mice with their obese siblings rescued weight gain, demonstrating the communicability of the obese phenotype. Ltbr−/− animals lacked interleukin 23 (IL-23) and IL-22 that can regulate SFB. Mice deficient in these pathways also resisted DIO, demonstrating that intact mucosal immunity guides diet-induced changes to the microbiota to enable obesity. PMID:22922363

  18. Unconscious collusion: An interpretative phenomenological analysis of the maternity care experiences of women with obesity (BMI≥30kg/m²).

    PubMed

    Atkinson, Sandra; McNamara, Patricia Mannix

    2017-06-01

    obstetric and midwifery literature continually emphasise incidence and consequence of obesity in pregnancy. However, they offer less consensus on how best to support women who are obese. Therefore, this study explores in depth the lived experience of women who have a Body Mass Index (BMI) ≥30kg/m². This exploration provides a bio-psycho-social understanding of the lived experience of women to identify how best to support them throughout their childbirth experience. an Interpretative Phenomenological Analysis (IPA) design was adopted for this qualitative study. Purposive sampling of participants was conducted on the postnatal wards of a maternity hospital in the Republic of Ireland. In total, 15 participants volunteered to take part in semi-structured interviews conducted at six to ten weeks postnatally. Data were analysed utilising the IPA framework. the results indicate that participants were conscious of the problematics of communicating obesity in pregnancy. The narrative data revealed an unconscious collusion between healthcare professionals and women as they navigate obesity related conversations. The behaviours related to unconscious collusion are incorporated in the sub-ordinate themes; 'just recorded and that's all', 'but what's eating healthy? 'pussy footing around' and 'I hate that word obesity. the findings highlight a lack of information received by participants from healthcare professionals regarding increased BMI or weight management. The data suggests that healthcare professionals appeared to collude with women to avoid challenging discussions regarding obesity. This may be related to avoidance on participants' part and/or may be linked with healthcare professionals' reluctance to communicate issues relating to increased BMI. Although participants were generally unhappy with the communication skills of health professionals, they readily acknowledged the sensitive nature of obesity related communications. The findings provide healthcare

  19. Inhibition of fetal bone development through epigenetic down- regulation of HoxA10 in obese rats fed high fat diet

    USDA-ARS?s Scientific Manuscript database

    Epidemiological studies show that maternal obesity during intrauterine and early postnatal life increases the risk of low bone mass and fracture later in life. Here, we show that bone development is inhibited in GED 18.5 embryos from rat dams made obese by feeding a high fat diet (HFD). Moreover, fe...

  20. Early Mitochondrial Adaptations in Skeletal Muscle to Obesity and Obesity Resistance Differentially Regulated by High-Fat Diet.

    PubMed

    Sun, Jingyu; Huang, Tao; Qi, Zhengtang; You, Songhui; Dong, Jingmei; Zhang, Chen; Qin, Lili; Zhou, Yunhe; Ding, Shuzhe

    2017-09-01

    The mechanism for different susceptibilities to obesity after short-term high-fat diet (HFD) feeding is largely unknown. Given the close association between obesity occurrence and mitochondrial dysfunction, the early events in skeletal muscle mitochondrial adaptations between HFD-induced obesity (DIO) and HFD-induced obesity resistant (DIO-R) lean phenotype under excess nutritional environment were explored.ICR/JCL male mice were randomly divided into 2 groups, as follows: low-fat diet (LFD) and HFD groups. After 6 weeks on HFD, HFD-fed mice were classified as DIO or DIO-R according to their body weight gain. Serum parameters, oxidative stress biomarkers, the activation of AMPK/ACC axis, and the expression profiles of mitochondrial biogenesis were measured by using corresponding methods among the LFD control, DIO, and DIO-R groups. Serum glucose, total cholesterol, low-density lipoprotein, and high-density lipoprotein levels were significantly increased in DIO and DIO-R mice compared with LFD controls. However, DIO-R mice had significantly higher MDA levels and exhibited a significantly higher level of AMP-activated protein kinase (AMPK) activation and acetyl-CoA carboxylase (ACC) inactivation than DIO mice. Furthermore, the transcript and protein levels of transcriptional coactivator peroxisome proliferator-activated receptor γ (PPARγ) coactivator 1α (PGC-1α) and estrogen-related receptor-α (ERRα) in DIO-R mice were significantly up-regulated compared with the DIO mice. Although the body weight gain differed, the DIO and DIO-R mice had similar metabolic disturbance of glucose and lipids after short-term HFD consumption. The diverse alterations on fatty acid oxidation and mitochondrial biogenesis pathway induced by AMPK activation might be involved in different susceptibilities to obesity when consuming HFD. © Georg Thieme Verlag KG Stuttgart · New York.

  1. Maternal depression and anxiety, social synchrony, and infant regulation of negative and positive emotions.

    PubMed

    Granat, Adi; Gadassi, Reuma; Gilboa-Schechtman, Eva; Feldman, Ruth

    2017-02-01

    Maternal postpartum depression (PPD) exerts long-term negative effects on infants; yet the mechanisms by which PPD disrupts emotional development are not fully clear. Utilizing an extreme-case design, 971 women reported symptoms of depression and anxiety following childbirth and 215 high and low on depressive symptomatology reported again at 6 months. Of these, mothers diagnosed with major depressive disorder (n = 22), anxiety disorders (n = 19), and controls (n = 59) were visited at 9 months. Mother-infant interaction was microcoded for maternal and infant's social behavior and synchrony. Infant negative and positive emotional expression and self-regulation were tested in 4 emotion-eliciting paradigms: anger with mother, anger with stranger, joy with mother, and joy with stranger. Infants of depressed mothers displayed less social gaze and more gaze aversion. Gaze and touch synchrony were lowest for depressed mothers, highest for anxious mothers, and midlevel among controls. Infants of control and anxious mothers expressed less negative affect with mother compared with stranger; however, maternal presence failed to buffer negative affect in the depressed group. Maternal depression chronicity predicted increased self-regulatory behavior during joy episodes, and touch synchrony moderated the effects of PPD on infant self-regulation. Findings describe subtle microlevel processes by which maternal depression across the postpartum year disrupts the development of infant emotion regulation and suggest that diminished social synchrony, low differentiation of attachment and nonattachment contexts, and increased self-regulation during positive moments may chart pathways for the cross-generational transfer of emotional maladjustment from depressed mothers to their infants. (PsycINFO Database Record (c) 2017 APA, all rights reserved).

  2. Environmental factors associated with overweight and obesity in taiwanese children.

    PubMed

    Chen, Yang-Ching; Chen, Pau-Chung; Hsieh, Wu-Shiun; Portnov, Boris A; Chen, Yu-An; Lee, Yungling Leo

    2012-11-01

    We explored the relationship among sociodemographic, behavioural, household environmental and perinatal factors, and risks of childhood overweight and obesity in Taiwan. A total of 7930 children aged 9 to 14 years were recruited from 14 randomly selected Taiwanese communities in 2007 and 2010. Height and weight were measured using standard protocols during school visits. Questionnaires that contained children's family information, birth conditions, exercise habits and household environmental factors were answered by the parents. Associations between risk factors and childhood overweight and obesity were estimated through odds ratio and 95% confidence interval from mixed models. In this cohort, 32.3% of the children were overweight and 17.5% were obese. Male gender, high birthweight, exposure to in utero maternal smoking and current exposure to household environmental tobacco smoke (stronger effect of maternal than paternal smoking) were positively associated with childhood overweight/obesity. In contrast, higher parental education level, number of siblings, active exercise habits and taking vitamins were associated with reduced risks of childhood obesity. Birthweight revealed a J-shaped relationship with the probability of childhood overweight/obesity. This study uncovers several modifiable risk factors for childhood overweight and obesity, and parents are encouraged to provide an anti-obesity environment such as quitting smoking, controlling birthweight of child during pregnancy and building up exercise habits. © 2012 Blackwell Publishing Ltd.

  3. Maternal obesogenic diet induces endometrial hyperplasia, an early hallmark of endometrial cancer, in a diethylstilbestrol mouse model.

    PubMed

    Owuor, Theresa O; Reid, Michaela; Reschke, Lauren; Hagemann, Ian; Greco, Suellen; Modi, Zeel; Moley, Kelle H

    2018-01-01

    Thirty-eight percent of US adult women are obese, meaning that more children are now born of overweight and obese mothers, leading to an increase in predisposition to several adult onset diseases. To explore this phenomenon, we developed a maternal obesity animal model by feeding mice a diet composed of high fat/ high sugar (HF/HS) and assessed both maternal diet and offspring diet on the development of endometrial cancer (ECa). We show that maternal diet by itself did not lead to ECa initiation in wildtype offspring of the C57Bl/6J mouse strain. While offspring fed a HF/HS post-weaning diet resulted in poor metabolic health and decreased uterine weight (regardless of maternal diet), it did not lead to ECa. We also investigated the effects of the maternal obesogenic diet on ECa development in a Diethylstilbestrol (DES) carcinogenesis mouse model. All mice injected with DES had reproductive tract lesions including decreased number of glands, condensed and hyalinized endometrial stroma, and fibrosis and increased collagen deposition that in some mice extended into the myometrium resulting in extensive disruption and loss of the inner and outer muscular layers. Fifty percent of DES mice that were exposed to maternal HF/HS diet developed several features indicative of the initial stages of carcinogenesis including focal glandular and atypical endometrial hyperplasia versus 0% of their Chow counterparts. There was an increase in phospho-Akt expression in DES mice exposed to maternal HF/HS diet, a regulator of persistent proliferation in the endometrium, and no difference in total Akt, phospho-PTEN and total PTEN expression. In summary, maternal HF/HS diet exposure induces endometrial hyperplasia and other precancerous phenotypes in mice treated with DES. This study suggests that maternal obesity alone is not sufficient for the development of ECa, but has an additive effect in the presence of a secondary insult such as DES.

  4. An ATF4-ATG5 signaling in hypothalamic POMC neurons regulates obesity.

    PubMed

    Xiao, Yuzhong; Deng, Yalan; Yuan, Feixiang; Xia, Tingting; Liu, Hao; Li, Zhigang; Chen, Shanghai; Liu, Zhixue; Ying, Hao; Liu, Yi; Zhai, Qiwei; Guo, Feifan

    2017-06-03

    ATF4 (activating transcription factor 4) is an important transcription factor that has many biological functions, while its role in hypothalamic POMC (pro-opiomelanocortin-α) neurons in the regulation of energy homeostasis has not been explored. We recently discovered that mice with an Atf4 deletion specific to POMC neurons (PAKO mice) are lean and have higher energy expenditure. Furthermore, these mice are resistant to high-fat diet (HFD)-induced obesity and obesity-related metabolic disorders. Mechanistically, we found the expression of ATG5 (autophagy-related 5) is upregulated in POMC neurons of PAKO mice, and ATF4 regulates ATG5 expression by binding directly to its promoter. Mice with Atf4 and Atg5 double knockout in POMC neurons have reduced energy expenditure and gain more fat mass compared with PAKO mice under a HFD. Finally, the effect of Atf4 knockout in POMC neurons is possibly mediated by enhanced ATG5-dependent macroautophagy/autophagy and α-melanocyte-stimulating hormone (α-MSH) production in the hypothalamus. Together, this work not only identifies a beneficial role for ATF4 in hypothalamic POMC neurons in the regulation of obesity, but also provides a new potential therapeutic target for obesity and obesity-related metabolic diseases.

  5. The Relation between Maternal Emotional Support and Child Physiological Regulation across the Preschool Years

    PubMed Central

    Perry, Nicole B.; Nelson, Jackie A.; Swingler, Margaret M.; Leerkes, Esther M.; Calkins, Susan D.; Marcovitch, Stuart; O’Brien, Marion

    2017-01-01

    Trajectories of baseline RSA (respiratory sinus arrhythmia), an index of reactivity, and vagal withdrawal, an index of regulation, across the preschool period were examined. In addition, maternal emotional support was investigated as a potential time-varying predictor of these trajectories. Physiological measures were obtained during frustration tasks, and a maternal emotional support measure was assessed via maternal report and direct observation. Children’s baseline RSA and vagal withdrawal scores were moderately stable across the preschool period. Growth models indicated that children’s baseline RSA scores changed linearly over the preschool years, and there was significant variability in withdrawal trajectories. Greater maternal emotional support predicted higher initial withdrawal levels and lower emotional support was associated with the greatest increase in withdrawal over time. This suggests that children of higher emotionally supportive mothers reached higher levels of physiological regulation earlier in development and therefore did not show the same increase across preschool as children of less supportive mothers. Maternal emotional support was not significantly related to trajectories of baseline RSA. PMID:22573287

  6. Individual Differences in Trajectories of Emotion Regulation Processes: The Effects of Maternal Depressive Symptomatology and Children's Physiological Regulation

    ERIC Educational Resources Information Center

    Blandon, Alysia Y.; Calkins, Susan D.; Keane, Susan P.; O'Brien, Marion

    2008-01-01

    Trajectories of emotion regulation processes were examined in a community sample of 269 children across the ages of 4 to 7 using hierarchical linear modeling. Maternal depressive symptomatology (Symptom Checklist-90) and children's physiological reactivity (respiratory sinus arrhythmia [RSA]) and vagal regulation ([delta]RSA) were explored as…

  7. Influence of maternal and child lifestyle-related characteristics on the socioeconomic inequality in overweight and obesity among 5-year-old children; the "Be Active, Eat Right" Study.

    PubMed

    Veldhuis, Lydian; Vogel, Ineke; van Rossem, Lenie; Renders, Carry M; Hirasing, Remy A; Mackenbach, Johan P; Raat, Hein

    2013-06-06

    It is unclear whether the socioeconomic inequality in prevalence of overweight and obesity is already present among very young children. This study investigates the association between overweight and socioeconomic status (SES, with maternal educational level as an indicator of SES) among 5-year-old children. This cross-sectional study uses baseline data from 5-year-olds of Dutch ethnicity (n = 5,582) and their mothers collected for the "Be active, eat right" study. Compared to children of mothers with the highest educational level, for children of mothers with the lowest educational level the odds ratio (adjusted for demographic characteristics) for having overweight was 2.10 (95% confidence interval: 1.57-2.82), and for having obesity was 4.18 (95% confidence interval: 2.32-7.55). Addition of maternal and child lifestyle-related characteristics decreased the odds ratios for overweight and obesity by 26.4% and 42.1%, respectively. The results show that an inverse SES-overweight/obesity association is already present at elementary school entry, and that watching TV by mother and child, the child consuming breakfast and, especially maternal weight status, are contributing factors in this association. These results should be taken into account when developing policies to reduce inequalities in (childhood) health.

  8. Psychological effects of dance-based group exergaming in obese adolescents.

    PubMed

    Wagener, T L; Fedele, D A; Mignogna, M R; Hester, C N; Gillaspy, S R

    2012-10-01

    In order to attract obese adolescents who are often reluctant to engage in traditional exercise, new forms of physical activity are needed. The purpose of the study was to investigate the impact of dance-based exergaming on a diverse sample of obese adolescents' perceived competence to exercise, psychological adjustment and body mass index (BMI). A diverse sample of 40 obese adolescents was randomized to either a 10-week group dance-based exergaming programme or a wait-list control condition. Baseline and follow-up measures included adolescent self-reported psychological adjustment and perceived competence to exercise, and maternal report of adolescent psychological adjustment and anthropometric measures. Compared with controls, participants in the dance-based exergaming condition significantly increased in self-reported perceived competence to exercise regularly and reported significant improvement in relations with parents from baseline to end-of-treatment. Maternal report of adolescent externalizing and internalizing symptomatology also decreased from baseline to end-of-treatment. No pre-post differences in BMI were seen within or between conditions. Results support the positive impact of dance-based exergaming on obese adolescents' psychological functioning and perceived competence to continue exercise. © 2012 The Authors. Pediatric Obesity © 2012 International Association for the Study of Obesity.

  9. The prevention and treatment of hypoadiponectinemia-associated human diseases by up-regulation of plasma adiponectin.

    PubMed

    Hossain, Md Murad; Mukheem, Abdul; Kamarul, Tunku

    2015-08-15

    Hypoadiponectinemia is characterized by low plasma adiponectin levels that can be caused by genetic factors, such as single nucleotide polymorphisms (SNPs) and mutations in the adiponectin gene or by visceral fat deposition/obesity. Reports have suggested that hypoadiponectinemia is associated with dyslipidemia, hypertension, hyperuricemia, metabolic syndrome, atherosclerosis, type 2 diabetes mellitus and various cardiovascular diseases. Previous studies have highlighted several potential strategies to up-regulate adiponectin secretion and function, including visceral fat reduction through diet therapy and exercise, administration of exogenous adiponectin, treatment with peroxisome proliferator-activating receptor gamma (PPARγ) agonists (e.g., thiazolidinediones (TZDs)) and ligands (e.g., bezafibrate and fenofibrate) or the blocking of the renin-angiotensin system. Likewise, the up-regulation of the expression and stimulation of adiponectin receptors by using adiponectin receptor agonists would be an effective method to treat obesity-related conditions. Notably, adiponectin is an abundantly expressed bioactive protein that also exhibits a wide spectrum of biological properties, such as insulin-sensitizing, anti-diabetic, anti-inflammatory and anti-atherosclerotic activities. Although targeting adiponectin and its receptors has been useful for treating diabetes and other metabolic-related diseases in experimental studies, current drug development based on adiponectin/adiponectin receptors for clinical applications is scarce, and there is a lack of available clinical trial data. This comprehensive review discusses the strategies that are presently being pursued to harness the potential of adiponectin up-regulation. In addition, we examined the current status of drug development and its potential for clinical applications. Copyright © 2015 Elsevier Inc. All rights reserved.

  10. Association of Maternal Prepregnancy BMI and Plasma Folate concentrations with Child Metabolic Health

    PubMed Central

    Wang, Guoying; Hu, Frank B.; Mistry, Kamila B.; Zhang, Cuilin; Ren, Fazheng; Huo, Yong; Paige, David; Bartell, Tami; Hong, Xiumei; Caruso, Deanna; Ji, Zhicheng; Chen, Zhu; Ji, Yuelong; Pearson, Colleen; Ji, Hongkai; Zuckerman, Barry; Cheng, Tina L.; Wang, Xiaobin

    2016-01-01

    Importance Previous reports have linked maternal prepregnancy obesity with low folate concentrations and child overweight or obesity (OWO) in separate studies. The role of maternal folate concentrations, alone or in combination with maternal OWO, in child metabolic health has not been examined in a prospective birth cohort. Objective We tested the hypotheses that maternal folate concentrations can significantly affect child metabolic health and that maternal sufficient folate concentrations can mitigate prepregnancy obesity-induced child metabolic risk. Design Prospective birth cohort study Setting The Boston Medical Center, MA, USA Participants This study included 1517 mother-child dyads recruited at birth from 1998–2012 and followed prospectively up to 9 years (median age: 6.2 years, range: 2–9 years). Main Outcomes and Measures Child BMI z-score calculated according to U.S. reference data, OWO defined as BMI≥85th percentile for age and gender, and metabolic biomarkers (leptin, insulin, and adiponectin). Results An “L-shaped” relationship between maternal folate concentrations and child OWO was observed: the risk of OWO was higher in the lowest quartile (Q1) as compared to Q2–Q4 with an odds ratio (OR) of 1.45 (95% confidence interval [CI], 1.13 to 1.87). The highest risk of child OWO was found among children of obese mothers with low folate concentrations (OR, 3.05, 95%CI, 1.91 to 4.86) compared to children of normal weight mothers with folate concentrations in Q2–Q4 after accounting for multiple covariables. Among children of obese mothers, their risk of OWO was associated with 43% reduction (OR, 0.57, 95%CI, 0.34–0.95) if their mothers had folate concentrations in Q2–Q4 compared to Q1. Similar patterns were observed for child metabolic biomarkers. Conclusions and Relevance In this urban low-income prospective birth cohort, we demonstrated an L-shaped relationship between maternal plasma folate concentrations and child OWO and the benefit of

  11. Maternal obesity, gestational weight gain and childhood cardiac outcomes: role of childhood body mass index.

    PubMed

    Toemen, L; Gishti, O; van Osch-Gevers, L; Steegers, E A P; Helbing, W A; Felix, J F; Reiss, I K M; Duijts, L; Gaillard, R; Jaddoe, V W V

    2016-07-01

    Maternal obesity may affect cardiovascular outcomes in the offspring. We examined the associations of maternal prepregnancy body mass index and gestational weight gain with childhood cardiac outcomes and explored whether these associations were explained by parental characteristics, infant characteristics or childhood body mass index. In a population-based prospective cohort study among 4852 parents and their children, we obtained maternal weight before pregnancy and in early, mid- and late pregnancy. At age 6 years, we measured aortic root diameter (cm) and left ventricular dimensions. We calculated left ventricular mass (g), left ventricular mass index (g m(-2.7)), relative wall thickness ((2 × left ventricular posterior wall thickness)/left ventricular diameter), fractional shorting (%), eccentric left ventricular hypertrophy and concentric remodeling. A one standard deviation score (SDS) higher maternal prepregnancy body mass index was associated with higher left ventricular mass (0.10 SDS (95% confidence interval (CI) 0.08, 0.13)), left ventricular mass index (0.06 SDS (95% CI 0.03, 0.09)) and aortic root diameter (0.09 SDS (95% CI 0.06, 0.12)), but not with relative wall thickness or fractional shortening. A one SDS higher maternal prepregnancy body mass index was associated with an increased risk of eccentric left ventricular hypertrophy (odds ratio 1.21 (95% CI 1.03, 1.41)), but not of concentric remodeling. When analyzing the effects of maternal weight in different periods simultaneously, only maternal prepregnancy weight and early pregnancy weight were associated with left ventricular mass, left ventricular mass index and aortic root diameter (P-values<0.05), independent of weight in other pregnancy periods. All observed associations were independent of parental and infant characteristics, but attenuated to non-significance after adjustment for childhood body mass index. Maternal prepregnancy body mass index and weight gain in early pregnancy are both

  12. Maternal RNA regulates Aurora C kinase during mouse oocyte maturation in a translation-independent fashion.

    PubMed

    Balboula, Ahmed Z; Blengini, Cecilia S; Gentilello, Amanda S; Takahashi, Masashi; Schindler, Karen

    2017-06-01

    During oocyte meiotic maturation, Aurora kinase C (AURKC) is required to accomplish many critical functions including destabilizing erroneous kinetochore-microtubule (K-MT)attachments and regulating bipolar spindle assembly. How localized activity of AURKC is regulated in mammalian oocytes, however, is not fully understood. Female gametes from many species, including mouse, contain stores of maternal transcripts that are required for downstream developmental events. We show here that depletion of maternal RNA in mouse oocytes resulted in impaired meiotic progression, increased incidence of chromosome misalignment and abnormal spindle formation at metaphase I (Met I), and cytokinesis defects. Importantly, depletion of maternal RNA perturbed the localization and activity of AURKC within the chromosomal passenger complex (CPC). These perturbations were not observed when translation was inhibited by cycloheximide (CHX) treatment. These results demonstrate a translation-independent function of maternal RNA to regulate AURKC-CPC function in mouse oocytes. © The Authors 2017. Published by Oxford University Press on behalf of Society for the Study of Reproduction. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

  13. Exercise rescues obese mothers' insulin sensitivity, placental hypoxia and male offspring insulin sensitivity.

    PubMed

    Fernandez-Twinn, Denise S; Gascoin, Geraldine; Musial, Barbara; Carr, Sarah; Duque-Guimaraes, Daniella; Blackmore, Heather L; Alfaradhi, Maria Z; Loche, Elena; Sferruzzi-Perri, Amanda N; Fowden, Abigail L; Ozanne, Susan E

    2017-03-14

    The prevalence of obesity during pregnancy continues to increase at alarming rates. This is concerning as in addition to immediate impacts on maternal wellbeing, obesity during pregnancy has detrimental effects on the long-term health of the offspring through non-genetic mechanisms. A major knowledge gap limiting our capacity to develop intervention strategies is the lack of understanding of the factors in the obese mother that mediate these epigenetic effects on the offspring. We used a mouse model of maternal-diet induced obesity to define predictive correlations between maternal factors and offspring insulin resistance. Maternal hyperinsulinemia (independent of maternal body weight and composition) strongly associated with offspring insulin resistance. To test causality, we implemented an exercise intervention that improved maternal insulin sensitivity without changing maternal body weight or composition. This maternal intervention prevented excess placental lipid deposition and hypoxia (independent of sex) and insulin resistance in male offspring. We conclude that hyperinsulinemia is a key programming factor and therefore an important interventional target during obese pregnancy, and propose moderate exercise as a promising strategy to improve metabolic outcome in both the obese mother and her offspring.

  14. Maternal overweight and obesity and risks of severe birth-asphyxia-related complications in term infants: a population-based cohort study in Sweden.

    PubMed

    Persson, Martina; Johansson, Stefan; Villamor, Eduardo; Cnattingius, Sven

    2014-05-01

    Maternal overweight and obesity increase risks of pregnancy and delivery complications and neonatal mortality, but the mechanisms are unclear. The objective of the study was to investigate associations between maternal body mass index (BMI) in early pregnancy and severe asphyxia-related outcomes in infants delivered at term (≥37 weeks). A nation-wide Swedish cohort study based on data from the Medical Birth Register included all live singleton term births in Sweden between 1992 and 2010. Logistic regression analyses were used to obtain odds ratios (ORs) with 95% CIs for Apgar scores between 0 and 3 at 5 and 10 minutes, meconium aspiration syndrome, and neonatal seizures, adjusted for maternal height, maternal age, parity, mother's smoking habits, education, country of birth, and year of infant birth. Among 1,764,403 term births, 86% had data on early pregnancy BMI and Apgar scores. There were 1,380 infants who had Apgar score 0-3 at 5 minutes (absolute risk  = 0.8 per 1,000) and 894 had Apgar score 0-3 at 10 minutes (absolute risk  = 0.5 per 1,000). Compared with infants of mothers with normal BMI (18.5-24.9), the adjusted ORs (95% CI) for Apgar scores 0-3 at 10 minutes were as follows: BMI 25-29.9: 1.32 (1.10-1.58); BMI 30-34.9: 1.57 (1.20-2.07); BMI 35-39.9: 1.80 (1.15-2.82); and BMI ≥40: 3.41 (1.91-6.09). The ORs for Apgar scores 0-3 at 5 minutes, meconium aspiration, and neonatal seizures increased similarly with maternal BMI. A study limitation was lack of data on effects of obstetric interventions and neonatal resuscitation efforts. Risks of severe asphyxia-related outcomes in term infants increase with maternal overweight and obesity. Given the high prevalence of the exposure and the severity of the outcomes studied, the results are of potential public health relevance and should be confirmed in other populations. Prevention of overweight and obesity in women of reproductive age is important to improve perinatal health.

  15. High Maternal Body Mass Index Is Associated with an Early-Onset of Overweight/Obesity in Pre-School-Aged Children in Malawi. A Multilevel Analysis of the 2015-16 Malawi Demographic and Health Survey.

    PubMed

    Ntenda, Peter Austin Morton; Mhone, Thomas Gabriel; Nkoka, Owen

    2018-05-25

    Overweight/obesity in young children is one of the most serious public health issues globally. We examined whether individual- and community-level maternal nutritional status is associated with an early onset of overweight/obesity in pre-school-aged children in Malawi. Data were obtained from the 2015-16 Malawi Demographic and Health Survey (MDHS). The maternal nutritional status as body mass index and childhood overweight/obesity status was assessed by using the World Health Organization (WHO) recommendations. To examine whether the maternal nutritional status is associated with overweight/obesity in pre-school-aged children, two-level multilevel logistic regression models were constructed on 4023 children of age less than five years dwelling in 850 different communities. The multilevel regression analysis showed that children born to overweight/obese mothers had increased odds of being overweight/obese [adjusted odds ratio (aOR) = 3.11; 95% confidence interval (CI): 1.13-8.54]. At the community level, children born to mothers from the middle (aOR: 1.68; 95% CI: 1.02-2.78) and high (aOR: 1.69; 95% CI: 1.00-2.90) percentage of overweight/obese women had increased odds of being overweight/obese. In addition, there were significant variations in the odds of childhood overweight/obesity in the communities. Strategies aimed at reducing childhood overweight/obesity in Malawi should address not only women and their children but also their communities. Appropriate choices of nutrition, diet and physical activity patterns should be emphasized upon in overweight/obese women of childbearing age throughout pregnancy and beyond.

  16. Maternal obesity in the ewe increases cardiac ventricular expression of glucocorticoid receptors, proinflammatory cytokines and fibrosis in adult male offspring

    PubMed Central

    Odhiambo, John F.; McCormick, Richard J.; Nathanielsz, Peter W.; Ford, Stephen P.

    2017-01-01

    Obesity during human pregnancy predisposes offspring to obesity and cardiovascular disease in postnatal life. In a sheep model of maternal overnutrition/obesity we have previously reported myocardial inflammation and fibrosis, as well as cardiac dysfunction in late term fetuses, in association with chronically elevated blood cortisol. Significant research has suggested a link between elevated glucocorticoid exposure in utero and hypertension and cardiovascular disease postnatally. Here we examined the effects of maternal obesity on myocardial inflammation and fibrosis of their adult offspring. Adult male offspring from control (CON) mothers fed 100% of National Research Council (NRC) recommendations (n = 6) and male offspring from obese mothers (MO) fed 150% NRC (n = 6), were put on a 12-week ad libitum feeding challenge then necropsied. At necropsy, plasma cortisol and left and right ventricular thickness were markedly increased (P<0.05) in adult male MO offspring. Myocardial collagen content and collagen-crosslinking were greater (P<0.05) in MO offspring compared to CON offspring in association with increased mRNA and protein expression of glucocorticoid receptors (GR). No group difference was found in myocardial mineralocorticoids receptor (MR) protein expression. Further, mRNA expression for the proinflammatory cytokines: cluster of differentiation (CD)-68, transforming growth factor (TGF)-β1, and tumor necrosis factor (TNF)-α were increased (P < 0.05), and protein expression of CD-68, TGF-β1, and TNF-α tended to increase (P<0.10) in MO vs. CON offspring. These data provide evidence for MO-induced programming of elevated plasma cortisol and myocardial inflammation and fibrosis in adult offspring potentially through increased GR. PMID:29267325

  17. Maternal obesity, obstetric interventions and post-partum anaemia increase the risk of post-partum sepsis: a population-based cohort study based on Swedish medical health registers.

    PubMed

    Axelsson, Daniel; Blomberg, Marie

    2017-10-01

    The objective was to estimate whether maternal obesity and/or obstetric interventions are associated with diagnosed maternal post-partum sepsis. A retrospective observational cohort study including all deliveries in Sweden between 1997 and 2012 (N = 1,558,752). Cases of sepsis (n = 376) were identified by International Classification of Diseases, (ICD-10) codes A40, A41 and O 85 in the Medical Birth Register and the National Patient Register. The reference population was non-infected, and therefore, women with any other infection diagnosis and/or with dispensed antibiotics within eight weeks post-partum were excluded. Information on dispensed drugs was available in the prescribed drug Register. Women with sepsis were compared with non-infected women concerning maternal characteristics and obstetric interventions. Adjusted odds ratios (aOR) were determined using the Mantel-Haenszel technique. Adjustments were made for maternal age, parity and smoking. Obese women (body mass index ≥30) had a doubled risk of sepsis (3.6/10,000) compared with normal weight women (2.0/10,000) (aOR 1.85 (95%CI: 1.37-2.48)). Induction of labour (aOR 1.44 (95%CI: 1.09-1.91)), caesarean section overall (aOR 3.06 (95%CI: 2.49-3.77)) and elective caesarean section (aOR 2.41 (95%CI: 1.68-3.45)) increased the risk of sepsis compared with normal vaginal delivery. Post-partum anaemia due to acute blood loss was associated with maternal sepsis (aOR 3.40 (95%CI: 2.59-4.47)). Maternal obesity, obstetric interventions and post-partum anaemia due to acute blood loss increased the risk of diagnosed post-partum sepsis indicating that interventions in obstetric care should be considered carefully and anaemia should be treated if resources are available.

  18. Proximal Tubular Cannabinoid-1 Receptor Regulates Obesity-Induced CKD.

    PubMed

    Udi, Shiran; Hinden, Liad; Earley, Brian; Drori, Adi; Reuveni, Noa; Hadar, Rivka; Cinar, Resat; Nemirovski, Alina; Tam, Joseph

    2017-12-01

    Obesity-related structural and functional changes in the kidney develop early in the course of obesity and occur independently of hypertension, diabetes, and dyslipidemia. Activating the renal cannabinoid-1 receptor (CB 1 R) induces nephropathy, whereas CB 1 R blockade improves kidney function. Whether these effects are mediated via a specific cell type within the kidney remains unknown. Here, we show that specific deletion of CB 1 R in the renal proximal tubule cells did not protect the mice from obesity, but markedly attenuated the obesity-induced lipid accumulation in the kidney and renal dysfunction, injury, inflammation, and fibrosis. These effects associated with increased activation of liver kinase B1 and the energy sensor AMP-activated protein kinase, as well as enhanced fatty acid β -oxidation. Collectively, these findings indicate that renal proximal tubule cell CB 1 R contributes to the pathogenesis of obesity-induced renal lipotoxicity and nephropathy by regulating the liver kinase B1/AMP-activated protein kinase signaling pathway. Copyright © 2017 by the American Society of Nephrology.

  19. Insulin-like signalling to the maternal germline controls progeny response to osmotic stress

    PubMed Central

    Burton, Nicholas O.; Furuta, Tokiko; Webster, Amy K.; Kaplan, Rebecca E. W.; Baugh, L. Ryan; Arur, Swathi; Horvitz, H. Robert

    2017-01-01

    In 1893 August Weismann proposed that information about the environment could not pass from somatic cells to germ cells1, a hypothesis now known as the Weismann barrier. However, recent studies have indicated that parental exposure to environmental stress can modify progeny physiology2–7 and that parental stress can contribute to progeny disorders8. The mechanisms regulating these phenomena are poorly understood. We report that the nematode C. elegans can protect itself from osmotic stress by entering a state of arrested development and can protect its progeny from osmotic stress by increasing the expression of the glycerol biosynthetic enzyme GPDH-2 in progeny. Both of these protective mechanisms are regulated by insulin-like signalling: insulin-like signalling to the intestine regulates developmental arrest, while insulin-like signalling to the maternal germline regulates glycerol metabolism in progeny. Thus, there is a heritable link between insulin-like signalling to the maternal germline and progeny metabolism and gene expression. We speculate that analogous modulation of insulin-like signalling to the germline is responsible for effects of the maternal environment on human diseases that involve insulin signalling, such as obesity and type-2 diabetes8. PMID:28166192

  20. Differential associations between maternal scaffolding and toddler emotion regulation in toddlers born preterm and full term

    PubMed Central

    Erickson, Sarah J.; Duvall, Susanne W.; Fuller, Janell; Schrader, Ron; MacLean, Peggy; Lowe, Jean

    2013-01-01

    Background Parental “scaffolding” behavior has been associated with developmental outcomes in at-risk children. Aims Because there are limited empirical data regarding how scaffolding is associated with emotion-based developmental skills, the purpose of this study was to compare associations between maternal verbal scaffolding and toddler emotion regulation, including fewer displays of negative affect and increased contentment and enjoyment during play, in toddlers born preterm and full term. Study Design This study was a cross-sectional cohort design. Maternal and toddler behavior was assessed during 5 minutes of videotaped free play with standardized toys. Subjects 131 toddlers (18-22 months) and their mothers were included (77 born preterm; 54 born full term). Outcome Measures Toddler emotion regulation, negative affect, and dyadic mutual enjoyment were coded from videotaped play. Results The association between maternal scaffolding and emotion regulation was different for dyads with a toddler born preterm versus full term, wherein the association was positive for toddlers born preterm and non-significant for toddlers born full term. Similarly, the association between maternal scaffolding and negative affect was different for the two groups: negative for toddlers born preterm and non-significant for toddlers born full term. Finally, the association between maternal scaffolding and mutual enjoyment was positive for toddlers born preterm and non-significant for toddlers born full term. Conclusions Our findings highlight early differences in mother-child interactive style correlates of children born preterm compared to those born full term. Maternal scaffolding behavior may be uniquely associated with emotion regulation and a positive dyadic encounter for toddlers born preterm. PMID:23773306

  1. Obesity in pregnancy: risks and management

    PubMed Central

    Fitzsimons, Kate J; Modder, Jo; Greer, Ian A

    2009-01-01

    Maternal obesity is now considered one of the most commonly occurring risk factors seen in obstetric practice. Compared with women with a healthy pre-pregnancy weight, women with obesity are at increased risk of miscarriage, gestational diabetes, preeclampsia, venous thromboembolism, induced labour, caesarean section, anaesthetic complications and wound infections, and they are less likely to initiate or maintain breastfeeding. Babies of obese mothers are at increased risk of stillbirth, congenital anomalies, prematurity, macrosomia and neonatal death. Intrauterine exposure to obesity is also associated with an increased risk of developing obesity and metabolic disorders in childhood. This article reviews the prevalence of obesity in pregnancy and the associated maternal and fetal complications. Recommendations and suggestions for pre-conception, antenatal and postnatal care of women with obesity are presented, and current research in the UK and future research priorities are considered. PMID:27582812

  2. The human obesity epidemic, the mismatch paradigm, and our modern "captive" environment.

    PubMed

    Power, Michael L

    2012-01-01

    In the distant past obesity in humans was rare and likely caused by metabolic dysregulation due to genetic or disease-related pathology. External factors precluded the ability of most people to overeat or under exert. Socio-cultural obesity came about due to the rareness of obesity and its difficulty to achieve. What is rare becomes valuable and what is difficult to achieve becomes a badge of prestige. The modern human obesity epidemic would appear to represent a third class of obesity: environmental obesity. Much like the captive environments which humans construct for the captive/companion animals in our care, the modern human environment has greatly decreased the challenges of life that would restrict food intake and enforce exertion. And like us, our captive/companion animal populations are also experiencing obesity epidemics. A further concern is that maternal obesity alters maternal signaling to offspring, in utero through the placenta and after birth through breast milk, in ways that perpetuate an enhanced vulnerability to obesity. Molecules such as leptin, produced by adipose tissue and placenta, have significant developmental effects on brain areas associated with feeding behavior. Leptin and other cytokines and growth factors are found in breast milk. These molecules have positive effects on gut maturation; their effects on metabolism and brain development are unclear. Placenta and brain also are hotspots for epigenetic regulation, and epigenetic changes may play significant roles in the later vulnerability to obesity and to the development of a diverse array of diseases, including heart disease, hypertension, and noninsulin-dependent diabetes. Copyright © 2012 Wiley Periodicals, Inc.

  3. Developmental origins of infant emotion regulation: Mediation by temperamental negativity and moderation by maternal sensitivity.

    PubMed

    Thomas, Jenna C; Letourneau, Nicole; Campbell, Tavis S; Tomfohr-Madsen, Lianne; Giesbrecht, Gerald F

    2017-04-01

    Emotion regulation is essential to cognitive, social, and emotional development and difficulties with emotion regulation portend future socioemotional, academic, and behavioral difficulties. There is growing awareness that many developmental outcomes previously thought to begin their development in the postnatal period have their origins in the prenatal period. Thus, there is a need to integrate evidence of prenatal influences within established postnatal factors, such as infant temperament and maternal sensitivity. In the current study, prenatal depression, pregnancy anxiety, and diurnal cortisol patterns (i.e., the cortisol awakening response (CAR) and diurnal slope) were assessed in 254 relatively low-risk mother-infant pairs (primarily White, middle-class) in early (M = 15 weeks) and late pregnancy (M = 33 weeks). Mothers reported on infant temperamental negativity (Infant Behavior Questionnaire-Revised) at 3 months. At 6 months, maternal sensitivity (Parent Child Interaction Teaching Scale) and infant emotion regulation behavior (Laboratory Temperament Assessment Battery) were assessed. Greater pregnancy anxiety in early pregnancy and a blunted CAR in late pregnancy predicted higher infant temperamental negativity at 3 months, and those infants with higher temperamental negativity used fewer attentional regulation strategies and more avoidance (i.e., escape behavior) at 6 months. Furthermore, this indirect effect was moderated by maternal sensitivity whereby infants with elevated negativity demonstrated maladaptive emotion regulation at below average levels of maternal sensitivity. These findings suggest that the development of infant emotion regulation is influenced by the ways that prenatal exposures shape infant temperament and is further modified by postnatal caregiving. (PsycINFO Database Record (c) 2017 APA, all rights reserved).

  4. Effects of early maternal distress and parenting on the development of children's self-regulation and externalizing behavior.

    PubMed

    Choe, Daniel Ewon; Olson, Sheryl L; Sameroff, Arnold J

    2013-05-01

    Emotional distress experienced by mothers increases young children's risk of externalizing problems through suboptimal parenting and child self-regulation. An integrative structural equation model tested hypotheses that mothers' parenting (i.e., low levels of inductive discipline and maternal warmth) would mediate adverse effects of early maternal distress on child effortful control, which in turn would mediate effects of maternal parenting on child externalizing behavior. This longitudinal study spanning ages 3, 6, and 10 included 241 children, mothers, and a subset of teachers. The hypothesized model was partially supported. Elevated maternal distress was associated with less inductive discipline and maternal warmth, which in turn were associated with less effortful control at age 3 but not at age 6. Inductive discipline and maternal warmth mediated adverse effects of maternal distress on children's effortful control. Less effortful control at ages 3 and 6 predicted smaller relative decreases in externalizing behavior at 6 and 10, respectively. Effortful control mediated effects of inductive discipline, but not maternal warmth, on externalizing behavior. Findings suggest elevated maternal distress increases children's risk of externalizing problems by compromising early parenting and child self-regulation.

  5. Parent-Child Interaction, Self-Regulation, and Obesity Prevention in Early Childhood.

    PubMed

    Anderson, Sarah E; Keim, Sarah A

    2016-06-01

    This paper describes the epidemiologic evidence linking parent-child relationships, self-regulation, and weight status with a focus on early childhood. The emotional quality of parent-child interactions may influence children's risk for obesity through multiple pathways. Prospective studies linking observer ratings of young children's self-regulation, particularly inhibitory control, to future weight status are discussed. Although findings are preliminary, promoting positive relationships between parents/caregivers and young children holds promise as a component of efforts to prevent childhood obesity. Multi-disciplinary collaborations between researchers with training in developmental science and child health should be encouraged.

  6. Self- and Co-regulation of Anger and Fear in Preschoolers with Autism Spectrum Disorders: The Role of Maternal Parenting Style and Temperament.

    PubMed

    Hirschler-Guttenberg, Yael; Feldman, Ruth; Ostfeld-Etzion, Sharon; Laor, Nathaniel; Golan, Ofer

    2015-09-01

    Emotion regulation (ER) difficulties are a major concern in children with autism spectrum disorder (ASD). Maternal temperament and parenting style have significant effects on children's ER. However, these effects have not been studied in children with ASD. Forty preschoolers with ASD and their mothers and forty matched controls engaged in fear and anger ER paradigms, micro-coded for child self- and co-regulatory behaviors and parent's regulation-facilitation. Mothers' parenting style and temperament were self-reported. In the ASD group only, maternal authoritarian style predicted higher self-regulation and lower co-regulation of anger and maternal authoritative style predicted higher self-regulation of fear. Maternal temperament did not predict child's ER. Findings emphasize the importance of maternal flexible parenting style in facilitating ER among children with ASD.

  7. An Evaluation of the Implementation of Maternal Obesity Pathways of Care: A Mixed Methods Study with Data Integration

    PubMed Central

    Heslehurst, Nicola; Dinsdale, Sarah; Sedgewick, Gillian; Simpson, Helen; Sen, Seema; Summerbell, Carolyn Dawn; Rankin, Judith

    2015-01-01

    Objectives Maternal obesity has multiple associated risks and requires substantial intervention. This research evaluated the implementation of maternal obesity care pathways from multiple stakeholder perspectives. Study Design A simultaneous mixed methods model with data integration was used. Three component studies were given equal priority. 1: Semi-structured qualitative interviews explored obese pregnant women’s experiences of being on the pathways. 2: A quantitative and qualitative postal survey explored healthcare professionals’ experiences of delivering the pathways. 3: A case note audit quantitatively assessed pathway compliance. Data were integrated using following a thread and convergence coding matrix methods to search for agreement and disagreement between studies. Results Study 1: Four themes were identified: women’s overall (positive and negative) views of the pathways; knowledge and understanding of the pathways; views on clinical and weight management advice and support; and views on the information leaflet. Key results included positive views of receiving additional clinical care, negative experiences of risk communication, and weight management support was considered a priority. Study 2: Healthcare professionals felt the pathways were worthwhile, facilitated good practice, and increased confidence. Training was consistently identified as being required. Healthcare professionals predominantly focussed on women’s response to sensitive obesity communication. Study 3: There was good compliance with antenatal clinical interventions. However, there was poor compliance with public health and postnatal interventions. There were some strong areas of agreement between component studies which can inform future development of the pathways. However, disagreement between studies included a lack of shared priorities between healthcare professionals and women, different perspectives on communication issues, and different perspectives on women

  8. Up-regulation of aldolase A and methylglyoxal production in adipocytes.

    PubMed

    Liu, Jianghai; Desai, Kaushik; Wang, Rui; Wu, Lingyun

    2013-04-01

    We previously reported that up-regulation of aldolase B, a key enzyme in fructose metabolism, was mainly responsible for vascular methylglyoxal (MG) overproduction under different pathological conditions. Here we investigated whether aldolase A, an enzyme of the glycolytic pathway, also caused MG overproduction in insulin-sensitive adipocytes. The relative contributions of different metabolic pathways or enzymes to MG generation were evaluated in cultured 3T3-L1 adipocytes. Glucose (25 mM) had no effect on aldolase A gene expression, but insulin (100 nM) up-regulated aldolase A mRNA and protein levels in the absence or presence of 25 mM glucose in adipocytes. Treatment with insulin increased levels of basal or glucose (25 mM)-induced MG and glucose 6-phosphate. However, insulin, glucose (25 mM) or their combination had no effect on cellular levels of sorbitol and fructose, but down-regulated gene expression of aldolase B to a similar extent, when compared with the control group. Incubation of 3T3-L1 adipocytes with fructose, acetone, acetol, threonine or glycine (25 mM), with or without insulin did not alter cellular MG levels. The elevated MG levels induced by insulin, glucose (25 mM) or their combination in adipocytes was completely reduced by siRNA knock down of aldolase A or application of 2-deoxy-D-glucose (a non-specific inhibitor of glucose uptake and glycolysis), but not by knock down of aldolase B. Insulin enhanced MG overproduction in insulin-sensitive adipocytes by up-regulating aldolase A, a mechanism that could be involved in the development of insulin resistance and obesity. © 2012 The Authors. British Journal of Pharmacology © 2012 The British Pharmacological Society.

  9. Modification of the fatty acid composition of an obesogenic diet improves the maternal and placental metabolic environment in obese pregnant mice.

    PubMed

    Gimpfl, Martina; Rozman, Jan; Dahlhoff, Maik; Kübeck, Raphaela; Blutke, Andreas; Rathkolb, Birgit; Klingenspor, Martin; Hrabě de Angelis, Martin; Öner-Sieben, Soner; Seibt, Annette; Roscher, Adelbert A; Wolf, Eckhard; Ensenauer, Regina

    2017-06-01

    Peri-conceptional exposure to maternal obesogenic nutrition is associated with in utero programming of later-life overweight and metabolic disease in the offspring. We aimed to investigate whether dietary intervention with a modified fatty acid quality in an obesogenic high-calorie (HC) diet during the preconception and gestational phases can improve unfavourable effects of an adipogenic maternal environment. In NMRI mice, peri-conceptional and gestational obesity was induced by feeding a HC diet (controls), and they were compared with dams on a fat-modified (Fat-mod) HC diet of the same energy content but enriched with medium-chain fatty acids (MCFAs) and adjusted to a decreased ratio of n-6 to n-3 long-chain polyunsaturated fatty acids (LC-PUFAs). Effects on maternal and placental outcomes at delivery (day 17.5 post coitum) were investigated. Despite comparable energy assimilation between the two groups of dams, the altered fatty acid composition of the Fat-mod HC diet induced lower maternal body weight, weights of fat depots, adipocyte size, and hepatic fat accumulation compared to the unmodified HC diet group. Further, there was a trend towards lower fasting glucose, insulin and leptin concentrations in dams fed the Fat-mod HC diet. Phenotypic changes were accompanied by inhibition of transcript and protein expression of genes involved in hepatic de novo lipogenesis comprising PPARG2 and its target genes Fasn, Acaca, and Fabp4, whereas regulation of other lipogenic factors (Srebf1, Nr1h3, Abca1) appeared to be more complex. The modified diet led to a sex-specific placental response by upregulating PPARG-dependent fatty acid transport gene expression in female versus male placentae. Qualitative modification of the fatty acid spectrum of a high-energy maternal diet, using a combination of both MCFAs and n-3 LC-PUFAs, seems to be a promising interventional approach to ameliorate the adipogenic milieu of mice before and during gestation. Copyright © 2017 Elsevier

  10. Effect of African- and European-American maternal attitudes and limit-setting strategies on children's self-regulation.

    PubMed

    LeCuyer, Elizabeth A; Swanson, Dena P; Cole, Robert; Kitzman, Harriet

    2011-12-01

    The effect of maternal attitudes and limit-setting strategies on children's self-regulation (measured as committed compliance) was compared in 151 African-American (AA) and 108 European-American (EA) mothers and their 3-year-old children. There were no ethnic differences in children's compliance, however ethnicity moderated the relationship between maternal authoritarian attitudes and children's compliance. Higher authoritarian attitudes predicted less children's compliance in the EA sample, but greater compliance in the AA sample. Observational limit-setting data revealed that in both ethnic groups, maternal authoritarian attitudes influenced children's self-regulation through maternal use of lower-power (gentle) verbal strategies, fewer physical strategies, and judicious use of higher-power verbal strategies. The findings indicate that the meaning and purpose of authoritarian attitudes varies across these mothers' socio-cultural contexts. Copyright © 2011 Wiley Periodicals, Inc.

  11. Prenatal programming of childhood overweight and obesity.

    PubMed

    Huang, Jennifer S; Lee, Tiffany A; Lu, Michael C

    2007-09-01

    To review the scientific evidence for prenatal programming of childhood overweight and obesity, and discuss its implications for MCH research, practice, and policy. A systematic review of observational studies examining the relationship between prenatal exposures and childhood overweight and obesity was conducted using MOOSE guidelines. The review included literature posted on PubMed and MDConsult and published between January 1975 and December 2005. Prenatal exposures to maternal diabetes, malnutrition, and cigarette smoking were examined, and primary study outcome was childhood overweight or obesity as measured by body mass index (BMI) for children ages 5 to 21. Four of six included studies of prenatal exposure to maternal diabetes found higher prevalence of childhood overweight or obesity among offspring of diabetic mothers, with the highest quality study reporting an odds ratio of adolescent overweight of 1.4 (95% CI 1.0-1.9). The Dutch famine study found that exposure to maternal malnutrition in early, but not late, gestation was associated with increased odds of childhood obesity (OR 1.9, 95% CI 1.5-2.4). All eight included studies of prenatal exposure to maternal smoking showed significantly increased odds of childhood overweight and obesity, with most odds ratios clustering around 1.5 to 2.0. The biological mechanisms mediating these relationships are unknown but may be partially related to programming of insulin, leptin, and glucocorticoid resistance in utero. Our review supports prenatal programming of childhood overweight and obesity. MCH research, practice, and policy need to consider the prenatal period a window of opportunity for obesity prevention.

  12. Predictors of Severe Obesity in Low-Income, Predominantly Hispanic/Latino Children: The Texas Childhood Obesity Research Demonstration Study

    PubMed Central

    Pérez, Adriana; Ranjit, Nalini; Kelder, Steven H.; Barlow, Sarah E.; Pont, Stephen J.; Butte, Nancy F.; Hoelscher, Deanna M.

    2017-01-01

    Introduction The objective of this study was to identify predictors of severe obesity in a low-income, predominantly Hispanic/Latino sample of children in Texas. Methods This cross-sectional analysis examined baseline data on 517 children from the secondary prevention component of the Texas Childhood Obesity Research Demonstration (TX CORD) study; data were collected from September 2012 through February 2014. Self-administered surveys were used to collect data from parents of children who were aged 2 to 12 years, had a body mass index (BMI) in the 85th percentile or higher, and resided in Austin, Texas, or Houston, Texas. Multivariable logistic regression models adjusted for sociodemographic covariates were used to examine associations of children’s early-life and maternal factors (large-for-gestational-age, exclusive breastfeeding for ≥4 months, maternal severe obesity [BMI ≥35.0 kg/m2]) and children’s behavioral factors (fruit and vegetable consumption, physical activity, screen time) with severe obesity (BMI ≥120% of 95th percentile), by age group (2–5 y, 6–8 y, and 9–12 y). Results Across all ages, 184 (35.6%) children had severe obesity. Among children aged 9 to 12 years, large-for-gestational-age at birth (odds ratio [OR] = 2.31; 95% confidence interval [CI], 1.13–4.73) was significantly associated with severe obesity. Maternal severe obesity was significantly associated with severe obesity among children aged 2 to 5 years (OR = 2.67; 95% CI, 1.10–6.47) and 9 to 12 years (OR = 4.12; 95% CI, 1.84–9.23). No significant association was observed between behavioral factors and severe obesity in any age group. Conclusion In this low-income, predominantly Hispanic/Latino sample of children, large-for-gestational-age and maternal severe obesity were risk factors for severe obesity among children in certain age groups. Promoting healthy lifestyle practices during preconception and prenatal periods could be an important intervention strategy for

  13. Maternal High-Fat Diet Programming of the Neuroendocrine System and Behavior

    PubMed Central

    Sullivan, Elinor L.; Riper, Kellie M.; Lockard, Rachel; Valleau, Jeanette C.

    2015-01-01

    Maternal obesity, metabolic state, and diet during gestation have profound effects on offspring development. The prevalence of neurodevelopmental and mental health disorders has risen rapidly in the last several decades in parallel with the rise in obesity rates. Evidence from epidemiological studies indicates that maternal obesity and metabolic complications increase the risk of offspring developing behavioral disorders such as attention deficit hyperactivity disorder (ADHD), autism spectrum disorders (ASD), and schizophrenia. Animal models show that a maternal diet high in fat similarly disrupts behavioral programming of offspring, with animals showing social impairments, increased anxiety and depressive behaviors, reduced cognitive development, and hyperactivity. Maternal obesity, metabolic conditions, and high fat diet consumption increase maternal leptin, insulin, glucose, triglycerides, and inflammatory cytokines. This leads to increased risk of placental dysfunction, and altered fetal neuroendocrine development. Changes in brain development that likely contribute to the increased risk of behavioral and mental health disorders include increased inflammation in the brain, as well as alterations in the serotonergic system, dopaminergic system and hypothalamic pituitary adrenal (HPA) axis. PMID:25913366

  14. Maternal and neonatal outcomes among obese women with weight gain below the new Institute of Medicine recommendations.

    PubMed

    Blomberg, Marie

    2011-05-01

    To estimate whether weight loss or low gestational weight gain in class I-III obese women is associated with adverse maternal and neonatal outcomes compared with gestational weight gain within the new Institute of Medicine recommendations. This was a population-based cohort study, which included 32,991 obesity class I, 10,068 obesity class II, and 3,536 obesity class III women who were divided into four gestational weight gain categories. Women with low (0-4.9 kg) or no gestational weight gain were compared with women gaining the recommended 5-9 kg concerning obstetric and neonatal outcome after suitable adjustments. Women in obesity class III who lost weight during pregnancy had a decreased risk of cesarean delivery (24.4%; odds ratio [OR] 0.77, 95% confidence interval [CI] 0.60-0.99), large-for-gestational-age births (11.2%, OR 0.64, 95% CI 0.46-0.90), and no significantly increased risk for pre-eclampsia, excessive bleeding during delivery, instrumental delivery, low Apgar score, or fetal distress compared with obese (class III) women gaining within the Institute of Medicine recommendations. There was an increased risk for small for gestational age, 3.7% (OR 2.34, 95% CI 1.15-4.76) among women in obesity class III losing weight, but there was no significantly increased risk of small for gestational age in the same group with low weight gain. Obese women (class II and III) who lose weight during pregnancy seem to have a decreased or unaffected risk for cesarean delivery, large for gestational age, pre-eclampsia, excessive postpartum bleeding, instrumental delivery, low Apgar score, and fetal distress. The twofold increased risk of small for gestational age in obesity class III and weight loss (3.7%) is slightly above the overall prevalence of small-for-gestational-age births in Sweden (3.6%).

  15. The effect of maternal obesity on pregnancy outcomes of women with gestational diabetes controlled with diet only, glyburide, or insulin.

    PubMed

    Joy, Saju; Roman, Ashley; Istwan, Niki; Rhea, Debbie; Desch, Cheryl; Stanziano, Gary; Saltzman, Daniel

    2012-09-01

    To examine the effect of obesity on maternal and neonatal outcomes in women diagnosed with gestational diabetes mellitus (GDM) and managed with diet only, glyburide, or insulin. Women with singleton gestations enrolled for outpatient services diagnosed with GDM and without history of pregnancy-related hypertension at enrollment or in a prior pregnancy were identified in a database. Women with GDM controlled by diet only (n = 3918), glyburide (n = 873), or insulin without prior exposure to oral hypoglycemic agents (n = 2229) were included. Pregnancy outcomes were compared for obese versus nonobese women within each treatment group and also compared across treatment groups within the obese and nonobese populations. Within each treatment group, obesity was associated with higher rates of cesarean delivery, pregnancy-related hypertension, macrosomia, and hyperbilirubinemia (all p < 0.05). Higher rates of pregnancy-related hypertension and hyperbilirubinemia were observed in women receiving glyburide. Obesity adversely affects pregnancy outcome in women with GDM. Higher rates of pregnancy-related hypertension and hyperbilirubinemia were observed in pregnant women receiving glyburide. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

  16. Maternal obesity induces fibrosis in fetal myocardium of sheep

    PubMed Central

    Huang, Yan; Yan, Xu; Zhao, Jun X.; Zhu, Mei J.; McCormick, Richard J.; Ford, Stephen P.; Nathanielsz, Peter W.; Ren, Jun

    2010-01-01

    Maternal obesity (MO) has harmful effects on both fetal development and subsequent offspring health. The impact of MO on fetal myocardium development has received little attention. Fibrogenesis is regulated by the transforming growth factor-β (TGF-β)/p38 signaling pathway. Using the well-established model of MO in pregnant sheep, we evaluated the effect of MO on TGF-β/p38 and collagen accumulation in fetal myocardium. Nonpregnant ewes were assigned to a control diet [Con, fed 100% of National Research Council (NRC) nutrient recommendations] or obesogenic diet (OB, fed 150% of NRC recommendations) from 60 days before conception. Fetal ventricular muscle was sampled at 75 and 135 days of gestation (dG). At 75 dG, the expression of precursor TGF-β was 39.9 ± 9.9% higher (P < 0.05) in OB than Con fetal myocardium, consistent with the higher content of phosphorylated Smad3 in OB myocardium. The phosphorylation of p38 tended to be higher in OB myocardium (P = 0.08). In addition, enhanced Smad complexes were bound to Smad-binding elements in 75 dG OB fetal myocardium measured by DNA mobility shift assay (130.2 ± 26.0% higher, P < 0.05). Similar elevation of TGF-β signaling was observed in OB fetal myocardium at 135 dG. Total collagen concentration in OB was greater than Con fetal myocardium (2.42 ± 0.16 vs. 1.87 ± 0.04%, P < 0.05). Matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-3 were higher in the Con group compared with OB sheep (43.86 ± 16.01 and 37.23 ± 7.97% respectively, P < 0.05). In summary, MO results in greater fetal heart connective tissue accumulation associated with an upregulated TGF-β/p38 signaling pathway at late gestation; such changes would be expected to negatively impact offspring heart function. PMID:20876759

  17. Women's safety alerts in maternity care: is speaking up enough?

    PubMed

    Rance, Susanna; McCourt, Christine; Rayment, Juliet; Mackintosh, Nicola; Carter, Wendy; Watson, Kylie; Sandall, Jane

    2013-04-01

    Patients' contributions to safety include speaking up about their perceptions of being at risk. Previous studies have found that dismissive responses from staff discouraged patients from speaking up. A Care Quality Commission investigation of a maternity service where serious incidents occurred found evidence that women had routinely been ignored and left alone in labour. Women using antenatal services hesitated to raise concerns that they felt staff might consider irrelevant. The Birthplace in England programme, which investigated the quality and safety of different places of birth for 'low-risk' women, included a qualitative organisational case study in four NHS Trusts. The authors collected documentary, observational and interview data from March to December 2010 including interviews with 58 postnatal women. A framework approach was combined with inductive analysis using NVivo8 software. Speaking up, defined as insistent and vehement communication when faced with failure by staff to listen and respond, was an unexpected finding mentioned in half the women's interviews. Fourteen women reported raising alerts about safety issues they felt to be urgent. The presence of a partner or relative was a facilitating factor for speaking up. Several women described distress and harm that ensued from staff failing to listen. Women are speaking up, but this is not enough: organisation-focused efforts are required to improve staff response. Further research is needed in maternity services and in acute and general healthcare on the effectiveness of safety-promoting interventions, including real-time patient feedback, patient toolkits and patient-activated rapid response calls.

  18. Prepregnancy obesity and pregnancy outcome.

    PubMed

    Ahmed, Salah R; Ellah, Mostafa A A; Mohamed, Osman A; Eid, Hesham M

    2009-07-01

    Maternal obesity has long been correlated with an increased risk of chronic hypertension and diabetes prior to pregnancy and adverse pregnancy outcomes including preeclampsia, gestational diabetes, fetal macrosomia, Cesarean deliveries, postpartum endometritis and a prolonged hospital stay To determine the effect of maternal pre-pregnancy obesity on pregnancy outcomes Methods: One hundred and twenty two women were recruited in the study. The patients were allocated into two groups, group 1 obese patients (68) BMI 30 or more and group 2 non obese patients (54) BMI between 19.8-24.9. About two - third of the study group were having mild obesity, moderate obesity comprised about 28% and about 4% only was morbidly obese. Hypertensive disorders were nine folds more among obese women (R.R 4.74). Obese pregnant women were significantly more prone to have gestational diabetes (R.R 6.35). Even anemia was significantly more amongst Obese women when compared to non obese ones (29/68, R.R 3.84). Ante partum hemorrhage had significantly more in obese women (R.R 3.14). There was no increased risk for PROM (R.R 0.71). Moreover The macrosomic babies were extremely commoner among obese (R.R 9.1). Pre-pregnancy obesity is a risk factor for gestational diabetes, preeclampsia, labor induction, cesarean section for fetal distress, and wound infection. They should be considered as high risk and counseled accordingly.

  19. Oxytocin Augmentation in Spontaneously Laboring, Nulliparous Women: Multilevel Assessment of Maternal BMI and Oxytocin Dose

    PubMed Central

    Carlson, Nicole S.; Corwin, Elizabeth J.; Lowe, Nancy K.

    2017-01-01

    Background Synthetic oxytocin, the primary tool for labor augmentation, is less effective among obese women, leading to more unplanned cesarean deliveries for slow labor progress. It is not known if obese women require higher doses of oxytocin due to maternal, fetal, or labor factors related to maternal obesity. Objectives This study had two main objectives: 1) Examine the influence of maternal body mass index (BMI) on hourly doses of oxytocin from augmentation initiation until vaginal delivery in obese women; and 2) Examine the influence of other maternal, fetal, and labor factors on hourly doses of oxytocin in obese women. Study design Longitudinal study of a cohort (N = 136) of healthy, nulliparous, spontaneously laboring obese women (BMI ≥ 30 kg/m2) who received oxytocin augmentation and achieved vaginal delivery. We performed iterative multilevel analyses to examine the influence of maternal BMI and other factors on hourly oxytocin doses. Results Maternal BMI explained 16.56% (95% CI [13.7-20.04], p < 0.001) of the variance in hourly oxytocin doses received in a multilevel model controlling for influence of maternal, fetal, and labor characteristics. Maternal age, gestational age, status of amniotic membranes at hospital admission, and admission cervical dilation examination were not significant; however, neonatal birthweight and cervical dilation at oxytocin initiation were significant predictors of hourly oxytocin dose in these women (p < 0.001). Conclusions Even when parturition preparation has progressed adequately for spontaneous labor initiation, there still may be some obesity-related blunting of myometrial contractility and response to oxytocin used for augmentation. PMID:28347147

  20. Oxytocin Augmentation in Spontaneously Laboring, Nulliparous Women: Multilevel Assessment of Maternal BMI and Oxytocin Dose.

    PubMed

    Carlson, Nicole S; Corwin, Elizabeth J; Lowe, Nancy K

    2017-07-01

    Synthetic oxytocin, the primary tool for labor augmentation, is less effective among obese women, leading to more unplanned cesarean deliveries for slow labor progress. It is not known if obese women require higher doses of oxytocin due to maternal, fetal, or labor factors related to maternal obesity. This study had two main objectives: (1) examine the influence of maternal body mass index (BMI) on hourly doses of oxytocin from augmentation initiation until vaginal delivery in obese women; and (2) examine the influence of other maternal, fetal, and labor factors on hourly doses of oxytocin in obese women. Longitudinal study of a cohort ( N = 136) of healthy, nulliparous, spontaneously laboring obese women (BMI ≥ 30 kg/m 2 ) who received oxytocin augmentation and achieved vaginal delivery. We performed iterative multilevel analyses to examine the influence of maternal BMI and other factors on hourly oxytocin doses. Maternal BMI explained 16.56% (95% confidence interval [CI] = [13.7, 20.04], p < .001) of the variance in hourly oxytocin doses received in a multilevel model controlling for influence of maternal, fetal, and labor characteristics. Maternal age, gestational age, status of amniotic membranes at hospital admission, and admission cervical dilation examination were not significant; however, neonatal birthweight and cervical dilation at oxytocin initiation were significant predictors of hourly oxytocin dose in these women ( p < .001). Even when parturition preparation has progressed adequately for spontaneous labor initiation, there still may be some obesity-related blunting of myometrial contractility and response to oxytocin used for augmentation.

  1. The role of sustained attention, maternal sensitivity, and infant temperament in the development of early self-regulation.

    PubMed

    Frick, Matilda A; Forslund, Tommie; Fransson, Mari; Johansson, Maria; Bohlin, Gunilla; Brocki, Karin C

    2018-05-01

    This study investigated infant predictors of early cognitive and emotional self-regulation from an intrinsic and caregiving environmental perspective. Sustained attention, reactive aspects of infant temperament, and maternal sensitivity were assessed at 10 months (n = 124) and early self-regulation (including executive functions, EF, and emotion regulation) was assessed at 18 months. The results indicated that sustained attention predicted early EF, which provide empirical support for the hierarchical framework of EF development, advocating early attention as a foundation for the development of cognitive self-regulation. Maternal sensitivity and surgency predicted emotion regulation, in that infants of sensitive mothers showed more regulatory behaviours and a longer latency to distress, whereas high levels of surgency predicted low emotion regulation, suggesting both the caregiving environment and temperament as important in the development of self-regulation. Interaction effects suggested high sustained attention to be a protective factor for children of insensitive mothers, in relation to emotion regulation. In addition, high levels of maternal sensitivity seemed to foster development of emotion regulation among children with low to medium levels of sustained attention and/or surgency. In all, our findings point to the importance of both intrinsic and extrinsic factors in infant development of self-regulation. © 2017 The British Psychological Society.

  2. Childhood obesity: Current and novel approaches.

    PubMed

    Sabin, Matthew A; Kiess, Wieland

    2015-06-01

    The prevalence of childhood obesity has increased over the last fifty years by approximately 5% per decade, and approximately a quarter of all children are now either overweight or obese. These children have a significantly increased risk of many future health problems including adult obesity, type 2 diabetes and heart disease. Despite this relentless increase, common-sense approaches aimed at prevention and treatment have failed to solve the problem. Current approaches at prevention have faced major challenges with some progress in implementing smaller scale programs and social marketing, but little action on broad public policy approaches which often appears unpalatable to society or individual governments. Meanwhile, treatment approaches have mainly focused on lifestyle change, and novel approaches are urgently needed. Prevention needs to shift to improving maternal health prior to conception, with more research focussed on the impact of early years in programming offspring to future overweight/obesity. Likewise, treatment paradigms need to move from simply thinking that obesity can be solved by readdressing diet and activity levels. Novel approaches are needed which take into consideration the complex physiology which regulates early childhood growth and the development of obesity in susceptible individuals. Copyright © 2015 Elsevier Ltd. All rights reserved.

  3. Maternal pre-gravid body mass index and adiposity influence umbilical cord gene expression at term in AGA infants

    USDA-ARS?s Scientific Manuscript database

    While maternal obesity is associated with unfavorable maternal and fetal outcomes, the influence of maternal obesity on fetal gene expression is less clear. Umbilical cords (UC) from 12 lean (pre-gravid BMI < 25) and 10 overweight/obese (OB, pre-gravid BMI =25) women without gestational diabetes wer...

  4. New evaluations of redox regulating system in adipose tissue of obesity.

    PubMed

    Park, Jiyoung; Chung, Jun-Jae; Kim, Jae Bum

    2007-09-01

    During the past several decades, the incidence of obesity has significantly increased worldwide. Enormous efforts have been devoted to understanding the molecular mechanisms underlying obesity and its related metabolic disorders such as type 2 diabetes, cardiovascular disease, atherosclerosis, and hypertension. It is now well-established that altered adipocyte metabolism in obese patients is closely associated with the induction of various metabolic stresses including hyperglycemia, hyperlipidemia, hyperinsulinemia, and chronic inflammation. However, the cellular factor(s) which sense metabolic changes and/or initiate the pathological progression of obesity-induced metabolic disorders remain to be elucidated. In this review, we will discuss the possible roles of cellular NADP(+)/NADPH, which function as redox potential regulators, in the induction of obesity-associated oxidative stress, chronic inflammation, and insulin resistance and suggest G6PD, a NADPH-generating enzyme, as a novel target for treating metabolic disorders.

  5. Maternal Diet, Metabolic State, and Inflammatory Response Exert Unique and Long-Lasting Influences on Offspring Behavior in Non-Human Primates

    PubMed Central

    Thompson, Jacqueline R.; Gustafsson, Hanna C.; DeCapo, Madison; Takahashi, Diana L.; Bagley, Jennifer L.; Dean, Tyler A.; Kievit, Paul; Fair, Damien A.; Sullivan, Elinor L.

    2018-01-01

    Nutritional status influences brain health and gestational exposure to metabolic disorders (e.g. obesity and diabetes) increases the risk of neuropsychiatric disorders. The aim of the present study was to further investigate the role of maternal Western-style diet (WSD), metabolic state, and inflammatory factors in the programming of Japanese macaque offspring behavior. Utilizing structural equation modeling, we investigated the relationships between maternal diet, prepregnancy adiposity, third trimester insulin response, and plasma cytokine levels on 11-month-old offspring behavior. Maternal WSD was associated with greater reactive and ritualized anxiety in offspring. Maternal adiposity and third trimester macrophage-derived chemokine (MDC) exerted opposing effects on offspring high-energy outbursts. Elevated levels of this behavior were associated with low maternal MDC and increased prepregnancy adiposity. This is the first study to show that maternal MDC levels influence offspring behavior. We found no evidence suggesting maternal peripheral inflammatory response mediated the effect of maternal diet and metabolic state on aberrant offspring behavior. Additionally, the extent of maternal metabolic impairment differentially influenced chemokine response. Elevated prepregnancy adiposity suppressed third trimester chemokines, while obesity-induced insulin resistance augmented peripheral chemokine levels. WSD also directly increased maternal interleukin-12. This is the first non-human primate study to delineate the effects of maternal diet and metabolic state on gestational inflammatory environment and subsequent offspring behavior. Our findings give insight to the complex mechanisms by which diet, metabolic state, and inflammation during pregnancy exert unique influences on offspring behavioral regulation. PMID:29740395

  6. Preclinical evidence for the addiction potential of highly palatable foods: Current developments related to maternal influence.

    PubMed

    Wiss, David A; Criscitelli, Kristen; Gold, Mark; Avena, Nicole

    2017-08-01

    It is well established that obesity has reached pandemic proportions. Over the last four decades the prevalence of obesity and morbid obesity have risen substantially in both men and women worldwide. Although there are many causative factors leading to excessive weight gain including genetics and sedentary lifestyle, the transformation of the food environment has undoubtedly contributed to the dangerously high rates of obesity. The current food landscape is inundated with food engineered to contain artificially high levels of sugar and fat. Overconsumption of these types of food overrides the homeostatic mechanisms, which under normal circumstances regulate appetite and body mass, leading to hedonic eating. Evidence from the animal literature has illustrated nutrition-influenced perturbations that occur within the mesolimbic dopamine pathway, as well as maladaptive behavioral responses that result from chronic ingestion of highly palatable foods. These neurobehavioral adaptations are similar to what is observed in drugs of abuse. Recent evidence also supports that maternal exposure to these foods is capable of provoking neurobehavioral alterations in offspring. Therefore the purpose of this review is to summarize the current developments on the addictive potential of highly palatable foods, as well as illuminate the impact of maternal hyperphagia and obesity on the reward-related neurocircuitry and addiction-like behaviors in the offspring. Published by Elsevier Ltd.

  7. Emerging effortful control in toddlerhood: the role of infant orienting/regulation, maternal effortful control, and maternal time spent in caregiving activities.

    PubMed

    Bridgett, David J; Gartstein, Maria A; Putnam, Samuel P; Lance, Kate Oddi; Iddins, Erin; Waits, Robin; Vanvleet, Jessica; Lee, Lindsay

    2011-02-01

    Latent growth modeling (LGM) was used to examine the contribution of changes in infant orienting/regulation (O/R) to the emergence of toddler effortful control (EC), the contributions of maternal EC to the development of infant O/R and the emergence of toddler EC, the influence of maternal time spent in caregiving activities on toddler EC and the slope of infant O/R, and the contribution of maternal EC to subsequent maternal time spent in caregiving activities. Mothers from 158 families completed a self-report measure of EC when their infants were 4 months of age, a measure of infant O/R when their infants were 4, 6, 8, 10, and 12 months of age, and a measure of toddler EC when their children reached 18 months of age. Information concerning maternal time spent in various interactive caregiving activities was collected when infants were 6 months old. Results indicated higher maternal EC predicted interindividual differences in the intercept (i.e., higher intercepts), but not slope, of infant O/R and that higher maternal EC, higher infant O/R intercept, and higher infant O/R slope contributed to higher toddler EC. Furthermore, higher maternal EC predicted greater maternal time spent in interactive caregiving activities with their infants and greater maternal time in interactive caregiving with infants also contributed to higher toddler EC after controlling for maternal EC. These findings contribute to the understanding of the influence of maternal EC, directly and through caregiving, on toddler EC. Additional implications as they are related to early developing regulatory aspects of temperament are discussed. Copyright © 2010 Elsevier Inc. All rights reserved.

  8. Children's Emotion Regulation Difficulties Mediate the Association Between Maternal Borderline and Antisocial Symptoms and Youth Behavior Problems Over 1 Year.

    PubMed

    Kaufman, Erin A; Puzia, Megan E; Mead, Hilary K; Crowell, Sheila E; McEachern, Amber; Beauchaine, Theodore P

    2017-04-01

    Borderline personality disorder (BPD) and antisocial personality disorder (ASPD) are among the most debilitating psychiatric conditions. Behaviors and traits associated with these disorders can have profound influences on those surrounding the affected individual. Accordingly, researchers have begun to examine effects of these symptoms on parent-child relationships. Theoretical and empirical work suggests that one mechanism linking maternal psychopathology to child symptoms is familial transmission of emotion dysregulation. The authors examined children's emotion regulation difficulties as a mediator between maternal BPD/ASPD symptoms and child behavior problems 1 year later. Analyses revealed that a composite of maternal BPD/ASPD symptoms had a direct effect on child internalizing, externalizing, and total symptoms. Associations between maternal BPD/ASPD symptoms and youth problems were partially mediated by child emotion regulation difficulties, even with maternal depression and other relevant covariates included in the models. Thus, maternal BPD/ASPD symptoms and child emotion regulation difficulties represent potential targets for prevention of psychopathology among youth.

  9. Evaluating Maternal and Child Health and Leadership Competencies of Emerging MCH Leaders: The MCHC/RISE-UP Experience.

    PubMed

    Belcher, Harolyn M E; Stone, Jacqueline D; McFadden, Jenese A; Hemmingson, Tyler A; Kreutzer, Cary; Harris, Lisa G; Wheeler, Barbara Y; Van Osdel, Joanne; Avila, Margaret; Yorker, Beatrice; Hoffman, Beth R; Turner-Musa, Jocelyn O

    2015-12-01

    This study examines maternal and child health core competencies and leadership characteristics of undergraduate students following participation in the Maternal and Child Health Careers/Research Initiatives for Student Enhancement-Undergraduate Program (MCHC/RISE-UP). MCHC/RISE-UP is a 10-week public health leadership program designed to promote diversity in public health workforce through mentored research, community engagement and advocacy, and clinical experiences for undergraduate students. The MCHC/RISE-UP is a national consortium of University Centers for Excellence in Developmental Disabilities including, (1) Kennedy Krieger Institute (Kennedy Krieger, lead institution) partnering with Morgan State University, a Historically Black University, (2) the University of South Dakota partnering with Tribal Serving Institutions; and (3) the University of Southern California Children's Hospital-Los Angeles and their partner institution, California State University Los Angeles, a Hispanic Serving Institution. Eighty-four junior and senior undergraduates and recent baccalaureate degree students who participated in the MCHC/RISE-UP worked on 48 maternal and child health projects. Following the MCHC/RISE-UP, students demonstrated statistically significant improvements in all maternal and child health core competencies. Transformational leadership characteristics also increased (mean increase 9.4, 95% CI 7.2-11.8; p < 0.001). At closing interview, over twice as many students endorsed a public health career goal compared to program admission (17.9 vs. 57.7%; p = 0.022). Multi-institutional collaborative public health leadership programs may extend the reach and recruitment of diverse students into the maternal and child health field. Experiential, didactic, and mentored learning opportunities may enhance student integration of maternal and child health competencies and transformational leadership characteristics.

  10. Links between Maternal and Child Psychopathology Symptoms: Mediation through Child Emotion Regulation and Moderation through Maternal Behavior

    ERIC Educational Resources Information Center

    Suveg, Cynthia; Shaffer, Anne; Morelen, Diana; Thomassin, Kristel

    2011-01-01

    This study examined the intergenerational transmission of psychopathology symptoms with 7-12 year-old children (N = 97; 44 boys, 53 girls, M age = 9.14, SD = 1.38) and their mothers (M age = 38.46, SD = 6.86). Child emotion regulation mediated the links between maternal psychopathology and child internalizing and externalizing symptoms. In turn,…

  11. Early markers of adult obesity: a review

    PubMed Central

    Brisbois, T D; Farmer, A P; McCargar, L J

    2012-01-01

    Summary The purpose of this review was to evaluate factors in early childhood (≤5 years of age) that are the most significant predictors of the development of obesity in adulthood. Factors of interest included exposures/insults in the prenatal period, infancy and early childhood, as well as other socio-demographic variables such as socioeconomic status (SES) or birth place that could impact all three time periods. An extensive electronic and systematic search initially resulted in 8,880 citations, after duplicates were removed. Specific inclusion and exclusion criteria were set, and following two screening processes, 135 studies were retained for detailed abstraction and analysis. A total of 42 variables were associated with obesity in adulthood; however, of these, only seven variables may be considered as potential early markers of obesity based on the reported associations. Possible early markers of obesity included maternal smoking and maternal weight gain during pregnancy. Probable early markers of obesity included maternal body mass index, childhood growth patterns (early rapid growth and early adiposity rebound), childhood obesity and father's employment (a proxy measure for SES in many studies). Health promotion programmes/agencies should consider these factors as reasonable targets to reduce the risk of adult obesity. PMID:22171945

  12. Modifiable Risk Factors and Interventions for Childhood Obesity Prevention within the First 1,000 Days.

    PubMed

    Dattilo, Anne M

    2017-01-01

    Worldwide, the prevalence of childhood obesity has increased, amounting to 42 million overweight or obese children, and there is increasing evidence that the origins are within the first 1,000 days: the period of conception through 2 years. Antecedents of early childhood obesity are multifactorial, and associations of varying strength have been documented for genetic/epigenetic, biologic, dietary, environmental, social, and behavioral influences. Modifiable factors in pregnancy and early infancy associated with childhood obesity include maternal overweight/obesity, maternal smoking, gestational weight gain, infant and young child feeding, caregiver responsive feeding practices, as well as sleep duration, and physical activity. Promising obesity prevention interventions include those beginning during the first 1,000 days, using a multicomponent approach, with roots in nutrition education theories or behavior change communication that can continue over time. However, the limited number of completed interventions to date (within pediatric clinics or in home-based or community settings) may not be scalable to the magnitude needed for sustainable obesity prevention. Scale-up interventions that can be maintained for the durations needed, addressing infant and young child feeding and other modifiable risk factors associated with childhood obesity are needed. © 2017 Nestec Ltd., Vevey/S. Karger AG, Basel.

  13. [Regulation of food advertising on television for the prevention of childhood obesity].

    PubMed

    Hidalgo, Catalina González; Samur, Eduardo Atalah

    2011-09-01

    Obesity is a serious global epidemic and the prevention strategies implemented have been insufficient. Numerous environmental factors have been associated with risk of obesity and their full consideration in prevention policies is important. The connection between food advertising on television and childhood obesity has been demonstrated. The large number of advertisements for unhealthy foods targeted at children through television and its possible impact on health has led some countries to legislate on this matter. However, a conceptual framework of reference enabling legislation must be internationally defined in order to achieve a real impact in preventing childhood obesity. This paper reviews scientific evidence on the relationship between food advertising and childhood obesity as a basis for developing public policies to regulate food marketing on television.

  14. Delta Healthy Sprouts: a randomized comparative effectiveness trial to promote maternal weight control and reduce childhood obesity in the Mississippi Delta.

    PubMed

    Thomson, Jessica L; Tussing-Humphreys, Lisa M; Goodman, Melissa H

    2014-05-01

    Excessive and inadequate gestational weight gain can complicate a woman's pregnancy and put her and her child at risk for poor delivery and birth outcomes. Further, feeding and activity habits established early in life can significantly impact the development of childhood obesity. The on-going Delta Healthy Sprouts Project is a randomized, controlled, comparative trial testing the efficacy of two Maternal, Infant, and Early Childhood Home Visiting programs on weight status and health behaviors of 150 mothers and their infants residing in the rural Mississippi Delta region of the United States. Women are enrolled in their second trimester of pregnancy and randomized to one of two treatment arms. The control arm curriculum is based on Parents as Teachers, an evidence based approach to increase parental knowledge of child development and improve parenting practices. The experimental arm, labeled Parents as Teachers Enhanced, builds upon the control curriculum by including culturally tailored nutrition and physical activity components specifically designed for the gestational and postnatal periods. We hypothesize that, as compared to the control arm, the experimental arm will be more effective in preventing inappropriate gestational weight gain, reducing postnatal weight retention, and decreasing infant obesity rates. We also will evaluate mother and child dietary and physical activity outcomes, breastfeeding initiation and continuation, and child feeding practices. The Delta Healthy Sprouts Project tests a novel, combined approach to maternal weight management and childhood obesity prevention in pregnant women and their children at high risk for obesity and chronic disease. Published by Elsevier Inc.

  15. Obstetric Obesity is Associated with Neonatal Hyperbilirubinemia with High Prevalence in Native Hawaiians and Pacific Island Women

    PubMed Central

    Rougée, Luc RA; Miyagi, Shogo J

    2016-01-01

    Obesity and pregnancy both place the liver under metabolic stress, but interactions between obstetric obesity and bilirubin metabolism have not been studied. We determined associations between obesity, maternal/neonatal bilirubin levels, and uridine 5′diphosphate-glucuronosyltransferase 1A1 (UGT1A1) enzyme that eliminates bilirubin. Adult livers were analyzed for UGT1A1 expression, activity, and bilirubin clearance by pharmacokinetic modeling. Then, matched maternal and neonatal sera (N = 450) were assayed for total and unconjugated bilirubin. Associations between obesity, UGT1A1, maternal and neonatal hyperbilirubinemia were determined statistically through correlation analysis (Pearson's test) as well as binned categories (one-way ANOVA). Morbid obesity decreased hepatic UGT1A1 protein levels, activity, and bilirubin clearance (P < .001). Increasing obesity corresponded to elevated maternal unconjugated bilirubin (P < .05). Maternal obesity was also significantly positively correlated with elevated neonatal bilirubin levels (P < .01, N = 450) and this was strongest in Native Hawaiians and Pacific Islander (NHPI) women (P < .01, n = 150). Obstetric obesity is associated with maternal and neonatal hyperbilirubinemia, likely through inhibition of hepatic UGT1A1. The NHPI cohort was the most obese and had the highest levels of maternal and neonatal unconjugated bilirubin. Neonates from obese mothers may be more susceptible to jaundice and side effects from parenteral nutrition. PMID:27980881

  16. Cognitive and Self-regulatory Mechanisms of Obesity Study (COSMOS): Study protocol for a randomized controlled weight loss trial examining change in biomarkers, cognition, and self-regulation across two behavioral treatments.

    PubMed

    Hawkins, M A W; Colaizzi, Janna; Gunstad, John; Hughes, Joel W; Mullins, Larry L; Betts, Nancy; Smith, Caitlin E; Keirns, Natalie G; Vohs, Kathleen D; Moore, Shirley M; Forman, Evan M; Lovallo, William R

    2018-03-01

    Obesity is a global epidemic, yet successful interventions are rare. Up to 60% of people fail to achieve clinically meaningful, short-term weight loss (5-10% of start weight), whereas up to 72% are unsuccessful at achieving long-term weight loss (5-10% loss for ≥5years). Understanding how biological, cognitive, and self-regulatory factors work together to promote or to impede weight loss is clearly needed to optimize obesity treatment. This paper describes the methodology of the Cognitive and Self-regulatory Mechanisms of Obesity Study (the COSMOS trial). COSMOS is the first randomized controlled trial to investigate how changes in multiple biopsychosocial and cognitive factors relate to weight loss and one another across two weight loss treatments. The specific aims are to: 1) Confirm that baseline obesity-related physiological dysregulation is linked to cognitive deficits and poorer self-regulation, 2) Evaluate pre- to post-treatment change across time to assess individual differences in biomarkers, cognition, and self-regulation, and 3) Evaluate whether the acceptance-based treatment (ABT) group has greater improvements in outcomes (e.g., greater weight loss and less weight regain, improvements in biomarkers, cognition, and self-regulation), than the standard behavioral treatment group (SBT) from pre- to post-treatment and 1-year follow-up. The results of COSMOS will provide critical information about how dysregulation in biomarkers, cognition, and/or self-regulation is related to weight loss and whether weight loss treatments are differentially associated with these factors. This information will be used to identify promising treatment targets that are informed by biological, cognitive, and self-regulatory factors in order to advance obesity treatment. Copyright © 2017 Elsevier Inc. All rights reserved.

  17. Risks of asphyxia-related neonatal complications in offspring of mothers with type 1 or type 2 diabetes: the impact of maternal overweight and obesity.

    PubMed

    Cnattingius, Sven; Lindam, Anna; Persson, Martina

    2017-07-01

    We aimed to compare the risks of severe asphyxia-related neonatal complications in the offspring of mothers with type 1 or type 2 diabetes, and to assess the impact of maternal overweight/obesity on these risks. This was a population-based study of 1,343,751 live-born singleton infants in Sweden between 1997 and 2011, including 5941 and 711 infants of mothers with type 1 and type 2 diabetes, respectively. ORs with 95% CIs were calculated for low Apgar score (0-6) at 5 min after birth, hypoxic ischaemic encephalopathy and neonatal seizures. The rates of a low Apgar score were 0.9%, 2.6% and 2.1% in the offspring of mothers without diabetes or with type 1 or type 2 diabetes, respectively. After controlling for maternal confounders (including BMI), the risk of a low Apgar score increased in the offspring of mothers with type 1 diabetes (OR 2.67, 95% CI 2.23, 3.20) but not in the offspring of mothers with type 2 diabetes (OR 1.25, 95% CI 0.66, 2.35). The ORs of hypoxic ischaemic encephalopathy or neonatal seizures were increased in the offspring of mothers with type 1 diabetes (OR 3.41, 95% CI 2.58, 4.49) and type 2 diabetes (OR 2.54, 95% CI 1.13, 5.69). Maternal overweight/obesity was a risk factor for asphyxia-related neonatal complications and low Apgar scores in the offspring of mothers with type 1 diabetes and mothers without diabetes. The risks of a low Apgar score and severe asphyxia-related neonatal complications are increased in the offspring of mothers with type 1 or type 2 diabetes. Maternal overweight/obesity is an important contributing factor.

  18. Perinatal and lifestyle factors mediate the association between maternal education and preschool children's weight status: the ToyBox study.

    PubMed

    Androutsos, Odysseas; Moschonis, George; Ierodiakonou, Despo; Karatzi, Kalliopi; De Bourdeaudhuij, Ilse; Iotova, Violeta; Zych, Kamila; Moreno, Luis A; Koletzko, Berthold; Manios, Yannis

    2018-04-01

    This study aimed to explore the associations among perinatal, sociodemographic, and behavioral factors and preschool overweight/obesity. Data were collected from 7541 European preschoolers in May/June 2012. Children's anthropometrics were measured, and parents self-reported all other data via questionnaires. Level of statistical significance was set at P ≤ 0.05. Certain perinatal factors (i.e., maternal prepregnancy overweight/obesity, maternal excess gestational weight gain, excess birth weight, and "rapid growth velocity"), children's energy balance-related behaviors (i.e., high sugar-sweetened beverage consumption, increased screen time, reduced active-play time), family sociodemographic characteristics (i.e., Eastern or Southern Europe, low maternal and paternal education), and parental overweight/obesity were identified as correlates of preschoolers' overweight/obesity. Furthermore, maternal prepregnancy overweight/obesity, children's "rapid growth velocity," and increased screen time mediated by 21.2%, 12.5%, and 5.7%, respectively, the association between maternal education and preschoolers' body mass index. This study highlighted positive associations of preschooler's overweight/obesity with excess maternal prepregnancy and gestational weight gain, excess birth weight and "rapid growth velocity," Southern or Eastern European region, and parental overweight/obesity. Moreover, maternal prepregnancy overweight/obesity, children's "rapid growth velocity," and increased screen time partially mediated the association between maternal education and preschoolers' body mass index. The findings of the present study may support childhood obesity prevention initiatives, because vulnerable population groups and most specifically low-educated families should be prioritized. Among other fields, these intervention initiatives should also focus on the importance of normal prepregnancy maternal weight status, normal growth velocity during infancy, and retaining

  19. Maternal choline intake alters the epigenetic state of fetal cortisol-regulating genes in humans.

    PubMed

    Jiang, Xinyin; Yan, Jian; West, Allyson A; Perry, Cydne A; Malysheva, Olga V; Devapatla, Srisatish; Pressman, Eva; Vermeylen, Francoise; Caudill, Marie A

    2012-08-01

    The in utero availability of methyl donors, such as choline, may modify fetal epigenetic marks and lead to sustainable functional alterations throughout the life course. The hypothalamic-pituitary-adrenal (HPA) axis regulates cortisol production and is sensitive to perinatal epigenetic programming. As an extension of a 12-wk dose-response choline feeding study conducted in third-trimester pregnant women, we investigated the effect of maternal choline intake (930 vs. 480 mg/d) on the epigenetic state of cortisol-regulating genes, and their expression, in placenta and cord venous blood. The higher maternal choline intake yielded higher placental promoter methylation of the cortisol-regulating genes, corticotropin releasing hormone (CRH; P=0.05) and glucocorticoid receptor (NR3C1; P=0.002); lower placental CRH transcript abundance (P=0.04); lower cord blood leukocyte promoter methylation of CRH (P=0.05) and NR3C1 (P=0.04); and 33% lower (P=0.07) cord plasma cortisol. In addition, placental global DNA methylation and dimethylated histone H3 at lysine 9 (H3K9me2) were higher (P=0.02) in the 930 mg choline/d group, as was the expression of select placental methyltransferases. These data collectively suggest that maternal choline intake in humans modulates the epigenetic state of genes that regulate fetal HPA axis reactivity as well as the epigenomic status of fetal derived tissues.

  20. Maternal obesity and metabolic risk to the offspring: why lifestyle interventions may have not achieved the desired outcomes.

    PubMed

    Catalano, P; deMouzon, S H

    2015-04-01

    Obesity during pregnancy is associated with an increased risk of short- and long-term metabolic dysfunction in the mother and her offspring. Both higher maternal pregravid body mass index (kg m(-2)) and excessive gestational weight gain (GWG) have been associated with adverse pregnancy outcomes such as gestational diabetes, preeclampsia and fetal adiposity. Multiple lifestyle intervention trials consisting of weight management using various diets, increased physical activity and behavioral modification techniques have been employed to avoid excessive GWG and improve perinatal outcomes. These randomized controlled trials (RCTs) have achieved modest success in decreasing excessive GWG, although the decrease in GWG was often not within the current Institute of Medicine guidelines. RCTs have generally not had any success with decreasing the risk of maternal gestational diabetes (GDM), preeclampsia or excessive fetal growth often referred to as macrosomia. Although the lack of success for these trials has been attributed to lack of statistical power and poor compliance with study protocols, our own research suggests that maternal pregravid and early pregnancy metabolic condition programs early placenta function and gene expression. These alterations in maternal/placental function occur in the first trimester of pregnancy prior to when most intervention trials are initiated. For example, maternal accrural of adipose tissue relies on prior activation of genes controlling lipogenesis and low-grade inflammation in early pregnancy. These metabolic alterations occur prior to any changes in maternal phenotype. Therefore, trials of lifestyle interventions before pregnancy are needed to demonstrate the safety and efficacy for both the mother and her offspring.

  1. Evidence that a maternal "junk food" diet during pregnancy and lactation can reduce muscle force in offspring.

    PubMed

    Bayol, Stéphanie A; Macharia, Raymond; Farrington, Samantha J; Simbi, Bigboy H; Stickland, Neil C

    2009-02-01

    Obesity is a multi-factorial condition generally attributed to an unbalanced diet and lack of exercise. Recent evidence suggests that maternal malnutrition during pregnancy and lactation can also contribute to the development of obesity in offspring. We have developed an animal model in rats to examine the effects of maternal overeating on a westernized "junk food" diet using palatable processed foods rich in fat, sugar and salt designed for human consumption. Using this model, we have shown that such a maternal diet can promote overeating and a greater preference for junk food in offspring at the end of adolescence. The maternal junk food diet also promoted adiposity and muscle atrophy at weaning. Impaired muscle development may permanently affect the function of this tissue including its ability to generate force. The aim of this study is to determine whether a maternal junk food diet can impair muscle force generation in offspring. Twitch and tetanic tensions were measured in offspring fed either chow alone (C) or with a junk food diet (J) during gestation, lactation and/or post-weaning up to the end of adolescence such that three groups of offspring were used, namely the CCC, JJC and JJJ groups. We show that adult offspring from mothers fed the junk food diet in pregnancy and lactation display reduced muscle force (both specific twitch and tetanic tensions) regardless of the post-weaning diet compared with offspring from mothers fed a balanced diet. Maternal malnutrition can influence muscle force production in offspring which may affect an individual's ability to exercise and thereby combat obesity.

  2. Emotional availability, understanding emotions, and recognition of facial emotions in obese mothers with young children.

    PubMed

    Bergmann, Sarah; von Klitzing, Kai; Keitel-Korndörfer, Anja; Wendt, Verena; Grube, Matthias; Herpertz, Sarah; Schütz, Astrid; Klein, Annette M

    2016-01-01

    Recent research has identified mother-child relationships of low quality as possible risk factors for childhood obesity. However, it remains open how mothers' own obesity influences the quality of mother-child interaction, and particularly emotional availability (EA). Also unclear is the influence of maternal emotional competencies, i.e. understanding emotions and recognizing facial emotions. This study aimed to (1) investigate differences between obese and normal-weight mothers regarding mother-child EA, maternal understanding emotions and recognition of facial emotions, and (2) explore how maternal emotional competencies and maternal weight interact with each other in predicting EA. A better understanding of these associations could inform strategies of obesity prevention especially in children at risk. We assessed EA, understanding emotions and recognition of facial emotions in 73 obese versus 73 normal-weight mothers, and their children aged 6 to 47 months (Mchild age=24.49, 80 females). Obese mothers showed lower EA and understanding emotions. Mothers' normal weight and their ability to understand emotions were positively associated with EA. The ability to recognize facial emotions was positively associated with EA in obese but not in normal-weight mothers. Maternal weight status indirectly influenced EA through its effect on understanding emotions. Maternal emotional competencies may play an important role for establishing high EA in interaction with the child. Children of obese mothers experience lower EA, which may contribute to overweight development. We suggest including elements that aim to improve maternal emotional competencies and mother-child EA in prevention or intervention programmes targeting childhood obesity. Copyright © 2015 Elsevier Inc. All rights reserved.

  3. Eating Self-Regulation in Overweight and Obese Adults: A Concept Analysis.

    PubMed

    Reed, Jill R; Yates, Bernice C; Houfek, Julia; Pullen, Carol H; Briner, Wayne; Schmid, Kendra K

    2016-04-01

    Poor eating behaviors greatly influence the development of becoming overweight or obese. Learning to better self-regulate eating is one area in which individuals can positively influence their own health. The purpose of this concept analysis is to provide an in-depth analysis of the concept eating self-regulation as it pertains to overweight and obese adults using Walker and Avant's method. The definition for eating self-regulation formulated as a result of this concept analysis and based on the critical attributes is the ability to initiate goal-related behaviors, to consistently self-monitor dietary intake, to regularly apply willpower to resist temptations, to self-evaluate where one stands in relationship to goal attainment, and finally to maintain motivation to positively change eating behaviors. Cognitive restraint, moderation, mindfulness, disinhibition, delayed gratification, emotions and moods, self-efficacy, social support, the environment, and physical activity are the antecedents that may influence eating self-regulation. Examining an individual's weight, body mass index, lipid levels, or blood pressure are some ways to determine if self-regulation of eating behavior is achieved. With a consistent definition of self-regulation and a better understanding of the critical factors that influence eating behaviors, research can better explore how to help individuals change their eating behaviors more effectively. © 2015 Wiley Periodicals, Inc.

  4. Newborn follow-up after discharge from the maternity unit: Compliance with national guidelines.

    PubMed

    Roisné, J; Delattre, M; Rousseau, S; Bourlet, A; Charkaluk, M-L

    2018-02-01

    In the context of shorter hospital stays in maternity units, in 2014 the French health authorities issued guidelines for newborn follow-up after discharge from maternity units. A medical visit is recommended between the 6th and 10th day of life, as are home visits from midwives. This study was designed to evaluate compliance with these guidelines. The study was observational, prospective, multicenter, and was conducted in March and April 2015 in three maternity units in northern France that participate in the Baby Friendly Hospital Initiative (BFHI). Follow-up practices (medical visit between the 6th and 10th day, home visits from a midwife) and demographic, social, and medical data were recorded during the stay in the maternity unit, and through a phone interview 1 month later, in singleton term-born infants. The study population included 108 mother-infant pairs. The recommended medical visit was effectively performed by a physician between the 6th and 10th day of life for 20 newborns (19%) (95% CI: [11; 26]). During the 1st month, at least one home visit from a midwife was recorded for 96 mother-infant pairs (89%). The only factor positively correlated with a medical visit between the 6th and 10th day was the mother's choice, made early during the hospital stay and independently of the real length of stay, for early discharge from the maternity unit. Compliance with national guidelines was poor for the recommended medical visit between the 6th and 10th day of life. Information needs to be improved. Copyright © 2017 Elsevier Masson SAS. All rights reserved.

  5. Maternal Chromium Restriction Leads to Glucose Metabolism Imbalance in Mice Offspring through Insulin Signaling and Wnt Signaling Pathways

    PubMed Central

    Zhang, Qian; Sun, Xiaofang; Xiao, Xinhua; Zheng, Jia; Li, Ming; Yu, Miao; Ping, Fan; Wang, Zhixin; Qi, Cuijuan; Wang, Tong; Wang, Xiaojing

    2016-01-01

    An adverse intrauterine environment, induced by a chromium-restricted diet, is a potential cause of metabolic disease in adult life. Up to now, the relative mechanism has not been clear. C57BL female mice were time-mated and fed either a control diet (CD), or a chromium-restricted diet (CR) throughout pregnancy and the lactation period. After weaning, some offspring continued the diet diagram (CD-CD or CR-CR), while other offspring were transferred to another diet diagram (CD-CR or CR-CD). At 32 weeks of age, glucose metabolism parameters were measured, and the liver from CR-CD group and CD-CD group was analyzed using a gene array. Quantitative real-time polymerase chain reaction (qPCR) and Western blot were used to verify the result of the gene array. A maternal chromium-restricted diet resulted in obesity, hyperglycemia, hyperinsulinemia, increased area under the curve (AUC) of glucose in oral glucose tolerance testing and homeostasis model assessment of insulin resistance (HOMA-IR). There were 463 genes that differed significantly (>1.5-fold change, p < 0.05) between CR-CD offspring (264 up-regulated genes, 199 down-regulated genes) and control offspring. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway and STRING (Search Tool for the Retrieval of Interacting Genes/Proteins) analysis revealed that the insulin signaling pathway and Wnt signaling pathway were in the center of the gene network. Our study provides the first evidence that maternal chromium deficiency influences glucose metabolism in pups through the regulation of insulin signaling and Wnt signaling pathways. PMID:27782077

  6. Prepregnancy Body Mass Index and Gestational Weight Gain Have No Negative Impact on Maternal or Neonatal Iron Status.

    PubMed

    Cao, Chang; Pressman, Eva K; Cooper, Elizabeth M; Guillet, Ronnie; Westerman, Mark; O'Brien, Kimberly O

    2016-05-01

    To assess the impact of maternal obesity and excessive gestational weight gain (GWG) on maternal and neonatal iron status and to explore the possible mediating role of inflammation on hepcidin. This analysis included 230 pregnant adolescents (13-18 years) enrolled in either a longitudinal or a cross-sectional study. Prepregnancy body mass index (ppBMI) and GWG were obtained from medical records. Maternal iron status (hemoglobin, serum iron, ferritin, transferrin receptor, total body iron, and hepcidin) and inflammation (interleukin-6 [IL-6] and leptin) were assessed at midgestation (26.2 ± 3.3 weeks) in the longitudinal cohort and at delivery (39.8 ± 1.3 weeks) in both study cohorts. Cord blood was collected in both studies and analyzed for iron indicators. Approximately 40% of the adolescents entered pregnancy overweight or obese. Multivariate analysis identified ppBMI as a negative predictor of serum iron at midgestation (P = .009) and a positive predictor of serum hepcidin at delivery (P = .02). None of the other maternal iron status indicators were significantly associated with ppBMI or GWG. Serum IL-6 was significantly positively associated with hepcidin at delivery (P = .0001) but not at midgestation. There was a positive relationship between ppBMI and cord hemoglobin (P = .03). These results suggest that adiposity-related inflammation does not override the iron-mediated signals that regulate hepcidin production during pregnancy, and in this adolescent cohort, there is no strong evidence for a detrimental effect of maternal obesity and excessive weight gain on iron status in the offspring at birth. © The Author(s) 2015.

  7. Early-pregnancy maternal vitamin D status and maternal hyperglycaemia.

    PubMed

    Tomedi, L E; Simhan, H N; Bodnar, L M

    2013-09-01

    To estimate the association between serum 25-hydroxyvitamin D concentrations and maternal hyperglycaemia (post-load glucose concentration ≥ 7.5 mmol/l). Pregnant women (n = 429; 61% black, 36% obese, 45% smokers) enrolled in a cohort study at <16 weeks gestation. Non-fasting blood samples were assayed for serum 25-hydroxyvitamin D at enrolment. At 24-28 weeks gestation, maternal hyperglycaemia was determined using a 50-g 1-h oral glucose challenge test. A total of 67% of women had 25-hydroxyvitamin D concentrations < 50 nmol/l and 11% had maternal hyperglycaemia. Among smokers, each 23-nmol/l increase in serum 25-hydroxyvitamin D was associated with a reduction in the odds of maternal hyperglycaemia [odds ratio: 0.30 (95% CI: 0.13, 0.68)] after adjustment for parity, race/ethnicity, age, pre-pregnancy BMI, marital status, income, family history of diabetes, and gestational age of gestational diabetes mellitus screening. Among non-smokers, we found no association between early pregnancy vitamin D status and maternal hyperglycaemia. Smoking status may modify the relationship between poor maternal vitamin D status and maternal hyperglycaemia. © 2013 The Authors. Diabetic Medicine © 2013 Diabetes UK.

  8. Latina mothers’ influences on child appetite regulation

    PubMed Central

    Silva, Karina; Power, Thomas G.; Fisher, Jennifer Orlet; O’Connor, Teresia M.; Hughes, Sheryl O.

    2016-01-01

    Parents influence child weight through interactions that shape the development of child eating behaviors. In this study we examined the association between maternal autonomy promoting serving practices and child appetite regulation. We predicted that maternal autonomy promoting serving practices would be positively associated with child appetite regulation. Participants were low-income Latino children—a group at high risk for the development of childhood obesity. A total of 186 low-income Latina mothers and their 4-5 year old children came to a laboratory on two separate days. On the first day, mothers and children chose foods for a meal from a buffet and were audio/videotaped so that maternal autonomy promoting serving practices could be later coded. On the second day, children completed the Eating in the Absence of Hunger (EAH) task to measure child appetite regulation. Mothers also completed the Child Eating Behavior Questionnaire (CEBQ) to measure other aspects of child appetite regulation (food responsiveness, satiety responsiveness, and emotional overeating). Maternal autonomy promotion during serving was assessed using seven separate measures of child and maternal behavior. Principal components analyses of these serving measures yielded three components: allows child choice, child serves food, and mother does not restrict. Consistent with hypotheses, maternal autonomy promoting serving practices (i.e., allows child choice and does not restrict) were negatively associated with maternal reports of child food responsiveness and emotional overeating (CEBQ). The results for the EAH task were more complex—mothers who were autonomy promoting in their serving practices had children who ate the most in the absence of hunger, but this linear effect was moderated somewhat by quadratic effect, with moderate levels of autonomy promotion during serving associated with the greatest child EAH. PMID:27083128

  9. Latina mothers' influences on child appetite regulation.

    PubMed

    Silva Garcia, Karina; Power, Thomas G; Fisher, Jennifer Orlet; O'Connor, Teresia M; Hughes, Sheryl O

    2016-08-01

    Parents influence child weight through interactions that shape the development of child eating behaviors. In this study we examined the association between maternal autonomy promoting serving practices and child appetite regulation. We predicted that maternal autonomy promoting serving practices would be positively associated with child appetite regulation. Participants were low-income Latino children-a group at high risk for the development of childhood obesity. A total of 186 low-income Latina mothers and their 4-5 year old children came to a laboratory on two separate days. On the first day, mothers and children chose foods for a meal from a buffet and were audio/videotaped so that maternal autonomy promoting serving practices could be later coded. On the second day, children completed the Eating in the Absence of Hunger (EAH) task to measure child appetite regulation. Mothers also completed the Child Eating Behavior Questionnaire (CEBQ) to measure other aspects of child appetite regulation (food responsiveness, satiety responsiveness, and emotional overeating). Maternal autonomy promotion during serving was assessed using seven separate measures of child and maternal behavior. Principal components analyses of these serving measures yielded three components: allows child choice, child serves food, and mother does not restrict. Consistent with hypotheses, maternal autonomy promoting serving practices (i.e., allows child choice and does not restrict) were negatively associated with maternal reports of child food responsiveness and emotional overeating (CEBQ). The results for the EAH task were more complex-mothers who were autonomy promoting in their serving practices had children who ate the most in the absence of hunger, but this linear effect was moderated somewhat by a quadratic effect, with moderate levels of autonomy promotion during serving associated with the greatest child EAH. Copyright © 2016 Elsevier Ltd. All rights reserved.

  10. The Influence of Maternal Psychosocial Characteristics on Infant Feeding Styles

    PubMed Central

    Barrett, Katherine J.; Thompson, Amanda L.; Bentley, Margaret E.

    2017-01-01

    Maternal feeding styles in infancy and early childhood are associated with children’s later risk for overweight and obesity. Maternal psychosocial factors that influence feeding styles during the complementary feeding period, the time during which infants transition from a milk-based diet to one that includes solid foods and other non-milk products, have received less attention. The present study explores how maternal psychosocial factors—specifically self-esteem, parenting self-efficacy, parenting satisfaction, and depression symptoms—influence mothers’ infant feeding styles at nine months of age, a time during which solid foods eating habits are being established. Participants included 160 low-income, African-American mother-infant pairs in central North Carolina who were enrolled in the Infant Care and Risk of Obesity Study. Regression models tested for associations between maternal psychosocial characteristics and pressuring and restrictive feeding styles. Models were first adjusted for maternal age, education, marital status and obesity status. To account for infant characteristics, models were then adjusted for infant weight-for-length, distress to limitations and activity level scores. Maternal self-esteem was negatively associated with pressuring to soothe. Maternal parenting self-efficacy was positively associated with restriction-diet quality. Maternal parenting satisfaction and depression symptoms were not associated with feeding styles in the final models. Focusing on strengthening maternal self-esteem and parenting self-efficacy may help to prevent the development of less desirable infant feeding styles. PMID:27174251

  11. The influence of maternal psychosocial characteristics on infant feeding styles.

    PubMed

    Barrett, Katherine J; Thompson, Amanda L; Bentley, Margaret E

    2016-08-01

    Maternal feeding styles in infancy and early childhood are associated with children's later risk for overweight and obesity. Maternal psychosocial factors that influence feeding styles during the complementary feeding period, the time during which infants transition from a milk-based diet to one that includes solid foods and other non-milk products, have received less attention. The present study explores how maternal psychosocial factors-specifically self-esteem, parenting self-efficacy, parenting satisfaction, and depression symptoms-influence mothers' infant feeding styles at nine months of age, a time during which solid foods eating habits are being established. Participants included 160 low-income, African-American mother-infant pairs in central North Carolina who were enrolled in the Infant Care and Risk of Obesity Study. Regression models tested for associations between maternal psychosocial characteristics and pressuring and restrictive feeding styles. Models were first adjusted for maternal age, education, marital status and obesity status. To account for infant characteristics, models were then adjusted for infant weight-for-length, distress to limitations and activity level scores. Maternal self-esteem was negatively associated with pressuring to soothe. Maternal parenting self-efficacy was positively associated with restriction-diet quality. Maternal parenting satisfaction and depression symptoms were not associated with feeding styles in the final models. Focusing on strengthening maternal self-esteem and parenting self-efficacy may help to prevent the development of less desirable infant feeding styles. Copyright © 2016 Elsevier Ltd. All rights reserved.

  12. Maternal body mass index and risk of birth and maternal health outcomes in low- and middle-income countries: a systematic review and meta-analysis.

    PubMed

    Rahman, M M; Abe, S K; Kanda, M; Narita, S; Rahman, M S; Bilano, V; Ota, E; Gilmour, S; Shibuya, K

    2015-09-01

    We conducted a systematic review and meta-analysis of population-based cohort studies of maternal body mass index (BMI) and risk of adverse birth and health outcomes in low- and middle-income countries. PubMed, Embase, CINAHL and the British Nursing Index were searched from inception to February 2014. Forty-two studies were included. Our study found that maternal underweight was significantly associated with higher risk of preterm birth (odds ratio [OR], 1.13; 95% confidence interval [CI], 1.01-1.27), low birthweight (OR, 1.66; 95% CI, 1.50-1.84) and small for gestational age (OR, 1.85; 95% CI, 1.69-2.02). Compared with mothers with normal BMI, overweight or obese mothers were at increased odds of gestational diabetes, pregnancy-induced hypertension, pre-eclampsia, caesarean delivery and post-partum haemorrhage. The population-attributable risk (PAR) indicated that if women were entirely unexposed to overweight or obesity during the pre-pregnancy or early pregnancy period, 14% to 35% fewer women would develop gestational diabetes, pre-eclampsia or pregnancy-induced hypertension in Brazil, China, India, Iran or Thailand. The highest PAR of low birthweight attributable to maternal underweight was found in Iran (20%), followed by India (18%), Thailand (10%) and China (8%). Treatment and prevention of maternal underweight, overweight or obesity may help reduce the burden on maternal and child health in developing countries. © 2015 World Obesity.

  13. Regulation of adipolin/CTRP12 cleavage by obesity.

    PubMed

    Enomoto, Takashi; Shibata, Rei; Ohashi, Koji; Kambara, Takahiro; Kataoka, Yoshiyuki; Uemura, Yusuke; Yuasa, Daisuke; Murohara, Toyoaki; Ouchi, Noriyuki

    2012-11-09

    Obesity is highly associated with the development of insulin resistance and type 2 diabetes. Recently we found that adipolin/CRTP12 is an adipocytokine that exerts beneficial actions on glucose metabolism. Here we investigated the regulation of circulating adipolin under conditions of obesity and assessed its potential mechanisms. Both full and cleaved forms of adipolin were observed in mouse plasma. Diet-induced obese (DIO) mice showed a significant reduction of plasma levels of full and total (full and cleaved) adipolin compared with control mice, resulting in an increase in the ratio of cleaved to full isoform. In vitro gene transfection studies using HEK293 cells revealed that a deletion mutant of adipolin gene (Δaa90-93) caused a reduction of cleaved production of adipolin in media. A bioinformatics analysis of adipolin amino acid sequence indicated the potential involvement of the family of proprotein convertases (PCs) in cleavage of adipolin. Treatment of 3T3-L1 adipocytes with an inhibitor for PCs abolished the expression of cleaved adipolin form in the media. The expression of furin, the member of PCs, was increased in adipose tissue of DIO mice. Furin expression was also increased in cultured adipocytes by treatment with an inducer of inflammation. These data suggest that obesity states facilitate the cleavage of adipolin presumably through upregulation of furin in adipose tissue. Copyright © 2012 Elsevier Inc. All rights reserved.

  14. Maternal lipids in pregnancy are associated with increased offspring cortisol reactivity in childhood.

    PubMed

    Mina, Theresia H; Lahti, Marius; Drake, Amanda J; Forbes, Shareen; Denison, Fiona C; Räikkönen, Katri; Norman, Jane E; Reynolds, Rebecca M

    2017-09-01

    Prenatal programming of hypothalamic-pituitary-adrenal (HPA) axis activity has long term implications for offspring health. Biological mechanisms underlying programming of the offspring HPA axis are poorly understood. We hypothesised that altered maternal metabolism including higher maternal obesity, glucose and lipids are novel programming factors for altered offspring HPA axis activity. Salivary cortisol levels were measured in 54 children aged 3-5 years under experimental conditions (before and after a delay of self-gratification test). Associations of child cortisol responses with maternal obesity in early pregnancy and with fasting glucose, triglycerides, HDL and total cholesterol measured in each pregnancy trimester were tested. Higher levels of maternal triglycerides and total cholesterol throughout pregnancy were associated with increased offspring cortisol reactivity. The associations were independent of maternal obesity and other confounders, suggesting that exposure to maternal lipids could be a biological mechanism of in utero programming of the offspring's HPA axis. Copyright © 2017. Published by Elsevier Ltd.

  15. The early origins of obesity and insulin resistance: timing, programming and mechanisms.

    PubMed

    Nicholas, L M; Morrison, J L; Rattanatray, L; Zhang, S; Ozanne, S E; McMillen, I C

    2016-02-01

    Maternal obesity is associated with an increased risk of developing gestational diabetes mellitus and it also results in an increased risk of giving birth to a large baby with increased fat mass. Furthermore, it is also contributes to an increased risk of obesity and insulin resistance in the offspring in childhood, adolescence and adult life. It has been proposed that exposure to maternal obesity may therefore result in an 'intergenerational cycle' of obesity and insulin resistance. There is significant interest in whether exposure to maternal obesity around the time of conception alone contributes directly to poor metabolic outcomes in the offspring and whether dieting in the obese mother before pregnancy or around the time of conception has metabolic benefits for the offspring. This review focusses on experimental and clinical studies that have investigated the specific impact of exposure to maternal obesity during the periconceptional period alone or extending beyond conception on adipogenesis, lipogenesis and on insulin signalling pathways in the fat, liver and muscle of the offspring. Findings from these studies highlight the need for a better evidence base for the development of dietary interventions in obese women before pregnancy and around the time of conception to maximize the metabolic benefits and minimize the metabolic costs for the next generation.

  16. Contextual risk, maternal parenting and adolescent externalizing behaviour problems: the role of emotion regulation.

    PubMed

    Walton, A; Flouri, Eirini

    2010-03-01

    The objective of this study was to test if emotion regulation mediates the association between mothers' parenting and adolescents' externalizing behaviour problems (conduct problems and hyperactivity). The parenting dimensions were warmth, psychological control and behavioural control (measured with knowledge, monitoring and discipline). Adjustment was made for contextual risk (measured with the number of proximal adverse life events experienced), gender, age and English as an additional language. Data were from a UK community sample of adolescents aged 11-18 from a comprehensive school in a disadvantaged area. At the multivariate level, none of the parenting variables predicted hyperactivity, which was associated only with difficulties in emotion regulation, contextual risk and English as a first language. The parenting variables predicting conduct problems at the multivariate level were warmth and knowledge. Knowledge did not predict emotion regulation. However, warmth predicted emotion regulation, which was negatively associated with conduct problems. Contextual risk was a significant predictor of both difficulties in emotion regulation and externalizing behaviour problems. Its effect on conduct problems was independent of parenting and was not via its association with difficulties in emotion regulation. The findings add to the evidence for the importance of maternal warmth and contextual risk for both regulated emotion and regulated behaviour. The small maternal control effects on both emotion regulation and externalizing behaviour could suggest the importance of paternal control for adolescent outcomes.

  17. The Impact of Maternal Obesity and Excessive Gestational Weight Gain on Maternal and Infant Outcomes in Maine: Analysis of Pregnancy Risk Assessment Monitoring System Results from 2000 to 2010.

    PubMed

    Baugh, Nancy; Harris, David E; Aboueissa, AbouEl-Makarim; Sarton, Cheryl; Lichter, Erika

    2016-01-01

    The objective of this study is to understand the relationships between prepregnancy obesity and excessive gestational weight gain (GWG) and adverse maternal and fetal outcomes. Pregnancy risk assessment monitoring system (PRAMS) data from Maine for 2000-2010 were used to determine associations between demographic, socioeconomic, and health behavioral variables and maternal and infant outcomes. Multivariate logistic regression analysis was performed on the independent variables of age, race, smoking, previous live births, marital status, education, BMI, income, rurality, alcohol use, and GWG. Dependent variables included maternal hypertension, premature birth, birth weight, infant admission to the intensive care unit (ICU), and length of hospital stay of the infant. Excessive prepregnancy BMI and excessive GWG independently predicted maternal hypertension. A high prepregnancy BMI increased the risk of the infant being born prematurely, having a longer hospital stay, and having an excessive birth weight. Excessive GWG predicted a longer infant hospital stay and excessive birth weight. A low pregnancy BMI and a lower than recommended GWG were also associated with poor outcomes: prematurity, low birth weight, and an increased risk of the infant admitted to ICU. These findings support the importance of preconception care that promotes achievement of a healthy weight to enhance optimal reproductive outcomes.

  18. The Impact of Maternal Obesity and Excessive Gestational Weight Gain on Maternal and Infant Outcomes in Maine: Analysis of Pregnancy Risk Assessment Monitoring System Results from 2000 to 2010

    PubMed Central

    Sarton, Cheryl; Lichter, Erika

    2016-01-01

    The objective of this study is to understand the relationships between prepregnancy obesity and excessive gestational weight gain (GWG) and adverse maternal and fetal outcomes. Pregnancy risk assessment monitoring system (PRAMS) data from Maine for 2000–2010 were used to determine associations between demographic, socioeconomic, and health behavioral variables and maternal and infant outcomes. Multivariate logistic regression analysis was performed on the independent variables of age, race, smoking, previous live births, marital status, education, BMI, income, rurality, alcohol use, and GWG. Dependent variables included maternal hypertension, premature birth, birth weight, infant admission to the intensive care unit (ICU), and length of hospital stay of the infant. Excessive prepregnancy BMI and excessive GWG independently predicted maternal hypertension. A high prepregnancy BMI increased the risk of the infant being born prematurely, having a longer hospital stay, and having an excessive birth weight. Excessive GWG predicted a longer infant hospital stay and excessive birth weight. A low pregnancy BMI and a lower than recommended GWG were also associated with poor outcomes: prematurity, low birth weight, and an increased risk of the infant admitted to ICU. These findings support the importance of preconception care that promotes achievement of a healthy weight to enhance optimal reproductive outcomes. PMID:27747104

  19. Self-regulation of eating and physical activity is lower in obese female college students as compared to their normal weight counterparts.

    PubMed

    Campos-Uscanga, Yolanda; Gutiérrez-Ospina, Gabriel; Morales-Romero, Jaime; Romo-González, Tania

    2017-06-01

    Obesity is characterized, among other features, by overeating, reduced physical activity and an abnormal accumulation of body fat. These features are thought to result, at least in part, from the individual's inability to self-regulate their eating and physical activity behaviors (E&PaB). Self-regulation of the E&PaB is a three-step sequential process: self-observation, self-evaluation and self-reaction. However, it is yet unclear whether deficient self-regulation of E&PaB could predispose, facilitate and/or consolidate obesity. Unraveling this issue is fundamental in order to more precisely define the role of self-regulation of E&PaB in the management of obesity. This research was focused on the question of whether or not self-regulation of E&PaB is related to obesity in female undergraduate students. This population segment seems especially vulnerable to developing obesity since they undergo a significant shift of their E&PaB upon their university enrollment. To address this question, a cross-sectional study with 108 female undergraduate students with normal weight (n = 80) or obesity (n = 28) was performed, in which self-regulation of eating habits and physical activity was measured by two validated scales and a personal data questionnaire. Female undergraduate students displaying lower E&PaB self-reactions were consistently overweight or obese. In addition, a multivariate analysis identified high levels of self-reaction towards eating habits related to a minor presence of overweight issues or obesity. Self-regulation should be an essential component in the strategies for obesity prevention as an integral approach that must include orientation about healthy eating and physical activity behaviors. In addition, further studies on the effect of self-regulation in the treatment of the obesity are needed.

  20. Changing perspectives in pre-existing diabetes and obesity in pregnancy: maternal and infant short- and long-term outcomes.

    PubMed

    Barbour, Linda A

    2014-08-01

    Climbing obesity rates in women have propelled the increasing prevalence of type 2 diabetes mellitus (T2DM) in pregnancy, and an increasing number of women with type 1 diabetes mellitus (T1DM) are also affected by obesity. Increasing recognition that an intrauterine environment characterized by obesity, insulin resistance, nutrient excess, and diabetes may be fueling the obesity epidemic in children has created enormous pressure to re-examine the conventional wisdom of our current approaches. Compelling data in pregnancies complicated by diabetes, in particular those accompanied by insulin resistance and obesity, support a fetal programming effect resulting in increased susceptibility to metabolic disease for the offspring later in life. Recent data also underscore the contribution of obesity, lipids, and lesser degrees of hyperglycemia on fetal fat accretion, challenging the wisdom of current gestational weight gain recommendations with and without diabetes. The risks of adverse pregnancy outcomes in T2DM are at least as high as in T1DM and there remains controversy about the ideal glucose treatment targets, the benefit of different insulin analogues, and the role of continuous glucose monitoring in T1DM and T2DM. It has become unmistakably evident that achieving optimal outcomes in mothers with diabetes is clearly impacted by ideal glycemic control but goes far beyond it. The intrauterine metabolic environment seems to have long-term implications on the future health of the offspring so that the effectiveness of our current approaches can no longer be simply measured by whether or not maternal glucose values are at goal.

  1. Obesity in mares promotes uterine inflammation and alters embryo lipid fingerprints and homeostasis.

    PubMed

    Sessions-Bresnahan, Dawn R; Heuberger, Adam L; Carnevale, Elaine M

    2018-05-07

    Maternal body composition can be an important determinant for development of obesity and metabolic syndrome in adult offspring. Obesity-related outcomes in offspring may include epigenetic alterations; however, mechanisms of fetal programming remain to be fully elucidated. This study was conducted to determine the impact of maternal obesity in the absence of a high fat diet on equine endometrium and preimplantation embryos. Embryos were collected from normal and obese mares at 8 and 16 d and a uterine biopsy at 16 d (0 d = ovulation). With the exception of 8 d embryos, each sample was divided into two pieces. One piece was analyzed for gene expression markers related to carbohydrate metabolism, lipid homeostasis, inflammation, endoplasmic reticulum stress, oxidative stress, mitochondrial stress, and components of the insulin-like growth factor (IGF) system. The second piece was analyzed for lipid content using matrix-assisted laser desorption/ionization mass spectrometry (MALDI-MS). Obese mares had elevated concentrations of insulin, leptin and total cholesterol, and they tended to have increased triglycerides and decreased insulin sensitivity. Embryos from obese mares had altered transcript abundance in genes for inflammation and lipid homeostasis, as well as, endoplasmic reticulum, oxidative and mitochondrial stress and altered lipid fingerprints. Endometrium from obese mares had increased expression of inflammatory cytokines, lipid homeostasis regulation, mitochondrial stress, and the IGF2 system. This study demonstrates increased adiposity in mares alters the uterine environment, transcript abundance of genes for cellular functions, and lipid profiles of embryos. These alterations could affect prenatal programming, with potential long-term effects in offspring.

  2. Obesity and diabetes: from genetics to epigenetics.

    PubMed

    Burgio, Ernesto; Lopomo, Angela; Migliore, Lucia

    2015-04-01

    Obesity is becoming an epidemic health problem. During the last years not only genetic but also, and primarily, environmental factors have been supposed to contribute to the susceptibility to weight gain or to develop complications such as type 2 diabetes. In spite of the intense efforts to identify genetic predisposing variants, progress has been slow and success limited, and the common obesity susceptibility variants identified only explains a small part of the individual variation in risk. Moreover, there is evidence that the current epidemic of obesity and diabetes is environment-driven. Recent studies indicate that normal metabolic regulation during adulthood besides requiring a good balance between energy intake and energy expenditure, can be also affected by pre- and post-natal environments. In fact, maternal nutritional constraint during pregnancy can alter the metabolic phenotype of the offspring by means of epigenetic regulation of specific genes, and this can be passed to the next generations. Studies focused on epigenetic marks in obesity found altered methylation and/or histone acetylation levels in genes involved in specific but also in more general metabolic processes. Recent researches point out the continuous increase of "obesogens", in the environment and food chains, above all endocrine disruptors, chemicals that interfere with many homeostatic mechanisms. Taken into account the already existing data on the effects of obesogens, and the multiple potential targets with which they might interfere daily, it seems likely that the exposure to obesogens can have an important role in the obesity and diabesity pandemic.

  3. Preconceptional and maternal obesity: epidemiology and health consequences.

    PubMed

    Poston, Lucilla; Caleyachetty, Rishi; Cnattingius, Sven; Corvalán, Camila; Uauy, Ricardo; Herring, Sharron; Gillman, Matthew W

    2016-12-01

    Obesity in women of reproductive age is increasing in prevelance worldwide. Obesity reduces fertility and increases time taken to conceive, and obesity-related comorbidities (such as type 2 diabetes and chronic hypertension) heighten the risk of adverse outcomes for mother and child if the woman becomes pregnant. Pregnant women who are obese are more likely to have early pregnancy loss, and have increased risk of congenital fetal malformations, delivery of large for gestational age infants, shoulder dystocia, spontaneous and medically indicated premature birth, and stillbirth. Late pregnancy complications include gestational diabetes and pre-eclampsia, both of which are associated with long-term morbidities post partum. Women with obesity can also experience difficulties during labour and delivery, and are more at risk of post-partum haemorrhage. Long-term health risks are associated with weight retention after delivery, and inherent complications for the next pregnancy. The wellbeing of the next generation is also compromised. All these health issues could be avoided by prevention of obesity among women of reproductive age, which should be viewed as a global public health priority. For women who are already obese, renewed efforts should be made towards improved management during pregnancy, especially of blood glucose, and increased attention to post-partum weight management. Effective interventions, tailored to ethnicity and culture, are needed at each of these stages to improve the health of women and their children in the context of the global obesity epidemic. Copyright © 2016 Elsevier Ltd. All rights reserved.

  4. Parental Obesity and Early Childhood Development.

    PubMed

    Yeung, Edwina H; Sundaram, Rajeshwari; Ghassabian, Akhgar; Xie, Yunlong; Buck Louis, Germaine

    2017-02-01

    Previous studies identified associations between maternal obesity and childhood neurodevelopment, but few examined paternal obesity despite potentially distinct genetic/epigenetic effects related to developmental programming. Upstate KIDS (2008-2010) recruited mothers from New York State (excluding New York City) at ∼4 months postpartum. Parents completed the Ages and Stages Questionnaire (ASQ) when their children were 4, 8, 12, 18, 24, 30, and 36 months of age corrected for gestation. The ASQ is validated to screen for delays in 5 developmental domains (ie, fine motor, gross motor, communication, personal-social functioning, and problem-solving ability). Analyses included 3759 singletons and 1062 nonrelated twins with ≥1 ASQs returned. Adjusted odds ratios (aORs) and 95% confidence intervals were estimated by using generalized linear mixed models accounting for maternal covariates (ie, age, race, education, insurance, marital status, parity, and pregnancy smoking). Compared with normal/underweight mothers (BMI <25), children of obese mothers (26% with BMI ≥30) had increased odds of failing the fine motor domain (aOR 1.67; confidence interval 1.12-2.47). The association remained after additional adjustment for paternal BMI (1.67; 1.11-2.52). Paternal obesity (29%) was associated with increased risk of failing the personal-social domain (1.75; 1.13-2.71), albeit attenuated after adjustment for maternal obesity (aOR 1.71; 1.08-2.70). Children whose parents both had BMI ≥35 were likely to additionally fail the problem-solving domain (2.93; 1.09-7.85). Findings suggest that maternal and paternal obesity are each associated with specific delays in early childhood development, emphasizing the importance of family information when screening child development. Copyright © 2017 by the American Academy of Pediatrics.

  5. Parental Obesity and Early Childhood Development

    PubMed Central

    Sundaram, Rajeshwari; Ghassabian, Akhgar; Xie, Yunlong; Buck Louis, Germaine

    2017-01-01

    BACKGROUND: Previous studies identified associations between maternal obesity and childhood neurodevelopment, but few examined paternal obesity despite potentially distinct genetic/epigenetic effects related to developmental programming. METHODS: Upstate KIDS (2008–2010) recruited mothers from New York State (excluding New York City) at ∼4 months postpartum. Parents completed the Ages and Stages Questionnaire (ASQ) when their children were 4, 8, 12, 18, 24, 30, and 36 months of age corrected for gestation. The ASQ is validated to screen for delays in 5 developmental domains (ie, fine motor, gross motor, communication, personal-social functioning, and problem-solving ability). Analyses included 3759 singletons and 1062 nonrelated twins with ≥1 ASQs returned. Adjusted odds ratios (aORs) and 95% confidence intervals were estimated by using generalized linear mixed models accounting for maternal covariates (ie, age, race, education, insurance, marital status, parity, and pregnancy smoking). RESULTS: Compared with normal/underweight mothers (BMI <25), children of obese mothers (26% with BMI ≥30) had increased odds of failing the fine motor domain (aOR 1.67; confidence interval 1.12–2.47). The association remained after additional adjustment for paternal BMI (1.67; 1.11–2.52). Paternal obesity (29%) was associated with increased risk of failing the personal-social domain (1.75; 1.13–2.71), albeit attenuated after adjustment for maternal obesity (aOR 1.71; 1.08–2.70). Children whose parents both had BMI ≥35 were likely to additionally fail the problem-solving domain (2.93; 1.09–7.85). CONCLUSIONS: Findings suggest that maternal and paternal obesity are each associated with specific delays in early childhood development, emphasizing the importance of family information when screening child development. PMID:28044047

  6. The Main and Interactive Effects of Maternal Interpersonal Emotion Regulation and Negative Affect on Adolescent Girls' Borderline Personality Disorder Symptoms.

    PubMed

    Dixon-Gordon, Katherine L; Whalen, Diana J; Scott, Lori N; Cummins, Nicole D; Stepp, Stephanie D

    2016-06-01

    The transaction of adolescent's expressed negative affect and parental interpersonal emotion regulation are theoretically implicated in the development of borderline personality disorder (BPD). Although problem solving and support/validation are interpersonal strategies that foster emotion regulation, little is known about whether these strategies are associated with less BPD severity among adolescents. Adolescent girls (age 16; N = 74) and their mothers completed a conflict discussion task, and maternal problem solving, support/validation, and girls' negative affect were coded. Girls' BPD symptoms were assessed at four time points. A 3-way interaction of girls' negative affect, problem solving, and support/validation indicated that girls' negative affect was only associated with BPD severity in the context of low maternal support/validation and high maternal problem solving. These variables did not predict changes in BPD symptoms over time. Although high negative affect is a risk for BPD severity in adolescent girls, maternal interpersonal emotion regulation strategies moderate this link. Whereas maternal problem solving coupled with low support/validation is associated with a stronger negative affect-BPD relation, maternal problem solving paired with high support/validation is associated with an attenuated relationship.

  7. The Main and Interactive Effects of Maternal Interpersonal Emotion Regulation and Negative Affect on Adolescent Girls’ Borderline Personality Disorder Symptoms

    PubMed Central

    Whalen, Diana J.; Scott, Lori N.; Cummins, Nicole D.; Stepp, Stephanie D.

    2015-01-01

    The transaction of adolescent’s expressed negative affect and parental interpersonal emotion regulation are theoretically implicated in the development of borderline personality disorder (BPD). Although problem solving and support/validation are interpersonal strategies that foster emotion regulation, little is known about whether these strategies are associated with less BPD severity among adolescents. Adolescent girls (age 16; N = 74) and their mothers completed a conflict discussion task, and maternal problem solving, support/validation, and girls’ negative affect were coded. Girls’ BPD symptoms were assessed at four time points. A 3-way interaction of girls’ negative affect, problem solving, and support/validation indicated that girls’ negative affect was only associated with BPD severity in the context of low maternal support/validation and high maternal problem solving. These variables did not predict changes in BPD symptoms over time. Although high negative affect is a risk for BPD severity in adolescent girls, maternal interpersonal emotion regulation strategies moderate this link. Whereas maternal problem solving coupled with low support/validation is associated with a stronger negative affect-BPD relation, maternal problem solving paired with high support/validation is associated with an attenuated relationship. PMID:27185969

  8. Impact of parental obesity on neonatal markers of inflammation and immune response.

    PubMed

    Broadney, M M; Chahal, N; Michels, K A; McLain, A C; Ghassabian, A; Lawrence, D A; Yeung, E H

    2017-01-01

    Maternal obesity may influence neonatal and childhood morbidities through increased inflammation and/or altered immune response. Less is known about paternal obesity. We hypothesized that excessive parental weight contributes to elevated inflammation and altered immunoglobulin (Ig) profiles in neonates. In the Upstate KIDS Study maternal pre-pregnancy body mass index (BMI) was obtained from vital records and paternal BMI from maternal report. Biomarkers were measured from newborn dried blood spots (DBS) among neonates whose parents provided consent. Inflammatory scores were calculated by assigning one point for each of five pro-inflammatory biomarkers above the median and one point for an anti-inflammatory cytokine below the median. Linear regression models and generalized estimating equations were used to estimate mean differences (β) and 95% confidence intervals (CI) in the inflammatory score and Ig levels by parental overweight/obesity status compared with normal weight. Among 2974 pregnancies, 51% were complicated by excessive maternal weight (BMI>25), 73% by excessive paternal weight and 28% by excessive gestational weight gain. Maternal BMI categories of overweight (BMI 25.0-29.9) and obese class II/III (BMI≥35) were associated with increased neonatal inflammation scores (β=0.12, 95% CI: 0.02, 0.21; P=0.02 and β=0.13, CI: -0.002, 0.26; P=0.05, respectively) but no increase was observed in the obese class I group (BMI 30-34.9). Mothers with class I and class II/III obesity had newborns with increased IgM levels (β=0.11, CI: 0.04, 0.17; P=0.001 and β=0.12, CI: 0.05, 0.19); P<0.001, respectively). Paternal groups of overweight, obese class I and obese class II/III had decreased neonatal IgM levels (β=-0.08, CI: -0.13,-0.03, P=0.001; β=-0.07, CI: -0.13, -0.01, P=0.029 and β=-0.11, CI:-0.19,-0.04, P=0.003, respectively). Excessive maternal weight was generally associated with increased inflammation and IgM supporting previous observations of maternal

  9. The New "Obstetrical Dilemma": Stunting, Obesity and the Risk of Obstructed Labour.

    PubMed

    Wells, Jonathan C K

    2017-04-01

    The "obstetrical dilemma" refers to the tight fit between maternal pelvic dimensions and neonatal size at delivery. Most interest traditionally focused on its generic significance for humans, for example our neonatal altriciality and our complex and lengthy birth process. Across contemporary populations, however, the obstetrical dilemma manifests substantial variability, illustrated by differences in the incidence of cephalo-pelvic disproportion, obstructed labour and cesarean section. Beyond accounting for 12% of maternal mortality worldwide, obstructed labour also imposes a huge burden of maternal morbidity, in particular through debilitating birth injuries. This article explores how the double burden of malnutrition and the global obesity epidemic may be reshaping the obstetrical dilemma. First, short maternal stature increases the risk of obstructed labour, while early age at marriage also risks pregnancy before pelvic growth is completed. Second, maternal obesity increases the risk of macrosomic offspring. In some populations, short maternal stature may also promote the risk of gestational diabetes, another risk factor for macrosomic offspring. These nutritional influences are furthermore sensitive to social values relating to issues such as maternal and child nutrition, gender inequality and age at marriage. Secular trends in maternal obesity are substantially greater than those in adult stature, especially in low- and middle-income countries. The association between the dual burden of malnutrition and the obstetrical dilemma is therefore expected to increase, because the obesity epidemic is emerging faster than stunting is being resolved. However, we currently lack objective population-specific data on the association between maternal obesity and birth injuries. Anat Rec, 300:716-731, 2017. © 2017 Wiley Periodicals, Inc. © 2017 Wiley Periodicals, Inc.

  10. Maternal prepregnancy body mass index and child psychosocial development at 6 years of age.

    PubMed

    Jo, Heejoo; Schieve, Laura A; Sharma, Andrea J; Hinkle, Stefanie N; Li, Ruowei; Lind, Jennifer N

    2015-05-01

    Both obesity and developmental disabilities have increased in recent decades. Limited studies suggest associations between maternal prepregnancy obesity and child neurodevelopment. The Infant Feeding Practices Study II, a US nationally distributed longitudinal study of maternal health and infant health and feeding practices, was conducted from 2005 to 2007. In 2012, mothers were recontacted for information on their children's health and development. We examined associations between maternal prepregnancy BMI and child psychosocial development in 1311 mother-child pairs included in this follow-up study. Children's development was assessed by maternal report of child psychosocial difficulties from the Strengths and Difficulties Questionnaire, past developmental diagnoses, and receipt of special needs services. Adjusting for sociodemographic factors, children of obese class II/III mothers (BMI >35.0) had increased odds of emotional symptoms (adjusted odds ratio [aOR] 2.24; 95% confidence interval [CI], 1.27-3.98), peer problems (aOR 2.07; 95% CI, 1.26-3.40), total psychosocial difficulties (aOR 2.17; 95% CI, 1.24-3.77), attention-deficit/hyperactivity disorder diagnosis (aOR 4.55; 95% CI, 1.80-11.46), autism or developmental delay diagnosis (aOR 3.13; 95% CI, 1.10-8.94), receipt of speech language therapy (aOR 1.93; 95% CI, 1.18-3.15), receipt of psychological services (aOR 2.27; 95% CI, 1.09-4.73), and receipt of any special needs service (aOR 1.99; 95% CI, 1.33-2.97) compared with children of normal weight mothers (BMI 18.5-24.9). Adjustment for potential causal pathway factors including pregnancy weight gain, gestational diabetes, breastfeeding duration, postpartum depression, and child's birth weight did not substantially affect most estimates. Children whose mothers were severely obese before pregnancy had increased risk for adverse developmental outcomes. published in the public domain by the American Academy of Pediatrics.

  11. The Interplay of Maternal Sensitivity and Toddler Engagement of Mother in Predicting Self-Regulation

    ERIC Educational Resources Information Center

    Ispa, Jean M.; Su-Russell, Chang; Palermo, Francisco; Carlo, Gustavo

    2017-01-01

    Using data from the Early Head Start Research and Evaluation Project, a cross-lag mediation model was tested to examine longitudinal relations among low-income mothers' sensitivity; toddlers' engagement of their mothers; and toddler's self-regulation at ages 1, 2, and 3 years (N = 2,958). Age 1 maternal sensitivity predicted self-regulation at…

  12. Prenatal programming in an obese swine model: sex-related effects of maternal energy restriction on morphology, metabolism and hypothalamic gene expression.

    PubMed

    Óvilo, Cristina; González-Bulnes, Antonio; Benítez, Rita; Ayuso, Miriam; Barbero, Alicia; Pérez-Solana, Maria L; Barragán, Carmen; Astiz, Susana; Fernández, Almudena; López-Bote, Clemente

    2014-02-01

    Maternal energy restriction during pregnancy predisposes to metabolic alterations in the offspring. The present study was designed to evaluate phenotypic and metabolic consequences following maternal undernutrition in an obese pig model and to define the potential role of hypothalamic gene expression in programming effects. Iberian sows were fed a control or a 50 % restricted diet for the last two-thirds of gestation. Newborns were assessed for body and organ weights, hormonal and metabolic status, and hypothalamic expression of genes implicated in energy homeostasis, glucocorticoid function and methylation. Weight and adiposity were measured in adult littermates. Newborns of the restricted sows were lighter (P <0·01), but brain growth was spared. The plasma concentration of TAG was lower in the restricted newborns than in the control newborns of both the sexes (P <0·01), while the concentration of cortisol was higher in females born to the restricted sows (P <0·04), reflecting a situation of metabolic stress by nutrient insufficiency. A lower hypothalamic expression of anorexigenic peptides (LEPR and POMC, P <0·01 and P <0·04, respectively) was observed in females born to the restricted sows, but no effect was observed in the males. The expression of HSD11B1 gene was down-regulated in the restricted animals (P <0·05), suggesting an adaptive mechanism for reducing the harmful effects of elevated concentrations of cortisol. At 4 and 7 months of age, the restricted females were heavier and fatter than the controls (P< 0·01). Maternal feed restriction induces asymmetrical growth retardation and metabolic alterations in the offspring. Differences in gene expression at birth and higher growth and adiposity in adulthood suggest a female-specific programming effect for a positive energy balance, possibly due to overexposure to endogenous stress-induced glucocorticoids.

  13. Self-regulation and household routines at age three and obesity at age eleven: longitudinal analysis of the UK Millennium Cohort Study

    PubMed Central

    Anderson, Sarah E; Sacker, Amanda; Whitaker, Robert C; Kelly, Yvonne

    2017-01-01

    Objective To examine, in a population-based cohort of three-year-old children, the association between self-regulation and exposure to the household routines of regular bedtime, regular mealtime, and limits on watching television/video; and to determine whether self-regulation and these routines predict the risk of obesity at age 11. Methods Analyses included 10 955 children in the nationally-representative UK Millennium Cohort Study. When children were age 3, parents reported whether children had a regular bedtime and mealtime and the amount of television/video watched. Emotional and cognitive self-regulation at age 3 were assessed by parent-report with the Child Social Behaviour Questionnaire. Children’s height and weight were measured at age 11 and obesity was defined using the International Obesity Task Force (IOTF) criteria. Results At age 3, 41% of children always had a regular bedtime, 47% always had a regular mealtime, and 23% were limited to ≤1 hour television/video daily. At age 11, 6.2% of children were obese. All three household routines were significantly associated with better emotional self-regulation, but not better cognitive self-regulation. In a multi-variable logistic regression model including emotional and cognitive self-regulation, all routines, and controlling for sociodemographic covariates, a 1 unit difference in emotional self-regulation at age 3 was associated with an OR (95% CI) for obesity of 1.38 (1.11, 1.71) at age 11, and inconsistent bedtimes with an OR (95% CI) for obesity of 1.87 (1.39, 2.51) at age 11. There was no evidence that emotional self-regulation mediated the relationship between regular bedtimes and later obesity. Cognitive self-regulation was not associated with later obesity. Conclusions Three-year-old children who had regular bedtimes, mealtimes, and limits on their television/video time had better emotional self-regulation. Lack of a regular bedtime and poorer emotional self-regulation at age 3 were independent

  14. Maternal dazap2 Regulates Germ Granules by Counteracting Dynein in Zebrafish Primordial Germ Cells.

    PubMed

    Forbes, Meredyth M; Rothhämel, Sophie; Jenny, Andreas; Marlow, Florence L

    2015-07-07

    Primordial germ cells (PGCs) are the stem cells of the germline. Generally, germline induction occurs via zygotic factors or the inheritance of maternal determinants called germ plasm (GP). GP is packaged into ribonucleoprotein complexes within oocytes and later promotes the germline fate in embryos. Once PGCs are specified by either mechanism, GP components localize to perinuclear granular-like structures. Although components of zebrafish PGC germ granules have been studied, the maternal factors regulating their assembly and contribution to germ cell development are unknown. Here, we show that the scaffold protein Dazap2 binds to Bucky ball, an essential regulator of oocyte polarity and GP assembly, and colocalizes with the GP in oocytes and in PGCs. Mutational analysis revealed a requirement for maternal Dazap2 (MDazap2) in germ-granule maintenance. Through molecular epistasis analyses, we show that MDazap2 is epistatic to Tdrd7 and maintains germ granules in the embryonic germline by counteracting Dynein activity. Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.

  15. Informed Decision Making in Maternity Care

    PubMed Central

    Goldberg, Holly

    2009-01-01

    In the United States, federal acts and regulations, as well as professional guidelines, clearly dictate that every pregnant woman has the right to base her maternity care decisions on accurate, up-to-date, comprehensible information. Despite these efforts, evidence suggests that informed consent within current health-care practice is restricted and inconsistently implemented. Patient access to evidence-based research is imperative under the scope of informed consent and is particularly important during a time when perinatal mortality and morbidity rates, interventions, and disparities are on the rise in the United States. This article describes the Coalition for Improving Maternity Services’ investigation of the breakdown of informed consent in maternity care. PMID:19436598

  16. Maternal fat, but not lean, mass is increased among overweight/obese women with excess gestational weight gain.

    PubMed

    Berggren, Erica K; Groh-Wargo, Sharon; Presley, Larraine; Hauguel-de Mouzon, Sylvie; Catalano, Patrick M

    2016-06-01

    Weight gain in pregnancy is an essential physiologic adaptation that supports growth and development of a fetus and is distributed among lean mass that includes total body water and fat mass gains. Although gestational weight gain provides a source of energy for the mother and fetus, excess gestational weight gain may underlie reported associations between parity and future metabolic disorders and is linked to postpartum weight retention and insulin resistance. Although weight gain often is proposed as a modifiable variable to mitigate adverse maternal and offspring health outcomes, our knowledge of specific maternal body composition changes with weight gain and the potential metabolic consequences is limited. Furthermore, although gestational weight gain alters maternal body composition, the impact of excess weight gain on fat and lean mass is not well-studied. Understanding the accrual of fat and lean body mass may improve our understanding of the role of excessive gestational weight gain and metabolic dysfunction. The purpose of our study was to quantify the relationship between gestational weight gain and maternal fat and lean body mass accrual and to compare fat and lean body mass accrual according to the 2009 Institute of Medicine Guidelines for Gestational Weight Gain in Pregnancy adherence. We hypothesized that exceeding current weight gain guidelines would be associated with greater fat, compared with lean body, mass accrual. This is a secondary analysis of a randomized controlled trial of 49 overweight/obese women; all 49 are included in this secondary analysis. Maternal weight and body composition were collected in early (13 0/6 to 16 6/7 weeks gestation) and late (34 0/7 to 36 6/7 weeks gestation) pregnancy with the use of air densitometry. Correlations were drawn between gestational weight gain and change in fat and lean body mass. We compared change in fat and lean body mass by adherence to the 2009 Institute of Medicine Guidelines for Gestational

  17. The relationship of prenatal maternal depression or anxiety to maternal caregiving behavior and infant behavior self-regulation during infant heel lance: an ethological time-based study of behavior.

    PubMed

    Warnock, Fay F; Craig, Kenneth D; Bakeman, Roger; Castral, Thaila; Mirlashari, Jila

    2016-09-07

    Sensitive and responsive maternal caregiving behavior strengthens infant self-regulatory capacities (HL), but this regulatory role may be diminished in some mothers with second-trimester prenatal exposure to depression and/ or anxiety (MDA). This study examined maternal and infant behavior during infant heel lance (HL) when mothers had or did not have MDA. Ethological methods and micro-analytic approaches capable of distinguishing and comparing time-based patterning in maternal and infant behavior were used to clarify biological mechanisms, such as MDA, that may underlie observed behavior. Aims were to examine group differences in caregiving behavior between mothers with and without MDA 5 min Pre-HL and 5 min Post-H, and relationships between MDA, maternal caregiving behavior and infant pain behavior self-regulation, concurrently. At second trimester, mothers were assessed for symptoms of mild-severe depression or anxiety. Mothers whose scores exceeded predetermined cut-off scores on one or more of the mental health measures were allocated to the MDA-exposure group, those below to the non-MDA-exposure group. Reliable observers, blinded to MDA status and study phases, coded video records of the caregiving behavior of each study mother for the full duration of the 5 min Pre-HL and 5 min Post-HL study phases. Group differences and associations between mean measures of maternal mental health scores, time-based measures of maternal behavior, and time-based measures of infant pain behavior regulation (previously coded) were concurrently analyzed using comparative and correlational statistics. MDA-exposed mothers spent significantly more time not embracing, engaging or responding to infant cues than maternal controls Pre-HL and Post-HL. MDA was associated with atypical maternal caregiving behavior, which in turn was related to atypical infant pain behavior self-regulation during and after the HL. Our findings have implication for practice. We recommend inclusion of

  18. Transcriptional integration of paternal and maternal factors in the Arabidopsis zygote

    PubMed Central

    Aichinger, Ernst; Gong, Wen; Groot, Edwin; Verstraeten, Inge; Vu, Lam Dai; De Smet, Ive; Higashiyama, Tetsuya; Umeda, Masaaki; Laux, Thomas

    2017-01-01

    In many plants, the asymmetric division of the zygote sets up the apical–basal axis of the embryo. Unlike animals, plant zygotes are transcriptionally active, implying that plants have evolved specific mechanisms to control transcriptional activation of patterning genes in the zygote. In Arabidopsis, two pathways have been found to regulate zygote asymmetry: YODA (YDA) mitogen-activated protein kinase (MAPK) signaling, which is potentiated by sperm-delivered mRNA of the SHORT SUSPENSOR (SSP) membrane protein, and up-regulation of the patterning gene WOX8 by the WRKY2 transcription factor. How SSP/YDA signaling is transduced into the nucleus and how these pathways are integrated have remained elusive. Here we show that paternal SSP/YDA signaling directly phosphorylates WRKY2, which in turn leads to the up-regulation of WOX8 transcription in the zygote. We further discovered the transcription factors HOMEODOMAIN GLABROUS11/12 (HDG11/12) as maternal regulators of zygote asymmetry that also directly regulate WOX8 transcription. Our results reveal a framework of how maternal and paternal factors are integrated in the zygote to regulate embryo patterning. PMID:28404632

  19. Cumulative Risk and Adolescent's Internalizing and Externalizing Problems: The Mediating Roles of Maternal Responsiveness and Self-Regulation

    ERIC Educational Resources Information Center

    Doan, Stacey N.; Fuller-Rowell, Thomas E.; Evans, Gary W.

    2012-01-01

    The purpose of the present study was to examine longitudinal associations among maternal responsiveness, self-regulation, and behavioral adjustment in adolescents. The authors used structural equation modeling to test a model that demonstrates that the effects of early cumulative risk on behavioral problems is mediated by maternal responsiveness…

  20. Screening for pre-eclampsia in the first trimester: role of maternal hemodynamics and bioimpedance in non-obese patients.

    PubMed

    Gagliardi, G; Tiralongo, G M; LoPresti, D; Pisani, I; Farsetti, D; Vasapollo, B; Novelli, G P; Andreoli, A; Valensise, H

    2017-11-01

    To test if maternal hemodynamics and bioimpedance, assessed at the time of combined screening for PE, are able to identify in the first trimester of gestation normotensive non-obese patients at risk for pre-eclampsia (PE) and/or intrauterine growth restriction (IUGR). One hundred and fifty healthy nulliparous non-obese women (body mass index < 30 kg/m 2 ) in the first trimester of pregnancy underwent assessment by UltraSonic Cardiac Output Monitor (USCOM) to detect hemodynamic parameters, bioimpedance analysis to characterize body composition, and combined screening for PE (assessment of maternal history, biophysical and maternal biochemical markers). Patients were followed until term, noting the appearance of PE and/or IUGR. One hundred and thirty-eight patients had an uneventful pregnancy (controls), while 12 (8%) developed complications (cases). USCOM showed, in cases compared with controls, lower cardiac output (5.6 ± 0.3 vs 6.7 ± 1.1 L/min, P < 0.001), lower inotropy index (1.54 ± 0.38 vs 1.91 ± 0.32 W/m 2 , P < 0.001) and higher total vascular resistance (1279.8 ± 166.4 vs 1061.4 ± 179.5 dynes × s/cm 5 , P < 0.001). Bioimpedance analysis showed, in cases compared with controls, lower total body water (53.7 ± 3.3% vs 57.2 ± 5.6%, P = 0.037). Combined screening was positive for PE in 8% of the controls and in 50% of the cases (P < 0.001). After identification of cut-off values for USCOM and bioimpedance parameters, forward multivariate logistic regression analysis identified as independent predictors of complications in pregnancy the inotropy index (derived by USCOM), fat mass (derived from bioimpedance analysis) and combined screening. Combined screening for PE and assessment of bioimpedance and maternal hemodynamics can be used to identify early markers of impaired cardiovascular adaptation and body composition that may lead to complications in the third trimester of pregnancy. Copyright