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Sample records for maternal obesity up-regulates

  1. 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) ...

  2. Maternal Dietary Restriction During the Periconceptional Period in Normal-Weight or Obese Ewes Results in Adrenocortical Hypertrophy, an Up-Regulation of the JAK/STAT and Down-Regulation of the IGF1R Signaling Pathways in the Adrenal of the Postnatal Lamb

    PubMed Central

    Zhang, Song; Morrison, Janna L.; Gill, Amreet; Rattanatray, Leewen; MacLaughlin, Severence M.; Kleemann, David; Walker, Simon K.

    2013-01-01

    Maternal dietary restriction during the periconceptional period results in an increase in adrenal growth and in the cortisol stress response in the offspring. The intraadrenal mechanisms that result in the programming of these changes are not clear. Activation of the IGF and the signal transducer and activator of transcription (STAT)/suppressors of cytokine signaling (SOCS) pathways regulate adrenal growth. We have used an embryo transfer model in sheep to investigate the impact of exposure to either dietary restriction in normal or obese mothers or to maternal obesity during the periconceptional period on adrenal growth and function in the offspring. We assessed the adrenal abundance of key signaling molecules in the IGF-I and Janus kinase/STAT/SOCS pathways including IGF-I receptor, IGF-II receptor, Akt, mammalian target of rapamycin, ribosomal protein S6, eukaryotic translation initiation factor 4E-binding protein 1, eukaryotic translation initiation factor 4E, STAT1, STAT3, STAT5, SOCS1, and SOCS3 in female and male postnatal lambs. Maternal dietary restriction in the periconceptional period resulted in the hypertrophy of the adrenocortical cells in the zona fasciculata-reticularis and an up-regulation in STAT1, phospho-STAT1, and phospho-STAT3 (Ser727) abundance and a down-regulation in IGF-I receptor, Akt, and phospho-Akt abundance in the adrenal cortex of the postnatal lamb. These studies highlight that weight loss around the time of conception, independent of the starting maternal body weight, results in the activation of the adrenal Janus kinase/STAT pathway and adrenocortical hypertrophy. Thus, signals of adversity around the time of conception have a long-term impact on the mechanisms that regulate adrenocortical growth. PMID:24108072

  3. Maternal dietary restriction during the periconceptional period in normal-weight or obese ewes results in adrenocortical hypertrophy, an up-regulation of the JAK/STAT and down-regulation of the IGF1R signaling pathways in the adrenal of the postnatal lamb.

    PubMed

    Zhang, Song; Morrison, Janna L; Gill, Amreet; Rattanatray, Leewen; MacLaughlin, Severence M; Kleemann, David; Walker, Simon K; McMillen, I Caroline

    2013-12-01

    Maternal dietary restriction during the periconceptional period results in an increase in adrenal growth and in the cortisol stress response in the offspring. The intraadrenal mechanisms that result in the programming of these changes are not clear. Activation of the IGF and the signal transducer and activator of transcription (STAT)/suppressors of cytokine signaling (SOCS) pathways regulate adrenal growth. We have used an embryo transfer model in sheep to investigate the impact of exposure to either dietary restriction in normal or obese mothers or to maternal obesity during the periconceptional period on adrenal growth and function in the offspring. We assessed the adrenal abundance of key signaling molecules in the IGF-I and Janus kinase/STAT/SOCS pathways including IGF-I receptor, IGF-II receptor, Akt, mammalian target of rapamycin, ribosomal protein S6, eukaryotic translation initiation factor 4E-binding protein 1, eukaryotic translation initiation factor 4E, STAT1, STAT3, STAT5, SOCS1, and SOCS3 in female and male postnatal lambs. Maternal dietary restriction in the periconceptional period resulted in the hypertrophy of the adrenocortical cells in the zona fasciculata-reticularis and an up-regulation in STAT1, phospho-STAT1, and phospho-STAT3 (Ser727) abundance and a down-regulation in IGF-I receptor, Akt, and phospho-Akt abundance in the adrenal cortex of the postnatal lamb. These studies highlight that weight loss around the time of conception, independent of the starting maternal body weight, results in the activation of the adrenal Janus kinase/STAT pathway and adrenocortical hypertrophy. Thus, signals of adversity around the time of conception have a long-term impact on the mechanisms that regulate adrenocortical growth.

  4. Potential involvement of adipocyte insulin resistance in obesity-associated up-regulation of adipocyte lysophospholipase D/autotaxin expression

    PubMed Central

    Boucher, Jérémie; Quilliot, Didier; Pradère, Jean-Philippe; Simon, Marie-Françoise; Grès, Sandra; Guigné, Charlotte; Prévot, Danielle; Ferry, Gilles; Boutin, Jean A.; Carpéné, Christian; Valet, Philippe; Saulnier-Blache, Jean Sébastien

    2005-01-01

    Aims/hypothesis Autotaxin (ATX) is an adipocyte-secreted lysophospholipase D which expression is substantially up-regulated in obese-diabetic db/db-mice. The aim of the present study was to depict the physiopathological and cellular mechanisms involved in regulation of adipocyte-ATX expression. Methods ATX mRNAs were quantified in adipose tissue from db/db mice (obese and highly diabetic Type 2), gold-thioglucose-treated (GTG) mice (highly obese and moderately diabetic Type 2), high fat diet-fed (HFD) mice (obese and moderately diabetic Type 2), streptozotocin-treated (STREPTO) mice (thin and diabetic Type 1), and massively obese humans exhibiting glucose intolerance. Results When compared to non-obese controls, ATX expression was significantly increased in db/db mice, but not in GTG-, HFD-, or STREPTO-mice. During db/db-mice development, up-regulation of ATX occurred only 3 weeks after emergence of hyper-insulinemia, and was concomitant to emergence of hyperglycaemia. Adipocytes from db/db-mice exhibited strong impairment in insulin-stimulated glucose uptake when compared with non-obese and HFD-induced obese mice. ATX expression was up-regulated by treatment with TNFα (insulin resistance-promoting cytokine), and down-regulated by rosiglitazone treatment (insulin-sensitizing compound) in 3T3F442A adipocytes. Finally, adipose tissue-ATX expression was significantly up-regulated in patients exhibiting both insulin-resistance and impaired glucose tolerance. Conclusions/interpretation The present work demonstrates the existence of a db/db-specific up-regulation of adipocyte-ATX expression which could be related to severe Type 2 diabetes phenotype and adipocyte insulin-resistance, rather than excess adiposity per se. The present work also revealed that Type 2 diabetes in human is also associated with up-regulation of adipocyte-ATX expression. PMID:15700135

  5. 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.

  6. Up-regulation of CD81 inhibits cytotrophoblast invasion and mediates maternal endothelial cell dysfunction in preeclampsia

    PubMed Central

    Shen, Li; Diao, Zhenyu; Sun, Hai-Xiang; Yan, Gui-Jun; Wang, Zhiqun; Li, Ruo-Tian; Dai, Yimin; Wang, Jingmei; Li, Jie; Ding, Hailing; Zhao, Guangfeng; Zheng, Mingming; Xue, Pingping; Liu, Mo; Zhou, Yan; Hu, Yali

    2017-01-01

    Preeclampsia (PE) is initiated by abnormal placentation in the early stages of pregnancy, followed by systemic activation of endothelial cells of the maternal small arterioles in the late second or third trimester (TM) of pregnancy. During normal pregnancy, placental cytotrophoblasts (CTBs) invade the maternal uterine wall and spiral arteries, whereas this process is interrupted in PE. However, it is not known how the malformed placenta triggers maternal endothelial crisis and the associated manifestations. Here, we have focused on the association of CD81 with PE. CD81, a member of the tetraspanin superfamily, plays significant roles in cell growth, adhesion, and motility. The function of CD81 in human placentation and its association with pregnancy complications are currently unknown. In the present study, we have demonstrated that CD81 was preferentially expressed in normal first TM placentas and progressively down-regulated with gestation advance. In patients with early-onset severe PE (sPE), CD81 expression was significantly up-regulated in syncytiotrophoblasts (STBs), CTBs and the cells in the villous core. In addition, high levels of CD81 were observed in the maternal sera of patients with sPE. Overexpressing CD81 in CTBs significantly decreased CTB invasion, and culturing primary human umbilical vein endothelial cells (HUVECs) in the presence of a high dose of exogenous CD81 resulted in interrupted angiogenesis and endothelial cell activation in vitro. Importantly, the phenotype of human PE was mimicked in the CD81-induced rat model. PMID:28167787

  7. The "Senobi" breathing exercise ameliorates depression in obese women through up-regulation of sympathetic nerve activity and hormone secretion.

    PubMed

    Sato, Kazunari; Kawamura, Toshihiko; Yamagiwa, Satoshi

    2011-04-01

    Obese individuals have an increased risk of developing depression. This study aimed to determine whether the "Senobi" breathing exercise (SBE), a stretching-breathing exercise that we have established, could relieve depression, especially in obese women. Forty premenopausal women, aged 40 to 49 years, participated in the present study. Twenty were healthy, and the other 20 were obese (body mass index > 25 and body fat > 30%) and in a depressive state (OWD). Sympathetic nerve activity determined by analyzing heart rate variability, and the hormone levels in the urine were investigated before and 30 min after one minute of SBE. The relative proportion of sympathetic nerve activity among healthy women in the daytime was 79.2 ± 2.3%, whereas that in OWD group was 30.4 ± 1.9%. After one minute of SBE, significant up-regulation of sympathetic nerve activity and increased concentrations of catecholamines, estradiol, and growth hormone (all P values < 0.001) were observed in OWD group. After 30 days of SBE, the sympathetic nerve activity and hormone levels had recovered in OWD group, and the depressive state, as evaluated by the Hamilton Depression Scale, had ameliorated. The "Senobi" breathing exercise was found to be effective for amelioration of depression in obese women possibly through up-regulation of sympathetic nerve activity and hormone secretion.

  8. Fetal and perinatal consequences of maternal obesity.

    PubMed

    Vasudevan, Chakrapani; Renfrew, Mary; McGuire, William

    2011-09-01

    In many industrialised countries, one in five women booking for antenatal care is obese. As well as affecting maternal health, maternal obesity may have important adverse consequences for fetal, neonatal and long-term health and well-being. Maternal obesity is associated with a higher risk of stillbirth, elective preterm birth and perinatal mortality. The incidence of severe birth defects, particularly neural tube and structural cardiac defects, appears to be higher in infants of obese mothers. Fetal macrosomia associated with maternal obesity and gestational diabetes predisposes infants to birth injuries, perinatal asphyxia and transitional problems such as neonatal respiratory distress and metabolic instability. Maternal obesity may also result in long-term health problems for offspring secondary to perinatal problems and to intrauterine and postnatal programming effects. Currently, the available interventions to prevent and treat maternal obesity are of limited proven utility and further research is needed to define the effects of maternal weight management interventions on fetal and neonatal outcomes.

  9. Maternal Obesity and Neck Circumference.

    PubMed

    Anglim, B; O'Higgins, A; Daly, N; Farren, M; Turner, M J

    2015-06-01

    Obese women are more likely to require general anaesthesia for an obstetric intervention than non-obese. Difficult tracheal intubation and oxygen desaturation is more common in pregnancy. Failed tracheal intubation has been associated with an increase in neck circumference (NC). We studied the relationship between maternal obesity and NC as pregnancy advanced in women attending a standard antenatal clinic. Of the 96 women recruited, 13.5% were obese. The mean NC was 36.8cm (SD 1.9) in the obese women compared with 31.5cm (SD 1.6) in women with a normal BMI (p < 0.001) at 18-22 weeks gestation. In the obese women it increased on average by 1.5cm by 36-40 weeks compared with an increase of 1.6 cm in women with a normal BMI. The antenatal measurement of NC is a simple, inexpensive tool that is potentially useful for screening obese women who may benefit from an antenatal anaesthetic assessment.

  10. Late-onset exercise in female rat offspring ameliorates the detrimental metabolic impact of maternal obesity.

    PubMed

    Bahari, Hasnah; Caruso, Vanni; Morris, Margaret J

    2013-10-01

    Rising rates of maternal obesity/overweight bring the need for effective interventions in offspring. We observed beneficial effects of postweaning exercise, but the question of whether late-onset exercise might benefit offspring exposed to maternal obesity is unanswered. Thus we examined effects of voluntary exercise implemented in adulthood on adiposity, hormone profiles, and genes involved in regulating appetite and metabolism in female offspring. Female Sprague Dawley rats were fed either normal chow or high-fat diet (HFD) ad libitum for 5 weeks before mating and throughout gestation/lactation. At weaning, female littermates received either chow or HFD and, after 7 weeks, half were exercised (running wheels) for 5 weeks. Tissues were collected at 15 weeks. Maternal obesity was associated with increased hypothalamic inflammatory markers, including suppressor of cytokine signaling 3, TNF-α, IL-1β, and IL-6 expression in the arcuate nucleus. In the paraventricular nucleus (PVN), Y1 receptor, melanocortin 4 receptor, and TNF-α mRNA were elevated. In the hippocampus, maternal obesity was associated with up-regulated fat mass and obesity-associated gene and TNF-α mRNA. We observed significant hypophagia across all exercise groups. In female offspring of lean dams, the reduction in food intake by exercise could be related to altered signaling at the PVN melanocortin 4 receptor whereas in offspring of obese dams, this may be related to up-regulated TNF-α. Late-onset exercise ameliorated the effects of maternal obesity and postweaning HFD in reducing body weight, adiposity, plasma leptin, insulin, triglycerides, and glucose intolerance, with greater beneficial effects in offspring of obese dams. Overall, hypothalamic inflammation was increased by maternal obesity or current HFD, and the effect of exercise was dependent on maternal diet. In conclusion, even after a significant sedentary period, many of the negative impacts of maternal obesity could be improved by

  11. 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

  12. Interrupting Intergenerational Cycles of Maternal Obesity.

    PubMed

    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 intergenerational 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.

  13. 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

  14. Maternal obesity, inflammation, and developmental programming.

    PubMed

    Segovia, Stephanie A; Vickers, Mark H; Gray, Clint; 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.

  15. Insulin up-regulates natriuretic peptide clearance receptor expression in the subcutaneous fat depot in obese subjects: a missing link between CVD risk and obesity?

    PubMed

    Pivovarova, Olga; Gögebakan, Özlem; Klöting, Nora; Sparwasser, Andrea; Weickert, Martin O; Haddad, Isam; Nikiforova, Victoria J; Bergmann, Andreas; Kruse, Michael; Seltmann, Anne-Cathrin; Blüher, Matthias; Pfeiffer, Andreas F H; Rudovich, Natalia

    2012-05-01

    Natriuretic peptides (NP) regulate cardiovascular homeostasis and have multiple metabolic properties. Decreased levels of NP or "natriuretic handicap" are signs of insulin resistance such as central obesity. Increased expression of NP clearance receptor (NPRC) in sc adipose tissue (SAT) was observed in insulin-resistant subjects. We hypothesized that insulin acutely regulates NP receptor expression in adipose tissue. NPRA, NPRB, and NPRC mRNA expression was measured in paired samples of visceral adipose tissue (VAT) and SAT from 157 subjects (108 with type 2 diabetes). The effect of insulin on NPR gene expression in SAT was studied in euglycemic-hyperinsulinemic and hyperglycemic-hyperinsulinemic clamp experiments. Additionally, the effect of insulin and glucose on NPR expression in the culture of primary human monocytes and macrophages was tested. NPRA and NPRC gene expression was higher in VAT compared with SAT (P < 0.01), but only NPRC gene expression strongly correlated with fasting insulin levels (r = 0.65, P = 0.04 × 10(-3); and r = 0.54, P = 0.002, for VAT and SAT, respectively). NPRB expression was lower in VAT than in SAT in subjects with type 2 diabetes and was lower compared with nondiabetic subjects. NPRC gene expression was up-regulated in SAT during both euglycemic- and hyperglycemic-hyperinsulinemic clamps (P = 0.038 and P = 0.048, respectively), and was increased in high glucose and insulin treatment in monocytes (70.2%; P = 0.01), but not in mature macrophages. Insulin increased expression of NPRC in SAT independently of circulating glucose concentrations. Thus, insulin might suppress circulating NP via up-regulation of NPRC expression in obesity, providing a novel link between hyperinsulinemia and obesity.

  16. 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.

  17. Maternal obesity, metabolism, and pregnancy outcomes.

    PubMed

    King, Janet C

    2006-01-01

    About one third of all pregnant women in the United States are obese. Maternal obesity at conception alters gestational metabolic adjustments and affects placental, embryonic, and fetal growth and development. Neural tube defects and other developmental anomalies are more common in infants born to obese women; these defects have been linked to poor glycemic control. Preeclampsia, a gestational disorder occurring more frequently in obese women, appears to be due to a subclinical inflammatory state that impairs early placentation and development of its blood supply. Fetal growth and development during the last half of pregnancy depends on maternal metabolic adjustments dictated by placental hormones and the subsequent oxygen and nutrient supply. Maternal obesity affects these metabolic adjustments as well. Basal metabolic rates are significantly higher in obese women, and maternal fat gain is lower, possibly in response to altered leptin function. The usual increase in insulin resistance seen in late pregnancy is enhanced in obese mothers, causing marked postprandial increases in glucose, lipids, and amino acids and excessive fetal exposure to fuel sources, which in turn increases fetal size, fat stores, and risk for disease postnatally. Impaired glucose tolerance, gestational diabetes, and hyperlipidemia are more common among obese mothers. To date, little attention has been given to the role of diet among obese women in preventing these problems. However, studies of women with impaired glucose tolerance show that replacing refined carbohydrates and saturated fat with complex, low-glycemic carbohydrates and polyunsaturated fatty acids improves metabolic homeostasis and pregnancy outcomes. Thus, current dietary guidelines regarding the amount and type of carbohydrates and fat for nonpregnant women seem appropriate for pregnant women as well.

  18. Maternal obesity and risk of postpartum hemorrhage.

    PubMed

    Blomberg, Marie

    2011-09-01

    To estimate whether maternal obesity was associated with an increased risk for postpartum hemorrhage more than 1,000 mL and whether there was an association between maternal obesity and causes of postpartum hemorrhage and mode of delivery. A population-based cohort study including 1,114,071 women with singleton pregnancies who gave birth in Sweden from January 1, 1997 through December 31, 2008, who were divided into six body mass index (BMI) classes. Obese women (class I-III) were compared with normal-weight women concerning the risk for postpartum hemorrhage after suitable adjustments. The use of heparin-like drugs over the BMI strata was analyzed in a subgroup. There was an increased prevalence of postpartum hemorrhage over the study period associated primarily with changes in maternal characteristics. The risk of atonic uterine hemorrhage increased rapidly with increasing BMI. There was a twofold increased risk in obesity class III (1.8%). No association was found between postpartum hemorrhage with retained placenta and maternal obesity. There was an increased risk for postpartum hemorrhage for women with a BMI of 40 or higher (5.2%) after normal delivery (odds ratio [OR] 1.23, 95% confidence interval [CI] 1.04-1.45]) compared with normal-weight women (4.4%) and even more pronounced (13.6%) after instrumental delivery (OR 1.69, 95% CI 1.22-2.34) compared with normal-weight women (8.8%). Maternal obesity was a risk factor for the use of heparin-like drugs (OR 2.86, 95% CI 2.22-3.68). The increased risk for atonic postpartum hemorrhage in the obese group has important clinical implications, such as considering administration of prophylactic postpartum uterotonic drugs to this group. II.

  19. Autotaxin is released from adipocytes, catalyzes lysophosphatidic acid synthesis, and activates preadipocyte proliferation. Up-regulated expression with adipocyte differentiation and obesity

    PubMed Central

    Ferry, Gilles; Tellier, Edwige; Try, Anne; Grés, Sandra; Naime, Isabelle; Simon, Marie Françoise; Rodriguez, Marianne; Boucher, Jérémie; Tack, Ivan; Gesta, Stéphane; Chomarat, Pascale; Dieu, Marc; Raes, Martine; Galizzi, Jean Pierre; Valet, Philippe; Boutin, Jean A.; Saulnier-Blache, Jean Sébastien

    2003-01-01

    Our group has recently demonstrated (Gesta et al. J. Lipid. Res, 2002, 43:904–910) the presence, in adipocyte conditioned-medium, of a soluble lysophospholipase D-activity (LPLDact) involved in synthesis of the bioactive phospholipid, lysophosphatidic acid (LPA). In the present report, LPLDact was purified from 3T3F442A-adipocyte conditioned-medium and identified as the type II ecto-nucleotide pyrophosphatase phosphodiesterase: autotaxin (ATX). A unique ATX cDNA was cloned from 3T3F442A-adipocytes, and its recombinant expression in COS-7 cells led to extracellular release of LPLDact. ATX mRNA expression was highly up-regulated during adipocyte differentiation of 3T3F442A-preadipocytes. This up-regulation was paralleled by the ability of newly differentiated adipocytes to release LPLDact and LPA. Differentiation-dependent up-regulation of ATX expression was also observed in primary culture of mouse preadipocytes. Treatment of 3T3F442A-preadipocytes with concentrated conditioned medium from ATX expressing-COS-7 cells led to an increase in cell number as compared with concentrated conditioned medium from ATX non-expressing-COS-7 cells. The specific effect of ATX on preadipocyte proliferation was completely suppressed by co-treatment with a LPA-hydrolyzing phospholipase, phospholipase B. Finally, ATX expression was found in mature adipocytes isolated from mouse adipose tissue, and was substantially increased in genetically obese-diabetic db/db mice when compared to their lean siblings. In conclusion, the present work shows that ATX is responsible for the LPLDact released by adipocytes, and exerts a paracrine control on preadipocyte growth via an LPA-dependent mechanism. Up-regulations of ATX expression with adipocyte differentiation and genetic obesity suggest a possible involvement of this released protein in the development of adipose tissue and obesity-associated pathologies. PMID:12642576

  20. Maternal obesity and neuroprotective magnesium sulfate.

    PubMed

    McPherson, Jessica; Smiley, Sarah; Stamilio, David

    2015-10-01

    Given the association between risk of cerebral palsy and children born to obese women, the study aim was to estimate whether maternal obesity is associated with reduced effectiveness of conventional antenatal magnesium sulfate dosing for the prevention of cerebral palsy and death. This is a secondary cohort analysis of a multicenter randomized clinical trial completed by the Maternal-Fetal Medicine Units Network. Women were included in the original trial if deemed high risk for preterm delivery in the subsequent 24 hours. The present study included singleton, nonanomalous fetuses that were randomized to and received magnesium sulfate with complete data available. Outcomes between obese (body mass index ≥30 kg/m(2)) and nonobese women were compared. A secondary analysis of outcomes between morbidly obese (body mass index ≥40 kg/m(2)) and nonmorbidly obese women was performed. The primary outcome was a composite of cerebral palsy or perinatal death before 15 months corrected age. Secondary outcomes included moderate to severe cerebral palsy or death, any cerebral palsy, moderate to severe cerebral palsy, and death. A logistic regression analysis was used to estimate the odds ratio of each outcome. Based on sample size, exposure rate (obesity) and an outcome rate of 10%, assuming an 80% power and a 0.05 alpha error, this study had sufficient power to detect a 2-fold increase in the primary outcome. Of 1188 women randomized to receive magnesium sulfate, 806 were included in this analysis. After adjusting for gestational age at delivery, maternal obesity was not associated with an increased risk of cerebral palsy or death in children born to women who received magnesium sulfate. Women with morbid obesity had higher rates of the primary outcome and cerebral palsy in an unadjusted analysis but did not have increased risks after adjusting for gestational age at delivery. In analyses stratified on gestational age, morbidly obese women who delivered after 28 weeks had

  1. Up-regulated expression of microRNA-143 in association with obesity in adipose tissue of mice fed high-fat diet.

    PubMed

    Takanabe, Rieko; Ono, Koh; Abe, Yukiko; Takaya, Tomohide; Horie, Takahiro; Wada, Hiromichi; Kita, Toru; Satoh, Noriko; Shimatsu, Akira; Hasegawa, Koji

    2008-11-28

    MicroRNAs (miRNAs) are short non-coding RNA that post-transcriptionally regulates gene expression. miR-143 has been proposed to play a role in the differentiation of adipocytes in culture. However, the mechanism regulating the expression of miR-143 in adult adipose tissue during the development of obesity in vivo is unknown. Here in, we showed that the expression of miR-143 in the mesenteric fat was up-regulated in mice fed a high-fat diet. Increased miR-143 expression was associated with an elevated body weight and mesenteric fat weight. Furthermore, miR-143 levels were closely correlated with expression levels of adipocyte differentiation markers such as PPARgamma and aP2 as well as plasma levels of leptin, one of the important adipocytokines involved in insulin resistance. These findings provide the first evidence for the up-regulated expression of miR-143 in the mesenteric fat of high-fat diet-induced obese mice, which might contribute to the regulated expression of adipocyte genes involved in the pathophysiology of obesity.

  2. RXR antagonism induces G0 /G1 cell cycle arrest and ameliorates obesity by up-regulating the p53-p21(Cip1) pathway in adipocytes.

    PubMed

    Nakatsuka, Atsuko; Wada, Jun; Hida, Kazuyuki; Hida, Aya; Eguchi, Jun; Teshigawara, Sanae; Murakami, Kazutoshi; Kanzaki, Motoko; Inoue, Kentaro; Terami, Takahiro; Katayama, Akihiro; Ogawa, Daisuke; Kagechika, Hiroyuki; Makino, Hirofumi

    2012-04-01

    The peroxisome proliferator activated receptor-γ (PPARγ) agonist, pioglitazone (PIO), exerts anti-diabetic properties associated with increased fat mass, whereas the retinoid X receptor (RXR) antagonist HX531 demonstrates anti-obesity and anti-diabetic effects with reduced body weight and fat pad mass. The cell cycle abnormality in adipocytes has not been well-investigated in obesity or during treatment with modulators of nuclear receptors. We therefore investigated cell size and cell cycle distributions of adipocytes in vivo and examined the expression of cell cycle regulators in cultured human visceral preadipocytes. The cell size distribution and cell cycle analyses of in vivo adipocytes derived from OLETF rats demonstrated that HX531 brought about G0/G1 cell cycle arrest associated with the inhibition of cellular hypertrophy, which resulted in the reduction of fat pad mass. In contrast, PIO promoted proliferation activities associated with the increase in M + late M:G0 + G1 ratio and the appearance of both small and hypertrophied adipocytes. In cultured human visceral preadipocytes HX531 up-regulated cell cycle regulators, p53, p21(Cip1), cyclin D1, Fbxw7 and Skp2, which are known contributors towards G0 /G1 cell cycle arrest. The knockdown of p53 with a shRNA lentivirus reversed the HX531-induced up-regulation of p21(Cip1), which is one of the major p53-effector molecules. We conclude that HX531 exerts anti-obesity and anti-diabetes properties by up-regulating the p53-p21(Cip1) pathway, resulting in G0/G1 cell cycle arrest and the inhibition of cellular hypertrophy of adipocytes. Copyright © 2012 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

  3. Maternal Obesity in Pregnancy Developmentally Programs Adipose Tissue Inflammation in Young, Lean Male Mice Offspring

    PubMed Central

    Alfaradhi, Maria Z.; Fernandez-Twinn, Denise S.; Pantaleão, Lucas C.; Carr, Sarah K.; Ferland-McCollough, David; Yeo, Giles S. H.; Bushell, Martin; Ozanne, Susan E.

    2016-01-01

    Obesity during pregnancy has a long-term effect on the health of the offspring including risk of developing the metabolic syndrome. Using a mouse model of maternal diet-induced obesity, we employed a genome-wide approach to investigate the microRNA (miRNA) and miRNA transcription profile in adipose tissue to understand mechanisms through which this occurs. Male offspring of diet-induced obese mothers, fed a control diet from weaning, showed no differences in body weight or adiposity at 8 weeks of age. However, offspring from the obese dams had up-regulated cytokine (Tnfα; P < .05) and chemokine (Ccl2 and Ccl7; P < .05) signaling in their adipose tissue. This was accompanied by reduced expression of miR-706, which we showed can directly regulate translation of the inflammatory proteins IL-33 (41% up-regulated; P < .05) and calcium/calmodulin-dependent protein kinase 1D (30% up-regulated; P < .01). We conclude that exposure to obesity during development primes an inflammatory environment in adipose tissue that is independent of offspring adiposity. Programming of adipose tissue miRNAs that regulate expression of inflammatory signaling molecules may be a contributing mechanism. PMID:27583789

  4. Autotaxin is released from adipocytes, catalyzes lysophosphatidic acid synthesis, and activates preadipocyte proliferation. Up-regulated expression with adipocyte differentiation and obesity.

    PubMed

    Ferry, Gilles; Tellier, Edwige; Try, Anne; Grés, Sandra; Naime, Isabelle; Simon, Marie Françoise; Rodriguez, Marianne; Boucher, Jérémie; Tack, Ivan; Gesta, Stéphane; Chomarat, Pascale; Dieu, Marc; Raes, Martine; Galizzi, Jean Pierre; Valet, Philippe; Boutin, Jean A; Saulnier-Blache, Jean Sébastien

    2003-05-16

    Our group has recently demonstrated (Gesta, S., Simon, M., Rey, A., Sibrac, D., Girard, A., Lafontan, M., Valet, P., and Saulnier-Blache, J. S. (2002) J. Lipid Res. 43, 904-910) the presence, in adipocyte conditioned-medium, of a soluble lysophospholipase d-activity (LPLDact) involved in synthesis of the bioactive phospholipid lysophosphatidic acid (LPA). In the present report, LPLDact was purified from 3T3F442A adipocyte-conditioned medium and identified as the type II ecto-nucleotide pyrophosphatase phosphodiesterase, autotaxin (ATX). A unique ATX cDNA was cloned from 3T3F442A adipocytes, and its recombinant expression in COS-7 cells led to extracellular release of LPLDact. ATX mRNA expression was highly up-regulated during adipocyte differentiation of 3T3F442A-preadipocytes. This up-regulation was paralleled by the ability of newly differentiated adipocytes to release LPLDact and LPA. Differentiation-dependent up-regulation of ATX expression was also observed in a primary culture of mouse preadipocytes. Treatment of 3T3F442A-preadipocytes with concentrated conditioned medium from ATX-expressing COS-7 cells led to an increase in cell number as compared with concentrated conditioned medium from ATX non-expressing COS-7 cells. The specific effect of ATX on preadipocyte proliferation was completely suppressed by co-treatment with a LPA-hydrolyzing phospholipase, phospholipase B. Finally, ATX expression was found in mature adipocytes isolated from mouse adipose tissue and was substantially increased in genetically obese-diabetic db/db mice when compared with their lean siblings. In conclusion, the present work shows that ATX is responsible for the LPLDact released by adipocytes and exerts a paracrine control on preadipocyte growth via an LPA-dependent mechanism. Up-regulations of ATX expression with adipocyte differentiation and genetic obesity suggest a possible involvement of this released protein in the development of adipose tissue and obesity

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

    SciTech Connect

    Liu, Wei-Xin; Wang, Ting; Zhou, Feng; Wang, Ying; Xing, Jun-Wei; Zhang, Shen; Gu, Shou-Zhi; Sang, Li-Xuan; Dai, Cong; Wang, Hai-Lan

    2015-04-10

    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-sedentary 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

  6. The Effect of Maternal Obesity on the Offspring

    PubMed Central

    Williams, Christine B.; Mackenzie, Kusaynyonon C.; Gahagan, Sheila

    2016-01-01

    Maternal obesity is inextricably linked to adverse health outcomes for the mother and her children. The peripartum period is a critical period of risk. In this chapter, we examine the importance of maternal pre-pregnancy weight status, gestational weight gain, breastfeeding, and postpartum weight loss in relation to subsequent risk for maternal obesity and obesity in the offspring. Promoting optimal maternal weight during the preconception, pregnancy and postpartum periods will provide lifelong benefits for maternal health and the health of her progeny. PMID:24936914

  7. Anti-obesity effect of total phenylpropanoid glycosides from Ligustrum robustum Blume in fatty diet-fed mice via up-regulating leptin.

    PubMed

    Yang, Run-mei; Liu, Fang; He, Zhen-dan; Ji, Min; Chu, Xin-xin; Kang, Zhuo-ying; Cai, Da-yong; Gao, Nan-nan

    2015-07-01

    In Chinese folk medicine, the leaves of Ligustrum robustum Blume (LR) were commonly used in the treatment of obesity and hyperlipidemia. This study aimed to evaluate the anti-obesity effect and mechanisms of total phenylpropanoid glycosides from Ligustrum robustum Blume (LRTPG) in fatty diet-fed C57BL/6J mice. C57BL/6J mice were divided randomly into 6 groups, i.e., control, model, positive (Orlistat 0.12g/kg), and LRTPG at three dosages (0.3, 0.6 or 1.2g/kg), respectively. Control mice were fed with standard diet; the others were fed with fatty diet. After 4 weeks׳ modeling, therapy mice were intragastrically administrated with positive drug or LRTPG for 5 weeks, respectively. Pharmacodynamic effects including body weight, fat weight, Lee׳s index, serum lipid levels, morphological changes and adipocyte area ratio were evaluated. The mechanisms were explored as the factors related to lipids metabolism in gene expressions by real-time PCR, and assured as the protein level of differential gene by Western blotting. The anti-obesity effects of LRTPG in all treated mice were shown as decreased body weight, fat mass, Lee׳s index, total cholesterol (TC) level, and adipocyte area. The mechanisms were demonstrated as elevated mRNA and protein levels of adipose leptin, and consequently decreasing mRNA of adipose acyl coenzyme A: diacylglycerol acyltransferase (DGAT) with increasing mRNA of hepatic cholesterol 7α-hydroxylase (CYP7A1), which led to inhibition of triglyceride (TG) synthesis and promotion of cholesterol catabolism. The anti-obesity effect of LRTPG in fatty diet-fed mice was related to the up-regulation of leptin, which may provide scientific evidence supporting the traditional usage of LR on obesity in China. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.

  8. Irbesartan treatment up-regulates hepatic expression of PPARα and its target genes in obese Koletsky (fak/fak) rats: a link to amelioration of hypertriglyceridaemia

    PubMed Central

    Rong, X; Li, Y; Ebihara, K; Zhao, M; Kusakabe, T; Tomita, T; Murray, M; Nakao, K

    2010-01-01

    BACKGROUND AND PURPOSE Hypertriglyceridaemia is associated with an increased risk of cardiovascular disease. Irbesartan, a well-established angiotensin II type 1 receptor (AT1) blocker, improves hypertriglyceridaemia in rodents and humans but the underlying mechanism of action is unclear. EXPERIMENTAL APPROACH Male obese Koletsky (fak/fak) rats, which exhibit spontaneous hypertension and metabolic abnormalities, received irbesartan (40 mg·kg−1·day−1) or vehicle by oral gavage over 7 weeks. Adipocyte-derived hormones in plasma were measured by ELISA. Gene expression in liver and other tissues was assessed by real-time PCR and Western immunoblotting. KEY RESULTS In Koletsky (fak/fak) rats irbesartan lowered plasma concentrations of triglycerides and non-esterified fatty acids, and decreased plasma insulin concentrations and the homeostasis model assessment of insulin resistance index. However, this treatment did not affect food intake, body weight, epididymal white adipose tissue weight, adipocyte size and plasma leptin concentrations, although plasma adiponectin was decreased. Irbesartan up-regulated hepatic expression of mRNAs corresponding to peroxisome proliferator-activated receptor (PPAR)α and its target genes (carnitine palmitoyltransferase-1a, acyl-CoA oxidase and fatty acid translocase/CD36) that mediate hepatic fatty acid uptake and oxidation; the increase in hepatic PPARα expression was confirmed at the protein level. In contrast, irbesartan did not affect expression of adipose PPARγ and its downstream genes or hepatic genes that mediate fatty acid synthesis. CONCLUSIONS AND IMPLICATIONS These findings demonstrate that irbesartan treatment up-regulates PPARα and several target genes in liver of obese spontaneously hypertensive Koletsky (fak/fak) rats and offers a novel insight into the lipid-lowering mechanism of irbesartan. PMID:20649581

  9. Irbesartan treatment up-regulates hepatic expression of PPARalpha and its target genes in obese Koletsky (fa(k)/fa(k)) rats: a link to amelioration of hypertriglyceridaemia.

    PubMed

    Rong, X; Li, Y; Ebihara, K; Zhao, M; Kusakabe, T; Tomita, T; Murray, M; Nakao, K

    2010-08-01

    Hypertriglyceridaemia is associated with an increased risk of cardiovascular disease. Irbesartan, a well-established angiotensin II type 1 receptor (AT(1)) blocker, improves hypertriglyceridaemia in rodents and humans but the underlying mechanism of action is unclear. Male obese Koletsky (fa(k)/fa(k)) rats, which exhibit spontaneous hypertension and metabolic abnormalities, received irbesartan (40 mg x kg(-1) x day(-1)) or vehicle by oral gavage over 7 weeks. Adipocyte-derived hormones in plasma were measured by ELISA. Gene expression in liver and other tissues was assessed by real-time PCR and Western immunoblotting. In Koletsky (fa(k)/fa(k)) rats irbesartan lowered plasma concentrations of triglycerides and non-esterified fatty acids, and decreased plasma insulin concentrations and the homeostasis model assessment of insulin resistance index. However, this treatment did not affect food intake, body weight, epididymal white adipose tissue weight, adipocyte size and plasma leptin concentrations, although plasma adiponectin was decreased. Irbesartan up-regulated hepatic expression of mRNAs corresponding to peroxisome proliferator-activated receptor (PPAR)alpha and its target genes (carnitine palmitoyltransferase-1a, acyl-CoA oxidase and fatty acid translocase/CD36) that mediate hepatic fatty acid uptake and oxidation; the increase in hepatic PPARalpha expression was confirmed at the protein level. In contrast, irbesartan did not affect expression of adipose PPARgamma and its downstream genes or hepatic genes that mediate fatty acid synthesis. These findings demonstrate that irbesartan treatment up-regulates PPARalpha and several target genes in liver of obese spontaneously hypertensive Koletsky (fa(k)/fa(k)) rats and offers a novel insight into the lipid-lowering mechanism of irbesartan.

  10. Maternal obesity and induction of labor.

    PubMed

    O'Dwyer, Vicky; O'Kelly, Sarah; Monaghan, Bernadette; Rowan, Ann; Farah, Nadine; Turner, Michael J

    2013-12-01

    To review induction of labor analyzed by body mass index (BMI) category in primigravidas and multigravidas. Prospective observational study. Women enrolled after sonographic confirmation of singleton pregnancy in the first trimester. Large university teaching hospital. Maternal height and weight were measured accurately before BMI calculation. Clinical details were recorded after review of individual obstetric records. Emergency cesarean section and obstetric interventions. Of 2000 women enrolled, 50.4% (n = 1008) were primigravidas and 17.3% (n = 346) were obese. The induction rate was 25.6% and the overall cesarean section rate 22.0%. Primigravidas were more likely to have labor induced than multigravidas (38.1% vs. 23.4%, p < 0.001). Compared with women with a normal BMI, obese primigravidas but not obese multigravidas were more likely to have labor induced. In primigravidas who had labor induced, the cesarean section rate was 20.6% (91/442) compared with 8.3% (17/206) in multigravidas who had labor induced (p < 0.001). In obese primigravidas, induction of labor was also more likely to be associated with other interventions such as epidural analgesia, fetal blood sampling and emergency cesarean section. In contrast, induction of labor in obese multigravidas was not only less common but also not associated with an increase in other interventions compared with multigravidas with a normal BMI. Due to the short-term and long-term implications of an unsuccessful induction in an obese primigravida, we recommend that induction of labor should only be undertaken for strict obstetric indications after careful consideration by an experienced clinician. © 2013 Nordic Federation of Societies of Obstetrics and Gynecology.

  11. 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.

  12. Impact of Maternal Obesity on Fetal Programming of Cardiovascular Disease

    PubMed Central

    Frias, Antonio E.; Grove, Kevin L.

    2015-01-01

    The in utero environment is a key determinant of long-term health outcomes; poor maternal metabolic state and placental insufficiency are strongly associated with these long-term health risks. Human epidemiological studies link maternal obesity and offspring cardiovascular disease in later life, but mechanistic studies in animal models are limited. Here, we review the literature pertaining to maternal consequences of obesity during pregnancy and the subsequent impact on fetal cardiovascular development. PMID:25933822

  13. Impact of maternal obesity on fetal programming of cardiovascular disease.

    PubMed

    Roberts, Victoria H J; Frias, Antonio E; Grove, Kevin L

    2015-05-01

    The in utero environment is a key determinant of long-term health outcomes; poor maternal metabolic state and placental insufficiency are strongly associated with these long-term health risks. Human epidemiological studies link maternal obesity and offspring cardiovascular disease in later life, but mechanistic studies in animal models are limited. Here, we review the literature pertaining to maternal consequences of obesity during pregnancy and the subsequent impact on fetal cardiovascular development. ©2015 Int. Union Physiol. Sci./Am. Physiol. Soc.

  14. Piperine's mitigation of obesity and diabetes can be explained by its up-regulation of the metabolic rate of resting muscle.

    PubMed

    Nogara, Leonardo; Naber, Nariman; Pate, Edward; Canton, Marcella; Reggiani, Carlo; Cooke, Roger

    2016-11-15

    We identify a target for treating obesity and type 2 diabetes, the consumption of calories by an increase in the metabolic rate of resting skeletal muscle. The metabolic rate of skeletal muscle can be increased by shifting myosin heads from the super-relaxed state (SRX), with a low ATPase activity, to a disordered relaxed state (DRX), with a higher ATPase activity. The shift of myosin heads was detected by a change in fluorescent intensity of a probe attached to the myosin regulatory light chain in skinned skeletal fibers, allowing us to perform a high-throughput screen of 2,128 compounds. The screen identified one compound, which destabilized the super-relaxed state, piperine (the main alkaloid component of black pepper). Destabilization of the SRX by piperine was confirmed by single-nucleotide turnover measurements. The effect was only observed in fast twitch skeletal fibers and not in slow twitch fibers or cardiac tissues. Piperine increased ATPase activity of skinned relaxed fibers by 66 ± 15%. The Kd was ∼2 µM. Piperine had little effect on the mechanics of either fully active or resting muscle fibers. Previous work has shown that piperine can mitigate both obesity and type 2 diabetes in rodent models of these conditions. We propose that the increase in resting muscle metabolism contributes to these positive effects. The results described here show that up-regulation of resting muscle metabolism could treat obesity and type 2 diabetes and that piperine would provide a useful lead compound for the development of these therapies.

  15. Piperine’s mitigation of obesity and diabetes can be explained by its up-regulation of the metabolic rate of resting muscle

    PubMed Central

    Naber, Nariman; Pate, Edward; Canton, Marcella; Reggiani, Carlo; Cooke, Roger

    2016-01-01

    We identify a target for treating obesity and type 2 diabetes, the consumption of calories by an increase in the metabolic rate of resting skeletal muscle. The metabolic rate of skeletal muscle can be increased by shifting myosin heads from the super-relaxed state (SRX), with a low ATPase activity, to a disordered relaxed state (DRX), with a higher ATPase activity. The shift of myosin heads was detected by a change in fluorescent intensity of a probe attached to the myosin regulatory light chain in skinned skeletal fibers, allowing us to perform a high-throughput screen of 2,128 compounds. The screen identified one compound, which destabilized the super-relaxed state, piperine (the main alkaloid component of black pepper). Destabilization of the SRX by piperine was confirmed by single-nucleotide turnover measurements. The effect was only observed in fast twitch skeletal fibers and not in slow twitch fibers or cardiac tissues. Piperine increased ATPase activity of skinned relaxed fibers by 66 ± 15%. The Kd was ∼2 µM. Piperine had little effect on the mechanics of either fully active or resting muscle fibers. Previous work has shown that piperine can mitigate both obesity and type 2 diabetes in rodent models of these conditions. We propose that the increase in resting muscle metabolism contributes to these positive effects. The results described here show that up-regulation of resting muscle metabolism could treat obesity and type 2 diabetes and that piperine would provide a useful lead compound for the development of these therapies. PMID:27799519

  16. 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.

  17. 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.

  18. Maternal obesity is associated with a lipotoxic placental environment

    USDA-ARS?s Scientific Manuscript database

    Maternal obesity is associated with placental lipotoxicity, oxidative stress, and inflammation, where MAPK activity may play a central role. Accordingly, we have previously shown that placenta from obese women have increased activation of MAPK-JNK. Here, we performed RNA-sequencing on term placenta ...

  19. 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.

  20. The impact of maternal obesity during pregnancy on offspring immunity

    PubMed Central

    Wilson, Randall; Messaoudi, Ilhem

    2015-01-01

    In the United States, approximately 64% of women of childbearing age are either overweight or obese. Maternal obesity during pregnancy is associated with a greater risk for adverse maternal-fetal outcomes. Adverse health outcomes for the offspring can persist into adulthood, increasing the incidence of several chronic conditions including cardiovascular disease, diabetes, and asthma. Since these diseases have a significant inflammatory component, these observations are indicative of perturbation of the normal development and maturation of the immune system of the offspring in utero. This hypothesis is strongly supported by data from several rodent studies. Although the mechanisms of these perturbations are not fully understood, it is thought that increased placental inflammation due to obesity may directly affect neonatal development through alterations in nutrient transport. In this review we examine the impact of maternal obesity on the neonatal immune system, and potential mechanisms for the changes observed. PMID:26232506

  1. 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.

  2. Maternal Obesity is Associated with a Lipotoxic Placental Environment

    PubMed Central

    Saben, Jessica; Lindsey, Forrest; Zhong, Ying; Thakali, Keshari; Badger, Thomas M.; Andres, Aline; Gomez-Acevedo, Horacio; Shankar, Kartik

    2014-01-01

    Maternal obesity is associated with placental lipotoxicity, oxidative stress, and inflammation, where MAPK activity may play a central role. Accordingly, we have previously shown that placenta from obese women have increased activation of MAPK-JNK. Here, we performed RNA-sequencing on term placenta from twenty-two subjects who were dichotomized based on pre-pregnancy BMI into lean (BMI 19–24 kg/m2; n = 12) and obese groups (BMI, 32–43 kg/m2; n = 12). RNA-seq revealed 288 genes to be significantly different in placenta from obese women by ≥1.4-fold. GO analysis identified genes related to lipid metabolism, angiogenesis, hormone activity, and cytokine activity to be altered in placenta from obese women. Indicative of a lipotoxic environment, increased placental lipid and CIDEA protein were associated with decreased AMPK and increased activation of NF-κB(p65) in placenta from obese women. Furthermore, we observed a 25% decrease in total antioxidant capacity and increased nuclear FOXO4 localization in placenta from obese women that was significantly associated with JNK activation, suggesting that maternal obesity may also be associated with increased oxidative stress in placenta. Maternal obesity was also associated with decreased HIF-1α protein expression, suggesting a potential link between increased inflammation/oxidative stress and decreased angiogenic factors. Together, these findings indicate that maternal obesity leads to a lipotoxic placental environment that is associated with decreased regulators of angiogenesis and increased markers of inflammation and oxidative stress. PMID:24484739

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

    PubMed

    Neri, Caterina; Edlow, Andrea G

    2015-09-03

    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. Copyright © 2016 Cold Spring Harbor Laboratory Press; all rights reserved.

  4. 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

  5. Maternal obesity and sex-specific differences in placental pathology.

    PubMed

    Leon-Garcia, Sandra M; Roeder, Hilary A; Nelson, Katharine K; Liao, Xiaoyan; Pizzo, Donald P; Laurent, Louise C; Parast, Mana M; LaCoursiere, D Yvette

    2016-02-01

    Adverse effects of obesity have been linked to inflammation in various tissues, but studies on placental inflammation and obesity have demonstrated conflicting findings. We sought to investigate the influence of pregravid obesity and fetal sex on placental histopathology while controlling for diabetes and hypertension. Placental histopathology focusing on inflammatory markers of a cohort of normal weight (BMI = 20-24.9) and obese (BMI ≥ 30) patients was characterized. Demographic, obstetric and neonatal variables were assessed. 192 normal and 231 obese women were included. Placental characteristics associated with obesity and fetal sex independent of diabetes and hypertension were placental disc weight >90(th) percentile, decreased placental efficiency, chronic villitis (CV), fetal thrombosis, and normoblastemia. Additionally, female fetuses of obese mothers had higher rates of CV and fetal thrombosis. Increasing BMI increased the risk of normoblastemia and CV. The final grade and extent of CV was significantly associated with obesity and BMI, but not fetal gender. Finally, CV was less common in large-for-gestation placentas. Maternal obesity results in placental overgrowth and fetal hypoxia as manifested by normoblastemia; it is also associated with an increased incidence of CV and fetal thrombosis, both more prevalent in female placentas. We have shown for the first time that the effect of maternal obesity on placental inflammation is independent of diabetes and hypertension, but significantly affected by fetal sex. Our data also point to the intriguing possibility that CV serves to normalize placental size, and potentially fetal growth, in the setting of maternal obesity. Copyright © 2015. Published by Elsevier Ltd.

  6. Maternal obesity increases oxidative stress in the newborn.

    PubMed

    Gallardo, Juan Manuel; Gómez-López, Jaqueline; Medina-Bravo, Patricia; Juárez-Sánchez, Francisco; Contreras-Ramos, Alejandra; Galicia-Esquivel, Matilde; Sánchez-Urbina, Rocío; Klünder-Klünder, Miguel

    2015-08-01

    Obesity before pregnancy is associated with a greater risk for the offspring to develop obesity and diabetes in childhood and adulthood. The aim of the present study was to determine the association between maternal overweight or obesity before pregnancy and newborn oxidative stress (OS). Seventy-two mother-child pairs were divided according to the pre-gestational body mass index (BMI) of the mothers as follows: eutrophic (n = 21), overweight (n = 32), and obese (n = 19). Malondialdehyde (MDA) and nitric oxide (NO) were measured in the plasma of a blood sample from the newborn's umbilical cord. The MDA levels of newborns increased with maternal BMI (P = 0.001), as did the levels of NO (P = 0.019). There was a direct correlation between MDA and NO levels in each of the three groups (eutrophic: R(2)  = 0.59, P < 0.001; overweight: R(2)  = 0.45, P < 0.001; and obese: R(2)  = 0.26, P = 0.024). Maternal overweight and obesity before pregnancy are associated with increased OS in the offspring. © 2015 The Obesity Society.

  7. 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...

  8. Associations of maternal obesity and smoking status with perinatal outcomes.

    PubMed

    Phillips, Julie K; Skelly, Joan M; King, Sarah E; Bernstein, Ira M; Higgins, Stephen T

    2017-05-14

    Maternal obesity and smoking are associated with adverse perinatal outcomes. These prevalent conditions contribute to health disparities. In this study, we examine whether maternal BMI moderates the impact of smoking cessation on short-term perinatal outcomes. This is a secondary analysis of assessments conducted from several prospective clinical trials examining the efficacy of incentives to promote smoking cessation during pregnancy. Participants were randomly assigned to receive financial incentives contingent upon smoking abstinence or a control condition. Pregnancy outcomes were abstracted from the medical record. ANCOVA and multiple logistic regression were used for statistical analysis. Among 388 women, there was a significant interaction between maternal pre-pregnancy BMI and smoking status on gestational age at delivery (p = .03) and admission to the NICU (p = .04). Among underweight/normal weight gravidas, smoking resulted in earlier deliveries and a greater likelihood of NICU admission than in those who abstained. Among overweight/obese gravidas, there was no effect of smoking on gestational age at delivery and infants of smokers were less likely to be admitted to the NICU. Maternal obesity and smoking have significant individual effects on perinatal outcome. Maternal overweight/obesity appears to moderate the effect of smoking on gestational age at delivery and on NICU admissions.

  9. Maternal obesity and inflammatory mediators: A controversial association.

    PubMed

    Pendeloski, Karen Priscilla Tezotto; Ono, Erika; Torloni, Maria Regina; Mattar, Rosiane; Daher, Silvia

    2017-03-22

    The link between maternal obesity and inflammatory mediators is still unclear. Our aim was to summarize the main findings of recently published studies on this topic. We performed a search in Medline for studies published in the last years on obesity, human pregnancy, and inflammatory mediators. We report the findings of 30 studies. The characteristics and number of participants, study design, gestational age at sample collection, and type of sample varied widely. Approximately two-thirds of them investigated more than one mediator, and 50% included participants in only one trimester of pregnancy. The most frequently investigated mediators were leptin, tumour necrosis factor-alpha (TNF-α), and interleukin (IL)-6. Almost all studies reported an association between maternal obesity, leptin, and C-reactive protein (CRP) serum levels but not with IL-1β and IL-10. The association of IL-6, TNF-α, monocyte chemo-attractant protein-1 (MCP-1), adiponectin, and resistin with maternal obesity is still controversial. To clarify the physiopathological link between maternal obesity and inflammation, more high-quality studies are needed.

  10. Maternal obesity during pregnancy is negatively associated with maternal and neonatal iron status

    PubMed Central

    Jones, Andrew D.; Zhao, Gengli; Jiang, Ya-ping; Zhou, Min; Xu, Guobin; Kaciroti, Niko; Zhang, Zhixiang; Lozoff, Betsy

    2015-01-01

    Background/Objectives Obesity among pregnant women may adversely affect both maternal iron status throughout pregnancy and placental transfer of iron. The objective of this study was to determine the association of maternal body mass index (BMI) with 1) maternal iron status and inflammation in mid and late pregnancy, 2) the change in maternal iron status throughout pregnancy, and 3) neonatal iron status. Subjects/Methods We examined longitudinal data from 1,613 participants in a pregnancy iron supplementation trial in rural China. Women with uncomplicated singleton pregnancies were enrolled in the early second trimester of pregnancy and followed through parturition. Maternal blood samples obtained at enrollment and in the third trimester, and cord blood samples were analyzed for a range of hematological and iron biomarkers. Results There was a negative association between maternal BMI and iron status at enrollment (transferrin receptor (sTfR): r=0.20, P<0.001; body iron (BI): r=−0.05; P=0.03). This association was markedly stronger among obese women. Maternal BMI was positively associated with maternal inflammation (C-reactive protein: r=0.33, P<0.001). In multiple linear regression models, maternal BMI was negatively associated with neonatal iron status (cord serum ferritin: −0.01, P=0.008; BI: −0.06, P=0.006) and associated with a lower decrease in iron status throughout pregnancy (sTfR: −4.6, P<0.001; BI: 1.1, P=0.004). Conclusions Maternal obesity during pregnancy may adversely affect both maternal and neonatal iron status, potentially through inflammatory pathways. PMID:26813939

  11. 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.

  12. Maternal Serum Leptin During Pregnancy and Infant Birth Weight: the Influence of Maternal Overweight and Obesity

    PubMed Central

    Misra, V. K.; Straughen, J. K.; Trudeau, S.

    2012-01-01

    Few studies have examined whether the distinct metabolic patterns found in obese and non-obese pregnant women may have different effects on the growing fetus. Our objective was to estimate the influence of longitudinal variation in maternal serum leptin levels on variation in infant birth weight in overweight/obese versus normal weight women. In a prospective cohort of 286 gravidas, we measured maternal weight and serum leptin levels at 6–10,10–14,16–20, 22–26, and 32–36 weeks gestation. Effects of leptin levels on infant birth weight adjusted for gestational age at delivery (aBW) were analyzed using a linear regression model that accounted for the relationship of time-varying predictors to the log transformed leptin concentrations. Overweight/obese and normal weight gravidas exhibit different relationships of aBW to maternal serum leptin and its rate of change across pregnancy. For normal weight women, aBW is not associated with either the magnitude of the logarithm of the leptin concentration nor with its rate of change in either the first or second half of pregnancy. Conversely, for overweight/obese women, we find that an increase in the rate of change in maternal serum leptin in the second half of pregnancy is significantly associated with a decrease in aBW. We find that this effect is distinct from that of maternal weight. Differences in the effect of maternal serum leptin on fetal growth between overweight/obese and normal weight women suggest metabolic and physiologic heterogeneity between these groups. Such differences may be involved in the long-term physiologic effects of the obese intrauterine environment on the health of the offspring. PMID:23784911

  13. Maternal serum leptin during pregnancy and infant birth weight: the influence of maternal overweight and obesity.

    PubMed

    Misra, Vinod K; Straughen, Jennifer K; Trudeau, Sheri

    2013-05-01

    Few studies have examined whether the distinct metabolic patterns found in obese and nonobese pregnant women have different effects on the growing fetus. Our objective was to estimate the influence of longitudinal variation in maternal serum leptin levels on variation in infant birth weight in overweight/obese versus normal-weight women. In a prospective cohort of 286 gravidas, maternal weight and serum leptin levels at 6-10, 10-14, 16-20, 22-26, and 32-36 weeks gestation were measured. Effects of leptin levels on infant birth weight adjusted for gestational age at delivery (aBW) were analyzed using a linear regression model that accounted for the relationship of time-varying predictors to the log-transformed leptin concentrations. Different relationships of aBW to maternal serum leptin and its rate of change across pregnancy were exhibited by overweight/obese and normal-weight gravidas. For normal-weight women, aBW is not associated with either the magnitude of the logarithm of the leptin concentration or with its rate of change in either the first or second half of pregnancy. Conversely, for overweight/obese women, an increase in the rate of change in maternal serum leptin in the second half of pregnancy is significantly associated with a decrease in aBW. This effect is distinct from that of maternal weight. Differences in the effect of maternal serum leptin on fetal growth between overweight/ obese and normal-weight women suggest metabolic and physiologic heterogeneity between these groups. Such differences may be involved in the long-term physiologic effects of the obese intrauterine environment on the health of the offspring. Copyright © 2012 The Obesity Society.

  14. 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.

  15. 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.

  16. Maternal Exposure of Rats to Isoflurane during Late Pregnancy Impairs Spatial Learning and Memory in the Offspring by Up-Regulating the Expression of Histone Deacetylase 2

    PubMed Central

    Hu, Yan; Zhao, Weilu; Zuo, Zhiyi; Yu, Qi; Liu, Zhiyi; Lin, Jiamei; Feng, Yunlin; Li, Binda; Wu, Liuqin; Xu, Lin

    2016-01-01

    Increasing evidence indicates that most general anesthetics can harm developing neurons and induce cognitive dysfunction in a dose- and time-dependent manner. Histone deacetylase 2 (HDAC2) has been implicated in synaptic plasticity and learning and memory. Our previous results showed that maternal exposure to general anesthetics during late pregnancy impaired the offspring’s learning and memory, but the role of HDAC2 in it is not known yet. In the present study, pregnant rats were exposed to 1.5% isoflurane in 100% oxygen for 2, 4 or 8 hours or to 100% oxygen only for 8 hours on gestation day 18 (E18). The offspring born to each rat were randomly subdivided into 2 subgroups. Thirty days after birth, the Morris water maze (MWM) was used to assess learning and memory in the offspring. Two hours before each MWM trial, an HDAC inhibitor (SAHA) was given to the offspring in one subgroup, whereas a control solvent was given to those in the other subgroup. The results showed that maternal exposure to isoflurane impaired learning and memory of the offspring, impaired the structure of the hippocampus, increased HDAC2 mRNA and downregulated cyclic adenosine monophosphate (cAMP) response element binding protein (CREB) mRNA, N-methyl-D-aspartate receptor 2 subunit B (NR2B) mRNA and NR2B protein in the hippocampus. These changes were proportional to the duration of the maternal exposure to isoflurane and were reversed by SAHA. These results suggest that exposure to isoflurane during late pregnancy can damage the learning and memory of the offspring rats via the HDAC2-CREB -NR2B pathway. This effect can be reversed by HDAC2 inhibition. PMID:27536989

  17. 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

  18. Maternal "isolated" obesity and obstetric complications.

    PubMed

    Gilead, Rami; Yaniv Salem, Shimrit; Sergienko, Ruslan; Sheiner, Eyal

    2012-12-01

    To investigate pregnancy outcomes, particularly cesarean delivery (CD), among women with "isolated" obesity (i.e. without additional comorbidities). We conducted a retrospective population-based study between the years 1988-2010. The pregnancy outcomes of obese (prepregnancy BMI ≥30 kg/m(2)) and nonobese patients were compared. Patients with chronic hypertension, pregestational diabetes mellitus, other preexisting chronic morbidities, multiple gestations, age above 40 years, grand multiparity (above 5 deliveries), lack of prenatal care, and following fertility treatments were excluded from the analysis. Stratified analyses, using multiple logistic regression models, were performed to control for confounders. During the study period, a total of 173,628 deliveries met the inclusion criteria; 1605 (0.9%) occurred in patients with "isolated" obesity. Higher rates of CD were found among patients with "isolated" obesity (30.7% vs. 12.3%; odds ration [OR] = 3.2; p < 0.001). When controlling for possible confounders, using a multivariable model with CD as the outcome variable, the association between "isolated" obesity and CD remained significant (adjusted OR = 2.6; p < 0.001). No significant differences were found in the risks of perinatal complications including perinatal mortality, shoulder dystocia, congenital malformations, and low 5-min Apgar score. "Isolated" obesity, although not a risk factor for adverse perinatal outcomes, is an independent risk factor for CD.

  19. Maternal obesity impairs specific regulatory pathways in human myometrial arteries.

    PubMed

    Hayward, Christina E; Cowley, Elizabeth J; Mills, Tracey A; Sibley, Colin P; Wareing, Mark

    2014-03-01

    Obese women (body mass index ≥30 kg/m(2)) are at greater risk than normal weight women of pregnancy complications associated with maternal and infant morbidity, particularly the development of cardiovascular disease and metabolic disorders in later life; why this occurs is unknown. Nonpregnant, obese individuals exhibit systemic vascular endothelial dysfunction. We tested the hypothesis that obese pregnant women have altered myometrial arterial function compared to pregnant women of normal (18-24 kg/m(2)) and overweight (25-29 kg/m(2)) body mass index. Responses to vasoconstrictors, U46619 (thromboxane mimetic) and arginine vasopressin, and vasodilators, bradykinin and the nitric oxide donor sodium nitroprusside, were assessed by wire myography in myometrial arteries from normal weight (n = 18), overweight (n = 18), and obese (n = 20) women with uncomplicated pregnancies. Thromboxane-prostanoid receptor expression was assessed using immunostaining in myometrial arteries of normal weight and obese women. Vasoconstriction and vasodilatation were impaired in myometrial arteries from obese women with otherwise uncomplicated pregnancies. Disparate agonist responses suggest that vascular function in obese women is not globally dysregulated but may be specific to thromboxane and nitric oxide pathways. Because obesity rates are escalating, it is important to identify the mechanisms underlying impaired vascular function and establish why some obese women compensate for vascular dysfunction and some do not. Future studies are needed to determine whether central adiposity results in an altered endocrine milieu that may promote vascular dysfunction by altering the function of perivascular adipose tissue.

  20. 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.

  1. 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

  2. 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.

  3. 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.

  4. Maternal obesity alters the apelinergic system at the feto-maternal interface.

    PubMed

    Hanssens, Sandy; Marx-Deseure, Aurore; Lecoutre, Simon; Butruille, Laura; Fournel, Audren; Knauf, Claude; Besengez, Capucine; Breton, Christophe; Storme, Laurent; Deruelle, Philippe; Lesage, Jean

    2016-03-01

    Apelin and its receptor APJ have been implicated in pathologies including cardiovascular disease, diabetes and obesity. Little is known about the function of the apelinergic system during gestation. We evaluated in mice this system at the feto-maternal interface in insulin-resistant obese female (HF) mice. Maternal apelinemia was decreased at term and fetal apelinemia was sixfold higher than maternal level. Ex-vivo, the placenta releases apelin at E12.5 and E18.5. In HF pregnant mice at term, apelinemia as well as placental apelin and APJ mRNA levels were increased whereas placental release of apelin was drastically reduced compared to controls. Copyright © 2016 Elsevier Ltd. All rights reserved.

  5. Fetal Syndrome of Endocannabinoid Deficiency (FSECD) In Maternal Obesity.

    PubMed

    Schlabritz-Loutsevitch, Natalia; German, Nadezhda; Ventolini, Gary; Larumbe, Eneko; Samson, Jacques

    2016-11-01

    The theory of a fetal origin of adult diseases links many pathological conditions to very early life events and is known as a "developmental programming" phenomenon. The mechanisms of this phenomenon are not quite understood and have been explained by inflammation, stress, etc. In particular the epidemic of obesity, with more than 64% of women being overweight or obese, has been associated with conditions in later life such as mental disorders, diabetes, asthma, and irritable bowel syndrome. Interestingly, these diseases were classified a decade ago as Clinical Syndrome of Endocannabinoid Deficiency (CECD), which was first described by Russo in 2004. Cannabinoids have been used for the treatment of chronic pain for millenniums and act through the mechanism of "kick-starting" the components of the endogenous cannabinoid system (ECS). ECS is a pharmacological target for the treatment of obesity, inflammation, cardiovascular and neuronal damage, and pain. We hypothesize that the deteriorating effect of maternal obesity on offspring health is explained by the mechanism of Fetal Syndrome of Endocannabinoid Deficiency (FSECD), which accompanies maternal obesity. Here we provide support for this hypothesis. Copyright © 2016 Elsevier Ltd. All rights reserved.

  6. 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…

  7. 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…

  8. Epigenetic changes in the hypothalamic pro-opiomelanocortin gene: a mechanism linking maternal undernutrition to obesity in the offspring?

    PubMed

    Stevens, Adam; Begum, Ghazala; White, Anne

    2011-06-11

    Maternal undernutrition is associated with programming of obesity in offspring. While previous evidence has linked programming to the hypothalamic, pituitary, and adrenal (HPA) axis it could also affect the hypothalamic neuropeptides which regulate food intake and energy balance. Alpha melanocyte stimulating hormone (αMSH), a key regulator of these neuronal pathways, is derived from pro-opiomelanocortin (POMC) which is therefore a prime target for the programming of obesity. Several models of maternal undernutrition have identified changes in POMC in hypothalami from foetuses or offspring at various ages. These models have also shown that the offspring go on to develop obesity and/or glucose intolerance. It is our hypothesis that programming leads to epigenetic changes in hypothalamic neuropeptide genes. Therefore when there is subsequent increased food availability, the epigenetic changes could cause dysfunctional transcriptional regulation of energy balance. We present evidence of epigenetic changes in the POMC gene promoter in foetal hypothalami after peri-conceptional undernutrition. In this model there are also epigenetic changes in the hypothalamic glucocorticoid receptor with consequent up-regulation of the receptor which could lead to alterations in the regulation of POMC and neuropeptide Y (NPY) in the hypothalamus. Thus maternal undernutrition could cause epigenetic changes in the POMC and glucocorticoid receptor genes, in the foetal hypothalamus, which may predispose the offspring to altered regulation of food intake, energy expenditure and glucose homeostasis, later in life. Crown Copyright © 2011. Published by Elsevier B.V. All rights reserved.

  9. The short- and long-term implications of maternal obesity on the mother and her offspring.

    PubMed

    Catalano, P M; Ehrenberg, H M

    2006-10-01

    Obesity's increasing prevalence has reached epidemic proportions in the USA, with close to one-third of the adult population affected in 2000. Additionally, there is increasing prevalence of obesity in other industrialised areas of the world such as Europe. Of potentially more concern is the potential risks associated with obesity and related metabolic complications in the developing world. The maternal, fetal, peripartum and neonatal complications of obesity in pregnancy have far-reaching implications for both mother and offspring. Of alarming interest is the increasing rate of obesity among adolescents and the cycle of obesity in future generations it portends. The purpose in this review is to briefly review the maternal perinatal morbidities associated with maternal pregravid obesity. Additionally, we will review evidence of both short- and long-term effect of maternal obesity on the in utero environment as it relates to fetal growth, neonatal body composition and adolescent obesity.

  10. 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.

  11. Maternal obesity - a risk factor for metabolic syndrome in children

    PubMed Central

    MOREA, MELINDA; MIU, NICOLAE; MOREA, VICENŢIU FLORIN; CORNEAN, RODICA

    2013-01-01

    Objective To determine the association between the metabolic syndrome in children (MS) and the pre-pregnancy nutritional status of the mother. Design and methods A total number of 180 children aged between 6–19 years were examined. Self reported data about parents and their children were collected. The children underwent physical examination; weight, height, waist circumference, blood pressure (BP) were measured. The nutritional status of the children was assessed by body mass index (BMI) and laboratory tests needed to diagnose MS were performed. IDF criteria for MS were used in children 10 years and older, and age and gender specific cut-off points in children younger than 10 years. The mothers were classified in the normal weight, overweight and obese categories according to the pre-pregnancy BMI. The statistical analysis of the data was descriptive and inferential analysis. In the bivariate analysis of the association between qualitative variables, we used the Chi-Square test and the exact Fisher test. The statistical analysis was performed with SPSS v 13.0. Results 73 (40.55%) children were normal weight, 54 (30%) were overweight and 53 (29.44%) were obese. None of the normal weight children, 16 (29.60%) of the overweight and 23 (43.40%) of the obese ones had MS; 125 (69.44%) of the mothers were normal weight, 44 (24.44%) were overweight and 11 (6.11%) were obese. Pre-pregnancy maternal BMI was significantly associated with offspring MS in both genders, obese children and in the 10–16 age group. Conclusions Pre-pregnancy maternal overweight/obesity represents a risk factor for offspring MS. The results are very difficult to compare between studies because of different cut-off values and definition of MS in children. If prevention is the goal rather than treatment, the perinatal period may be an important focus for future research. PMID:26527958

  12. The effect of teenage maternal obesity on perinatal outcomes.

    PubMed

    Haeri, Sina; Guichard, Isabelle; Baker, Arthur M; Saddlemire, Stephanie; Boggess, Kim A

    2009-02-01

    To estimate the effect of obesity on perinatal outcomes among inner-city teenage pregnant women. In this retrospective cohort study, we reviewed all nulliparous teenaged (aged 18 years and younger) deliveries at the Washington Hospital Center between 2000 and 2004. Overweight and obese teenagers (body mass index at or above 25.0 kg/m) were compared with normal-weight (body mass index less than 25.0 kg/m) teenagers. Frequencies and odds ratios for adverse maternal-fetal outcomes were calculated. Of the 10,322 deliveries that occurred during the study period, 712 (7%) were to teenagers. Among the 458 nulliparous teenaged mothers, 274 (60%) were normal weight and 184 (40%) were overweight/obese. Compared with normal-weight teens (n=274), obese teens (n=78) were at higher risk for cesarean delivery (adjusted odds ration [OR] 4.3, 95% confidence interval [CI] 2.4-7.6) and gestational diabetes (adjusted OR 4.2, 95% CI 1.5-12.1). Overweight teens (n=106) had lower risk for preterm birth at less than 37 and less than 34 weeks of gestation (adjusted OR 0.28, 95% CI 0.10-0.77 and adjusted OR 0.11, 95% CI 0.01-0.80, respectively). Overweight and obese teenage mothers are at increased risk for adverse perinatal outcomes. Research on optimal weight for pregnant teens and weight control interventions is needed. II.

  13. Maternal obesity and the early origins of childhood obesity: weighing up the benefits and costs of maternal weight loss in the periconceptional period for the offspring.

    PubMed

    Zhang, Song; Rattanatray, Leewen; Morrison, Janna L; Nicholas, Lisa M; Lie, Shervi; McMillen, I Caroline

    2011-01-01

    There is a need to understand the separate or interdependent contributions of maternal prepregnancy BMI, gestational weight gain, glycaemic control, and macronutrient intake on the metabolic outcomes for the offspring. Experimental studies highlight that there may be separate influences of maternal obesity during the periconceptional period and late gestation on the adiposity of the offspring. While a period of dietary restriction in obese mothers may ablate the programming of obesity, it is associated with an activation of the stress axis in the offspring. Thus, maternal obesity may result in epigenetic changes which predict the need for efficient fat storage in postnatal life, while maternal weight loss may lead to epigenetic changes which predict later adversity. Thus, development of dietary interventions for obese mothers during the periconceptional period requires a greater evidence base which allows the effective weighing up of the metabolic benefits and costs for the offspring. Copyright © 2011 Song Zhang et al.

  14. 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

  15. Maternal obesity and major intraoperative complications during cesarean delivery.

    PubMed

    Smid, Marcela C; Vladutiu, Catherine J; Dotters-Katz, Sarah K; Boggess, Kim A; Manuck, Tracy A; Stamilio, David M

    2017-06-01

    Multiple studies have demonstrated an association between maternal obesity and postoperative complications, but there is a dearth of information about the impact of obesity on intraoperative complications. To estimate the association between maternal obesity at delivery and major intraoperative complications during cesarean delivery (CD). This is a secondary analysis of the deidentified Maternal-Fetal Medicine Unit Cesarean Registry of women with singleton pregnancies. Maternal body mass index (BMI) at delivery was categorized as BMI 18.5 to 29.9 kg/m(2), BMI 30 to 39.9 kg/m(2), BMI 40 to 49.9 kg/m(2), and BMI ≥ 50 kg/m(2). The primary outcome, any intraoperative complication, was defined as having at least 1 major intraoperative complication, including perioperative blood transfusion, intraoperative injury (bowel, bladder, ureteral injury; broad ligament hematoma), atony requiring surgical intervention, repeat laparotomy, and hysterectomy. Log-binomial models were used to estimate risk ratios of intraoperative complication in 2 models: model 1 adjusting for maternal race, and preterm delivery <37 weeks; and model 2 adjusting for confounders in Model 1 as well as emergency CD, and type of skin incision. A total of 51,218 women underwent CD; 38% had BMI 18.5 to 29.9 kg/m(2), 47% BMI 30 to 39.9 kg/m(2), 12% BMI 40 to 49.9 kg/m(2) and 3% BMI ≥ 50 kg/m(2). Having at least 1 intraoperative complication was uncommon (3.4%): 3.8% for BMI 18.5 to 29.9 kg/m(2), 3.2% BMI 30 to 39.9 kg/m(2), 2.6% BMI 40 to 49.9 kg/m(2) and 4.3% BMI ≥ 50 kg/m(2) (P < .001). In the fully adjusted model 2, women with BMI 40 to 49.9 kg/m(2) had a lower risk of any intraoperative complication (adjusted risk ratio [ARR], 0.76; 95% confidence interval [CI], 0.64 to 0.89) compared with women with BMI 18.5 to 29.9 kg/m(2). Women with BMI 30 to 39.9 kg/m(2) (ARR, 0.93; 95% CI, 0.84 to 1.03) had a similar risk of any intraoperative complication compared with nonobese women. Among super obese women

  16. 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

  17. Maternal obesity alters endoplasmic reticulum homeostasis in offspring pancreas.

    PubMed

    Soeda, Jumpei; Mouralidarane, Angelina; Cordero, Paul; Li, Jiawei; Nguyen, Vi; Carter, Rebeca; Kapur, Sabrina R; Pombo, Joaquim; Poston, Lucilla; Taylor, Paul D; Vinciguerra, Manlio; Oben, Jude A

    2016-06-01

    The prevalence of non-alcoholic fatty pancreas disease (NAFPD) is increasing in parallel with obesity rates. Stress-related alterations in endoplasmic reticulum (ER), such as the unfolded protein response (UPR), are associated with obesity. The aim of this study was to investigate ER imbalance in the pancreas of a mice model of adult and perinatal diet-induced obesity. Twenty female C57BL/6J mice were assigned to control (Con) or obesogenic (Ob) diets prior to and during pregnancy and lactation. Their offspring were weaned onto Con or Ob diets up to 6 months post-partum. Then, after sacrifice, plasma biochemical analyses, gene expression, and protein concentrations were measured in pancreata. Offspring of Ob-fed mice had significantly increased body weight (p < 0.001) and plasma leptin (p < 0.001) and decreased insulin (p < 0.01) levels. Maternal obesogenic diet decreased the total and phosphorylated Eif2α and increased spliced X-box binding protein 1 (XBP1). Pancreatic gene expression of downstream regulators of UPR (EDEM, homocysteine-responsive endoplasmic reticulum-resident (HERP), activating transcription factor 4 (ATF4), and C/EBP homologous protein (CHOP)) and autophagy-related proteins (LC3BI/LC3BII) were differently disrupted by obesogenic feeding in both mothers and offspring (from p < 0.1 to p < 0.001). Maternal obesity and Ob feeding in their offspring alter UPR in NAFPD, with involvement of proapoptotic and autophagy-related markers. Upstream and downstream regulators of PERK, IRE1α, and ATF6 pathways were affected differently following the obesogenic insults.

  18. 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...

  19. 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…

  20. 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…

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

    PubMed

    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

    In addition to immediate implications for pregnancy complications, increasing evidence implicates maternal obesity as a major determinant of offspring health during childhood and later adult life. Observational studies provide evidence for effects of maternal obesity on her offspring's risks of obesity, coronary heart disease, stroke, type 2 diabetes, and asthma. Maternal obesity could also lead to poorer cognitive performance and 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, which are mediated at least partly through changes in epigenetic processes, such as alterations in DNA methylation, and perhaps through alterations in the gut microbiome. Although the offspring of obese women who lose weight before pregnancy have a reduced risk of obesity, few controlled intervention studies have been done in which maternal obesity is reversed and the consequences for offspring have been examined. Because the long-term effects of maternal obesity could have profound public health implications, there is an urgent need for studies on causality, underlying mechanisms, and effective interventions to reverse the epidemic of obesity in women of childbearing age and to mitigate consequences for offspring.

  2. 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

  3. Maternal obesity, mode of delivery, and neonatal outcome.

    PubMed

    Blomberg, Marie

    2013-07-01

    To evaluate whether adverse neonatal outcome, defined as birth injuries or severe illnesses in the newborn, was associated with maternal body mass index (BMI) in singleton pregnancies overall and depending on mode of delivery. This was a cohort study including 1,024,471 women. Data were collected from the Swedish Medical Birth Registry. Women were categorized into six classes of BMI. Obese women were compared with normal weight women regarding adverse neonatal outcome after suitable adjustments. Four modes of delivery were evaluated: vaginal delivery; instrumental vaginal delivery; elective cesarean delivery; and emergency cesarean delivery. Compared with neonates born to women of normal weight, neonates born to women with BMIs of 40 or more (morbidly obese) were at increased risk of birth injury to the peripheral nervous system (odds ratio [OR] 3.80, 95% confidence interval [CI] 2.83-5.12; 0.2% compared with 0.6%), birth injury to the skeleton (OR 2.59, 95% CI 2.10-3.21; 0.5% compared with 1.1%), respiratory distress syndrome (OR 2.08, 95% CI 1.88-2.30; 2.9 compared with 5.8%), bacterial sepsis (OR 2.90, 95% CI 2.43-3.46; 0.6% compared with 1.7%), convulsions (OR 3.43, 95% CI 2.63-4.47; 0.2% compared with 0.8%), and hypoglycemia (OR 3.48, 95% CI 3.20-3.78; 2.4% compared with 7.9%). For morbidly obese women, elective cesarean delivery and vaginal delivery were associated with twice the increased risk of adverse neonatal outcomes when compared with women of normal weight. Neonates born to morbidly obese women are at markedly increased risk of adverse neonatal outcome regardless of mode of delivery. Obstetricians should not disregard the neonatal problems associated with elective cesarean delivery for morbidly obese women. II.

  4. 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.

  5. Maternal Obesity in Early Pregnancy and Risk of Adverse Outcomes

    PubMed Central

    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

    Objectives 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. Methods 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. Results 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). Conclusion Obesity and overweight status at the beginning of pregnancy increase the adverse outcomes of the pregnancy. It is important to promote

  6. 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

  7. 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.

  8. 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.

  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. Maternal obesity leads to an inflammatory response and insulin resistance in ovarian tissue

    USDA-ARS?s Scientific Manuscript database

    Maternal obesity during the pre-conception period may influence ovarian functions and affect embryo development. Lean and obese (OB) Sprague-Dawley dams were examined during the preimplantation period at dpc 4.5. Obesity was induced by controlled overfeeding (40% excess calories for 28 d) via total ...

  11. Maternal obesity promotes a proinflammatory signature in rat uterus and blastocyst

    USDA-ARS?s Scientific Manuscript database

    Maternal obesity at conception increases the risk of offspring obesity, thus propagating an intergenerational vicious cycle. Male offspring born to obese dams are hyper-responsive to high fat diets, gaining greater body weight, fat mass and additional metabolic sequelae compared to lean controls. ...

  12. Maternal and grandmaternal obesity and environmental factors as determinants of daughter's obesity

    PubMed Central

    Shin, Mi Na; Lee, Kyung Hea; Lee, Hye Sang; Sasaki, Satoshi; Oh, Hea Young; Lyu, Eun Soon

    2013-01-01

    Obesity may be the consequence of various environmental or genetic factors, which may be highly correlated with each other. We aimed to examine whether grandmaternal and maternal obesity and environmental risk factors are related to obesity in daughters. Daughters (n = 182) recruited from female students, their mothers (n = 147) and their grandmothers (n = 67) were included in this study. Multivariable logistic regression was used to analyze the association between the daughter's obesity and maternal, grandmaternal, and environmental factors. Maternal heights of 161-175cm (OD: 8.48, 95% CI: 3.61-19.93) and 156-160 cm (2.37, 1.14-4.91) showed positive associations with a higher height of daughter, compared to those of 149-155 cm. Mothers receiving a university or a higher education had a significant OR (3.82, 1.27-11.50) for a higher height of daughter compared to those having a low education (elementary school). Mother having the heaviest weight at current time (59-80 kg, 3.78, 1.73-8.28) and the heaviest weight at 20 years of age (51-65 kg, 3.17, 1.53-6.55) had significant associations with a higher height of daughters, compared to those having the lightest weight at the same times. There was no association between the height, weight, and BMI of daughters and the characteristics and education of her grandmothers. In conclusion, although genetic factors appear to influence the daughter's height more than environmental factors, the daughter's weight appears to be more strongly associated with individual factors than the genetic factors. PMID:24133620

  13. Maternal infant feeding behaviors and disparities in early child obesity.

    PubMed

    Gross, Rachel S; Mendelsohn, Alan L; Fierman, Arthur H; Hauser, Nicole R; Messito, Mary Jo

    2014-04-01

    Although disparities in child obesity exist during infancy, the underlying mechanisms are unclear. Assessing dissimilarities in feeding practices, styles, and beliefs may provide a better understanding of these mechanisms. This study sought to identify modifiable maternal-infant feeding behaviors that may contribute to disparities in early child obesity. This study is a cross-sectional analysis comparing mothers with infants (2 weeks to 6 months old) in a low-risk group of high-income white mothers to a high-risk group of low-income Hispanic mothers. Regression analysis was used to explore relationships between each group and (1) infant feeding practices, including breastfeeding, giving juice, and adding cereal to bottles, (2) controlling feeding styles, (3) beliefs about infant hunger and satiety, and (4) infant weight status. The sample included 412 mothers (low-risk group, n = 208; high-risk group, n = 204). The high-risk group was less likely to exclusively breastfeed (adjusted odds ratio [AOR], 0.43; 95% confidence interval [CI], 0.22-0.83), more likely to introduce juice (AOR, 12.25; 95% CI, 3.44-43.62), and add cereal to the bottle (AOR, 10.61; 95% CI, 2.74-41.0). The high-risk group exhibited greater restrictive and pressuring feeding styles and was more likely to believe that mothers can recognize infant hunger and satiety and less likely to believe that infants know their own hunger and satiety. High-risk infants were more likely to have a weight-for-length percentile >85th percentile (AOR, 2.66; 95% CI, 1.10-6.45). Differences in infant feeding behaviors may contribute to disparities in early child obesity. Longitudinal studies are needed to determine the effect of these differences on child obesity.

  14. Obesity during pregnancy alters maternal oxidant balance and micronutrient status.

    PubMed

    Sen, S; Iyer, C; Meydani, S N

    2014-02-01

    Little is known about the effect of obesity on inflammatory status in pregnant women. The objective of this study was to determine the effect of obesity on markers of inflammation, oxidative stress and micronutrient status in obese pregnant women and their infants compared with lean controls (Lc). This was a prospective case-control study. A total of 15 obese (Ob; body mass index (BMI) >30 kg m(-2)) and 15 lean (BMI 18-25 kg m(-2)) women were recruited based on prepregnancy BMI. Vitamins A, B6, C, E and 25-hydroxyvitamin D (25(OH)D), zinc, red blood cell (RBC) folate, C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-α and oxidized and reduced glutathione were measured from maternal blood between 24 and 28 weeks of gestation. Vitamins A, B6, C and E, 25(OH)D, zinc, red blood cell folate, CRP and IL-6 were measured from cord blood at delivery. Ob pregnant women have statistically significantly lower levels of vitamin B6, vitamin C, vitamin E, RBC folate, higher CRP and IL-6 levels and higher ratio of oxidized to reduced glutathione compared with Lc pregnant women. Infants born to Ob mothers did not have statistically significantly higher measures of inflammation or oxidative stress. There were no differences in micronutrient concentrations between Lc and Ob infants, but folate, vitamin B6 and zinc levels correlated strongly between mother and infant. There was no statistically significant difference in any parameter between Ob and Lc cord blood. Ob pregnant women have increased inflammation and oxidative stress, and lower levels of nutritional antioxidant defenses compared with Lc pregnant women. We speculate that lower antioxidant defenses combined with increased oxidative stress and inflammation may contribute to the adverse outcomes associated with pregnancy in Ob women.

  15. 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.

  16. Effects of maternal obesity on fetal growth and body composition: implications for programming and future health.

    PubMed

    Freeman, Dilys J

    2010-04-01

    Since the hypothesis linking low birth weight and poor fetal growth with future risk of cardiovascular disease was first proposed, there has been much interest in the early origins of disease. As rates of obesity increase and as maternal obesity has become common, interest has been directed towards the early origins of obesity. It is likely that a complex interaction of inherited gene effects and in-utero environment may interact in the developing fetus to programme pathways leading to future obesity. It is clear that maternal metabolism is disturbed in pregnancy in obese women, and that offspring of obese mothers have a higher percentage of body fat and are insulin resistant. This review discusses the ideas contributing to the current working concept of obesity programming, and discusses several potential mechanisms that may underlie obesity programming and susceptibility to future metabolic and vascular disease.

  17. Maternal obesity is associated with younger age at obesity onset in U.S. adolescent offspring followed into adulthood.

    PubMed

    Gordon-Larsen, Penny; Adair, Linda S; Suchindran, Chirayath M

    2007-11-01

    The objective was to test the hypothesis that maternal obesity is associated with younger age of offspring's obesity onset. We used prospective, nationally representative, longitudinal data collected across Waves I (1995; 12 to 20 years), II (1996; 13 to 20 years), and III (2001; 18 to 28 years) of the National Longitudinal Study of Adolescent Health (N = 14,654; 49% female). Interval regression analysis was used to assess the association between maternal obesity and age at offspring's obesity onset (International Obesity Task Force BMI >or=30 equivalent age- and sex-specific cut-off points for adolescents and BMI >or=30 for young adults) using self-reported heights and weights, adjusting for race/ethnicity, sex, parental education, and family income, accounting for complex sampling design. The net effect of having an obese mother varied by race/ethnicity and was associated with a significantly earlier age at obesity onset (p = 0.0001) for whites [beta= -8.1 year, 95% confidence interval (CI), -9.3; -6.9)], blacks (beta = -10.8 years, 95% CI, -12.4; -9.2), Hispanics (beta = -7.0 years, 95% CI, -9.2; -4.8), and Asians (beta = -8.6 years, 95% CI, -13.3; -3.9). Earlier obesity onset (<18 years) was associated with increased severity at young adulthood (mean BMI, 36.0 +/- 0.3 kg/m(2)) vs. onset after age 18 (mean BMI, 34.4 +/- 0.2 kg/m(2); p = 0.0001). There were no sex differences in the association of maternal obesity to age at obesity onset. Having an obese mother was associated with earlier age at obesity onset across all race/ethnic groups, particularly non-Hispanic blacks. Early obesity onset has important health consequences because of its association with more severe adult obesity.

  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.

  19. 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

  20. 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.

  1. 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

  2. Racial differences in the association between maternal prepregnancy obesity and children's behavior problems.

    PubMed

    Tanda, Rika; Salsberry, Pamela J

    2014-01-01

    Evidence for the adverse effects of prepregnancy obesity on offspring's neurodevelopmental outcomes has begun to emerge. The authors examined the association between prepregnancy obesity and children's behavioral problems and if the association would differ by race. This observational study used a total of 3395 white (n = 2127) and African-American (n = 1268) children aged 96 to 119 months from the National Longitudinal Survey of Youth. Behavior Problem Index (BPI) total and subscale scores were used to measure children's behavioral problems. The association between maternal prepregnancy obesity and the BPI scores for each racial group was examined using multivariate linear and logistic regressions, controlling for prenatal, child, maternal, and family background factors. Maternal prepregnancy obesity was independently associated with an increase in the BPI total scores among the white sample only. Among the African-Americans, prepregnancy obesity was not associated with the BPI scores. Subsample analyses using externalizing and internalizing subscales also revealed similar trends. Among the white sample, children born to obese women were more socially disadvantaged than those born to nonobese women, whereas no such trend was observed in children of African-American obese and nonobese women. The impact of maternal prepregnancy obesity on children's behavioral problems differed by racial groups. Obesity-related metabolic dysregulations during the intrauterine period may not contribute to later children's behavioral problems. Social and psychological factors seem to play key roles in the association between prepregnancy obesity and childhood behavioral problems among whites.

  3. Risk factors and outcomes of maternal obesity and excessive weight gain during pregnancy.

    PubMed

    Gaillard, Romy; Durmuş, Büşra; Hofman, Albert; Mackenbach, Johan P; Steegers, Eric A P; Jaddoe, Vincent W V

    2013-05-01

    The prevalence of overweight and obesity among women of reproductive age is increasing. We aimed to determine risk factors and maternal, fetal and childhood consequences of maternal obesity and excessive gestational weight gain. The study was embedded in a population-based prospective cohort study among 6959 mothers and their children. The study was based in Rotterdam, The Netherlands (2001-2005). Maternal lower educational level, lower household income, multiparity, and FTO risk allel were associated with an increased risk of maternal obesity, whereas maternal European ethnicity, nulliparity, higher total energy intake, and smoking during pregnancy were associated with an increased risk of excessive gestational weight gain (all p-values <0.05). As compared to normal weight, maternal obesity was associated with increased risks of gestational hypertension (OR 6.31 (95% CI 4.30, 9.26)), preeclampsia (OR (3.61, (95% CI 2.04, 6.39)), gestational diabetes (OR 6.28 (95%CI 3.01, 13.06)), caesarean delivery (OR 1.91 (95% CI 1.46, 2.50)), delivering large size for gestational age infants (OR 2.97 (95% CI 2.16, 4.08)), and childhood obesity (OR 5.02 (95% CI:2.97, 8.45)). Weaker associations of excessive gestational weight gain with maternal, fetal and childhood outcomes were observed, with the strongest effects for first trimester weight gain. Our study shows that maternal obesity and excessive weight gain during pregnancy are associated with socio-demographic, lifestyle, and genetic factors and with increased risks of adverse maternal, fetal and childhood outcomes. As compared to prepregnancy overweight and obesity, excessive gestational weight gain has a limited influence on adverse pregnancy outcomes. Copyright © 2013 The Obesity Society.

  4. 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

  5. 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.

  6. The combined effect of maternal obesity and fetal macrosomia on pregnancy outcomes.

    PubMed

    Gaudet, Laura; Wen, Shi Wu; Walker, Mark

    2014-09-01

    To examine the combined effect of macrosomia and maternal obesity on adverse pregnancy outcomes using a retrospective cohort. Infants with a birth weight of ≥ 4000g (macrosomia) were identified from an institutional birth cohort. Demographic characteristics and maternal, fetal, neonatal, and pregnancy outcomes of macrosomic infants whose mothers were obese were compared with those whose mothers were non-obese. Pregnancies in obese women resulting in macrosomic infants are more likely to be complicated by gestational diabetes, gestational hypertension, and smoking than pregnancies in non-obese women with macrosomic infants. Mothers whose infants are macrosomic are significantly more likely to require induction of labour (OR 1.42; 95% CI 1.10 to 1.98) and delivery by Caesarean section (OR 1.45; 95% CI 1.04 to 2.01), particularly for maternal indications (OR 3.7; 95% CI 1.47 to 9.34), if they are obese. Finally, macrosomic infants of obese mothers are significantly more likely to require neonatal resuscitation in the form of free flow oxygen (OR 1.57; 95% CI 1.03 to 2.42) than macrosomic infants of non-obese mothers. When both maternal obesity and macrosomia are present, adverse pregnancy outcomes are more common than when fetal macrosomia occurs in a woman of normal weight.

  7. 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.

  8. Maternal Obesity and Vitamin D Sufficiency Are Associated with Cord Blood Vitamin D Insufficiency

    PubMed Central

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

    2013-01-01

    Context: 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. Objective: 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. Design, Setting, and Patients: 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. Outcome Measures: Maternal and cord blood sera were assayed for 25-OH D, and neonatal body composition was measured by air displacement plethysmography. Results: 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 (r2 = 0.66). Conclusion: 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. PMID:23144468

  9. 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.

  10. The Maternal Obesity Management (MOM) Trial Protocol: a lifestyle intervention during pregnancy to minimize downstream obesity.

    PubMed

    Adamo, Kristi B; Ferraro, Zachary M; Goldfield, Gary; Keely, Erin; Stacey, Dawn; Hadjiyannakis, Stasia; Jean-Philippe, Sonia; Walker, Mark; Barrowman, Nicholas J

    2013-05-01

    Maternal obesity and/or high gestational weight gain (GWG) are associated with downstream child obesity. Pregnancy represents a critical period for prevention as women are highly motivated and more receptive to behavior change. This pilot study was developed to test the feasibility of intervening with the mother, specifically keeping her GWG within the Institute of Medicine (IOM) limits, with the intended target of preventing obesity in her child downstream. We are testing the practicality of delivering a structured physical activity and nutrition intervention to pregnant women during gestation and then following mom and baby to 24 months of age. This study is a two-arm, parallel group, randomized controlled trial being conducted in Ottawa. Pregnant women, with pregravid BMI >18.5, between 12 and 20 weeks gestation are randomized to one of two groups: intervention (n=30) who receive the MOM trial Handbook (guide to healthy gestation) plus a structured physical activity and nutrition program, or a standard clinical care control group (n=30). The intervention lasts 25-28 weeks (6 months) depending on anticipated delivery date, with follow-up assessment on mother and child at 3, 6, 12 and 24 months post-delivery. Pregnancy, a critical time of growth, development and physiological change, provides an opportunity for early lifestyle intervention. The goal of identifying an effective lifestyle program for the gestational period that leads to healthy fetal development and subsequently normal weight offspring, less likely to develop obesity and its co-morbidities, is unique and could possibly attenuate the inter-generational cycle of obesity. Copyright © 2013 Elsevier Inc. All rights reserved.

  11. Maternal obesity is a risk factor for orofacial clefts: a meta-analysis.

    PubMed

    Blanco, R; Colombo, A; Suazo, J

    2015-10-01

    Orofacial clefts are the most prevalent birth defects that affect craniofacial structures and implicate genetic and environmental factors in their aetiology. Maternal metabolic state and nutrition have been related to these and other structural malformations, and studies of maternal obesity before pregnancy have shown controversial results about its association with the risk of orofacial clefts in their offspring. Our aim was to assess the combined effect of several single studies of maternal obesity on the risk of orofacial clefts using meta-analysis. We searched for these reports in the PubMed database, and selected 8 studies that met our criteria for eligibility. As a result of this analysis, and using maternal normal weight as a reference, we found that maternal obesity does increase the risk of orofacial clefts in their offspring (OR 1.18, 95% CI 1.11 to 1.26). When these clefts are considered separately, maternal obesity is associated with cleft lip with or without cleft palate (OR 1.13, 95% CI 1.04 to 1.23), and with cleft palate alone (OR 1.22, 95% CI 1.09 to 1.35). Our results support the relation between maternal obesity and orofacial clefts, and confirm two previous meta-analyses that considered fewer studies. However, the molecular mechanisms underlying this statistical evidence have not been fully elucidated.

  12. Maternal obesity enhances white adipose tissue differentiation and alters genome-scale DNA methylation in male rat offspring

    USDA-ARS?s Scientific Manuscript database

    The risk of obesity in adulthood is strongly influenced by maternal body composition. Here we examined the hypothesis that maternal obesity influences white adipose tissue (WAT) transcriptome and increases propensity for adipogenesis in the offspring, prior to the development of obesity, using an es...

  13. 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.

  14. 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...

  15. Maternal diet-induced obesity alters mitochondrial activity and redox status in mouse oocytes and zygotes.

    PubMed

    Igosheva, Natalia; Abramov, Andrey Y; Poston, Lucilla; Eckert, Judith J; Fleming, Tom P; Duchen, Michael R; McConnell, Josie

    2010-04-09

    The negative impact of obesity on reproductive success is well documented but the stages at which development of the conceptus is compromised and the mechanisms responsible for the developmental failure still remain unclear. Recent findings suggest that mitochondria may be a contributing factor. However to date no studies have directly addressed the consequences of maternal obesity on mitochondria in early embryogenesis.Using an established murine model of maternal diet induced obesity and a live cell dynamic fluorescence imaging techniques coupled with molecular biology we have investigated the underlying mechanisms of obesity-induced reduced fertility. Our study is the first to show that maternal obesity prior to conception is associated with altered mitochondria in mouse oocytes and zygotes. Specifically, maternal diet-induced obesity in mice led to an increase in mitochondrial potential, mitochondrial DNA content and biogenesis. Generation of reactive oxygen species (ROS) was raised while glutathione was depleted and the redox state became more oxidised, suggestive of oxidative stress. These altered mitochondrial properties were associated with significant developmental impairment as shown by the increased number of obese mothers who failed to support blastocyst formation compared to lean dams. We propose that compromised oocyte and early embryo mitochondrial metabolism, resulting from excessive nutrient exposure prior to and during conception, may underlie poor reproductive outcomes frequently reported in obese women.

  16. 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.

  17. Maternal Behaviors during Pregnancy Impact Offspring Obesity Risk

    PubMed Central

    Phelan, Suzanne; Hart, Chantelle; Phipps, Maureen; Abrams, Barbara; Schaffner, Andrew; Adams, Angelica; Wing, Rena

    2011-01-01

    This study investigated the effects of maternal changes during pregnancy in diet, exercise, and psychosocial factors on offspring weight parameters at birth and 6 months. In overweight/obese (OW/OB; n = 132) mothers, greater % kcal from sweets early in pregnancy was the strongest, independent predictor of higher weight for age (WFA) (beta = 0.19; P = 0.004), higher odds of macrosomia (OR = 1.1 (1.0–1.2); P = 0.004) andWFA >90th percentile at birth (OR = 1.2 (1.1–1.3); P = 0.002) and higher WFA at 6 months (beta = 0.30; P = 0.002). In normal weight (n = 153) mothers, higher intake of soft drinks was the strongest predictor of higher offspring WFA at birth (beta = 0.16; P = 0.04) but not at 6 months. Prenatal physical activity, depressive symptoms, and sleep-related variables did not significantly predict offspring weight outcomes. Mothers' eating behaviors during pregnancy, especially intake of sweets in OW/OB mothers, may have a lasting effect on child weight. PMID:22110475

  18. Maternal Obesity Enhances White Adipose Tissue Differentiation and Alters Genome-Scale DNA Methylation in Male Rat Offspring

    PubMed Central

    Borengasser, Sarah J.; Zhong, Ying; Kang, Ping; Lindsey, Forrest; Ronis, Martin J. J.; Badger, Thomas M.; Gomez-Acevedo, Horacio

    2013-01-01

    The risk of obesity (OB) in adulthood is strongly influenced by maternal body composition. Here we examined the hypothesis that maternal OB influences white adipose tissue (WAT) transcriptome and increases propensity for adipogenesis in the offspring, prior to the development of OB, using an established model of long-term metabolic programming. Employing an overfeeding-based rat model, in which exposure to OB is limited to preconception and gestation alone, we conducted global transcriptomic profiling in WAT, and gene/protein expression analysis of lipogenic and adipogenic pathways and examined adipogenic differentiation of WAT stromal-vascular cells ex vivo. Using reduced representation bisulfite sequencing we also evaluated genome-scale changes in DNA methylation in offspring WAT. Maternal OB led to extensive changes in expression of genes (±1.8-fold, P ≤ .05), revealing a distinct up-regulation of lipogenic pathways in WAT. mRNA expression of a battery of sterol regulatory element-binding protein-1-regulated genes was increased in OB-dam offspring, which were confirmed by immunoblotting. In conjunction with lipogenic gene expression, OB-dam offspring showed increased glucose transporter-4 mRNA/protein expression and greater AKT phosphorylation following acute insulin challenge, suggesting sensitization of insulin signaling in WAT. Offspring of OB dams also exhibited increased in vivo expression of adipogenic regulators (peroxisome proliferator-activated receptor-γ, CCAAT enhancer binding protein α [C/EBP-α] and C/EBP-β), associated with greater ex vivo differentiation of WAT stromal-vascular cells. These transcriptomic changes were associated with alterations in DNA methylation of CpG sites and CGI shores, proximal to developmentally important genes, including key pro-adipogenic factors (Zfp423 and C/EBP-β). Our findings strongly suggest that the maternal OB in utero alters adipocyte commitment and differentiation via epigenetic mechanisms. PMID:23959936

  19. 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.

  20. 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

  1. 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.

  2. The Association of Maternal Obesity and Diabetes With Autism and Other Developmental Disabilities.

    PubMed

    Li, Mengying; Fallin, M Daniele; Riley, Anne; Landa, Rebecca; Walker, Sheila O; Silverstein, Michael; Caruso, Deanna; Pearson, Colleen; Kiang, Shannon; Dahm, Jamie Lyn; Hong, Xiumei; Wang, Guoying; Wang, Mei-Cheng; Zuckerman, Barry; Wang, Xiaobin

    2016-02-01

    Obesity and diabetes are highly prevalent among pregnant women in the United States. No study has examined the independent and combined effects of maternal prepregnancy obesity and maternal diabetes on the risk of autism spectrum disorder (ASD) in parallel with other developmental disorders (DDs). This study is based on 2734 children (including 102 ASD cases), a subset of the Boston Birth Cohort who completed at least 1 postnatal study visit at Boston Medical Center between 1998 and 2014. Child ASD and other DDs were based on physician diagnoses as documented in electronic medical records. Risks of ASD and other DDs were compared among 6 groups defined by maternal prepregnancy obesity and diabetes status by using Cox proportional hazard regression controlling for potential confounders. When examined individually, maternal prepregnancy obesity and pregestational diabetes (PGDM) were each associated with risk of ASD. When examined in combination, only mothers with obesity and PGDM (hazard ratio 3.91, 95% confidence interval 1.76-8.68) and those with obesity and gestational diabetes (hazard ratio 3.04, 95% confidence interval 1.21-7.63) had a significantly increased risk of offspring ASD. Intellectual disabilities (IDs), but not other DDs, showed a similar pattern of increased risk associated with combined obesity and PGDM. This pattern of risk was mostly accounted for by cases with co-occurring ASD and ID. Maternal prepregnancy obesity and maternal diabetes in combination were associated with increased risk for ASD and ID. ASD with ID may be etiologically distinct from ASD without ID. Copyright © 2016 by the American Academy of Pediatrics.

  3. [Maternal obesity: effects on labor and delivery: Excluding other diseases that might modify obstetrical management].

    PubMed

    Hamon, C; Fanello, S; Catala, L; Parot, E

    2005-04-01

    The aim of this survey was to analyze the effects on labor, delivery, afterbirth, and neonatal status of maternal obesity, independently of other diseases that might modify obstetrical management. Cross-sectional survey of cases during one year in the obstetrics department of a university hospital center. The inclusion criterion was obesity, defined as BMI > 30. The exclusion criteria were hypertension, pregnancy-related hypoxemia, diabetes (pre-existing or pregnancy-related), maternal cardio-pulmonary disease, uterine scar, multiple pregnancy, and non-cephalic presentation. Two groups, one obese and the other not, were matched for age and parity. The rate of post-term deliveries was higher among obese women (p = 0.04), induction of labor more frequent (p = 0.05), and the duration of its first phase longer (p = 0.003); the cesarean rate was seven times higher (14.6% versus 2.1%) and the mean weight of the newborns significantly higher (p = 0.01). Multivariate analysis found the following factors to be significantly associated with maternal obesity: longer duration of the first phase of labor, less frequent spontaneous vaginal delivery, higher cesarean rate, and higher rate of lack of progress in dilatation. This study shows that maternal obesity is a risk factor for complications during pregnancy, independently of its standard complications--pregnancy-related diabetes and hypertension. It compromises the smooth progression of labor and delivery. Pregnancy in obese women must be considered to be "at risk", regardless of any complications of obesity. It is thus important to help obese women become more aware of the importance of a balanced diet for themselves and their children. The presence of an obese adult in the household quadruples the risk of obesity in children.

  4. Maternal obesity (Class I-III), gestational weight gain and maternal leptin levels during and after pregnancy: a prospective cohort study.

    PubMed

    Carlhäll, Sara; Bladh, Marie; Brynhildsen, Jan; Claesson, Ing-Marie; Josefsson, Ann; Sydsjö, Gunilla; Thorsell, Annika; Blomberg, Marie

    2016-01-01

    Maternal obesity is accompanied by maternal and fetal complications during and after pregnancy. The risks seem to increase with degree of obesity. Leptin has been suggested to play a role in the development of obesity related complications. Whether maternal leptin levels differ between obese and morbidly obese women, during and after pregnancy, have to our knowledge not been previously described. Neither has the association between maternal leptin levels and gestational weight gain in obese women. The aim was to evaluate if maternal plasma leptin levels were associated with different degrees of maternal obesity and gestational weight gain. Prospective cohort study including women categorized as obesity class I-III (n = 343) and divided into three gestational weight gain groups (n = 304). Maternal plasma leptin was measured at gestational week 15, 29 and 10 weeks postpartum. Maternal Body Mass Index (BMI) was calculated from early pregnancy weight. Gestational weight gain was calculated using maternal weight in delivery week minus early pregnancy weight. The mean value and confidence interval of plasma-leptin were analysed with a two-way ANOVA model. Interaction effect between BMI and gestational weight gain group was tested with a two-way ANOVA model. The mean maternal leptin concentrations were significantly higher in women with obesity class III compared to women in obesity class I, at all times when plasma leptin were measured. The mean leptin concentrations were also significantly higher in women with obesity class II compared to women in obesity class I, except in gestational week 29. There was no difference in mean levels of plasma leptin between the gestational weight gain groups. No significant interaction between BMI and gestational weight gain group was found. Plasma leptin levels during and after pregnancy were associated with obesity class but not with degree of gestational weight gain. These results are in concordance with epidemiological

  5. Maternal Obesity During Pregnancy Associates With Premature Mortality and Major Cardiovascular Events in Later Life.

    PubMed

    Lee, Kuan Ken; Raja, Edwin A; Lee, Amanda J; Bhattacharya, Sohinee; Bhattacharya, Siladitya; Norman, Jane E; Reynolds, Rebecca M

    2015-11-01

    One in 5 pregnant women is obese but the impact on later health is unknown. We aimed to determine whether maternal obesity during pregnancy associates with increased premature mortality and later life major cardiovascular events. Maternity records of women who gave birth to their first child between 1950 and 1976 (n=18 873) from the Aberdeen Maternity and Neonatal databank were linked to the National Register of Deaths, Scotland and Scottish Morbidity Record. The effect of maternal obesity at first antenatal visit on death and hospital admissions for cardiovascular events was tested using time-to-event analysis with Cox proportional hazard regression to compare outcomes of mothers in underweight, overweight, or obese body mass index (BMI) categories compared with normal BMI. Median follow-up was at 73 years. All-cause mortality was increased in women who were obese during pregnancy (BMI>30 kg/m(2)) versus normal BMI after adjustment for socioeconomic status, smoking, gestation at BMI measurement, preeclampsia, and low birth weight (hazard ratio, 1.35; 95% confidence interval, 1.02-1.77). In adjusted models, overweight and obese mothers had increased risk of hospital admission for a cardiovascular event (1.16; 1.06-1.27 and 1.26; 1.01-1.57) compared with normal BMI mothers. Adjustment for parity largely unchanged the hazard ratios (mortality: 1.43, 1.09-1.88; cardiovascular events overweight: 1.17, 1.07-1.29; and obese: 1.30, 1.04-1.62). In conclusion, maternal obesity is associated with increased risk of premature death and cardiovascular disease. Pregnancy and early postpartum could represent an opportunity for interventions to identify obesity and reduce its adverse consequences.

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

    PubMed Central

    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. PMID:28125591

  7. 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.

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

    PubMed

    Thakali, Keshari M; Faske, Jennifer B; Ishwar, Arjun; Alfaro, Maria P; Cleves, Mario A; Badger, Thomas M; Andres, Aline; Shankar, Kartik

    2017-09-01

    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 targeted DNA methylation association analysis of maternal obesity and excessive GWG with DNA methylation of select metabolism-related and imprinted genes. Umbilical cord (UC) tissue from infants born to normal weight and overweight/obese women from the Glowing study were utilized (n = 78). In multivariable linear regression adjusted for relevant confounders, Institute on Medicine (IOM) GWG category and infant sex were significantly associated with UC IGFBP1 methylation, while gestation length was significantly associated with UC PRKAA1 methylation. In addition, infant fat mass (%) at 2 weeks of age was significantly associated with umbilical cord methylation of RAPTOR. While regression tree analysis confirmed findings from multivariable models demonstrating that maternal early pregnancy BMI and IOM GWG category are associated with fetal UC DNA methylation patterns for select metabolic and imprinted genes, in general, effect sizes were quite small and statistical significance was not maintained when accounting for multiple testing. Our findings suggest that maternal obesity and excessive GWG are weakly correlated with offspring DNA methylation patterns at birth. Copyright © 2017 Elsevier Ltd. All rights reserved.

  9. Update on Prepregnancy Maternal Obesity: Birth Defects and Childhood Outcomes

    PubMed Central

    Iessa, Noha; Bérard, Anick

    2015-01-01

    Obesity is a growing global health epidemic. It is estimated that more than 20% of pregnancies are complicated by obesity. Prepregnancy obesity has been associated with birth defects such as neural tube defects, macrosomia, fetal death, and long-term effects such as asthma on the offspring. We provide a summary of the most recent studies and meta-analyses on obesity and birth outcome. Possible mechanisms of actions are explored and recommendations for further research are highlighted. PMID:27617118

  10. 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

  11. Association Between Maternal Intimate Partner Violence and Incident Obesity in Preschool-Aged Children

    PubMed Central

    Boynton-Jarrett, Renée; Fargnoli, Jessica; Suglia, Shakira Franco; Zuckerman, Barry; Wright, Rosalind J.

    2015-01-01

    Objective To examine the impact of chronicity of maternal intimate partner violence (IPV) on obesity risk among preschool-aged children. Design Prospective cohort study. Setting Several large US cities. Participants A subsample of the Fragile Families and Child Well-being Study participants (n = 1595), who were children born between 1998 and 2000 and their parents interviewed at baseline and at 12, 36, and 60 months. Main Exposure Maternal report of restrictive, sexual, and physical abuse from an intimate partner. Chronic IPV was defined as any maternal IPV exposure during both pregnancy or infancy (0–12 months) and early childhood (36–60 months). Main Outcome Measure Repeated measures of child body mass index. Results Among the 1595 children, 16.5% were obese at age 5 years and 49.4% of the mothers reported some form of IPV. Compared with those who had no IPV exposure, children whose mothers reported chronic IPV had an elevated risk for obesity at age 5 years (adjusted odds ratio = 1.80; 95% confidence interval, 1.24–2.61). Stratified analyses indicated increased risk for obesity among girls with a maternal history of chronic IPV (adjusted odds ratio = 2.21; 95% confidence interval, 1.30–3.75) compared with boys (adjusted odds ratio = 1.66; 95% confidence interval, 0.94–2.93) and a larger effect of any maternal IPV on obesity among children living in less safe neighborhoods (adjusted odds ratio = 1.56; 95% confidence interval, 1.03–2.36). Conclusions Chronic maternal IPV is associated with increased risk of obesity among preschool-aged children. Preventing family violence and improving community safety may help reduce childhood obesity. PMID:20530304

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

    PubMed

    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.

  13. Maternal obesity is associated with a low serum progesterone level in early pregnancy.

    PubMed

    Goh, Jia Ying; He, Song; Allen, John Carson; Malhotra, Rahul; Tan, Thiam Chye

    2016-09-01

    Progesterone is an important biomarker of early pregnancy failure. However, literature is limited regarding factors that influence progesterone levels in early pregnancy. Maternal obesity has been associated with adverse pregnancy outcomes such as miscarriages. We investigated the association between maternal body mass index (BMI) and serum progesterone level in first trimester singleton pregnancies for 194 women at a tertiary maternity hospital in Singapore, from January 2012 to February 2014. Maternal characteristics and study outcomes were retrieved from clinical records. Multivariate analysis demonstrated an inverse relationship between first trimester maternal BMI category and serum progesterone level (p=0.012). Obesity (maternal BMI ≥30 kg/m2), relative to normal weight (BMI 18.5-24.9 kg/m2), conferred an increased risk for serum progesterone <35 nmol/L (adjusted OR: 9.14; 95% CI: 2.12 - 39.5; p=0.003). The overall miscarriage rate in our study population was 13.9%. This study indicates that maternal obesity is associated with low first trimester serum progesterone. Pre-pregnancy weight optimization may be beneficial in regulation of serum progesterone level and maintenance of healthy pregnancy.

  14. Maternal inflammation during late pregnancy is lower in physically active compared with inactive obese women.

    PubMed

    Tinius, Rachel A; Cahill, Alison G; Strand, Eric A; Cade, W Todd

    2016-02-01

    The primary purpose of this study was to compare maternal plasma inflammation between physically active and inactive obese women during late pregnancy. The secondary purpose was to examine the relationships between maternal plasma inflammation and lipid metabolism and maternal and neonatal metabolic health in these women. A cross-sectional, observational study design was performed in 16 obese-inactive (OBI; means ± SD; age, 25.0 ± 4.8 years; prepregnancy body mass index (BMI), 36.3 ± 4.3 kg/m(2); body fat percentage in late gestation, 37.7% ± 3.5%) and 16 obese-active (OBA; age, 28.9 ± 4.8 years; prepregnancy BMI, 34.0 ± 3.7 kg/m(2); body fat in late gestation, 36.6% ± 3.8%) women during the third trimester of pregnancy. Maternal plasma inflammation (C -reactive protein (CRP)) and insulin resistance (Homeostatic Model Assessment-Insulin Resistance) were measured at rest. Plasma lipid concentration and metabolism (lipid oxidation and lipolysis) were measured at rest, during a 30-min bout of low-intensity (40% peak oxygen uptake) exercise, and during a resting recovery period using indirect calorimetry. Umbilical cord blood was collected for measurement of neonatal plasma insulin resistance, inflammation, and lipid concentration. Neonatal body composition was measured via air displacement plethysmography. Maternal plasma CRP concentration was significantly higher in OBI compared with OBA women (9.1 ± 4.0 mg/L vs. 6.3 ± 2.5 mg/L, p = 0.02). Maternal plasma CRP concentration was significantly associated with maternal lipolysis (r = 0.43, p = 0.02), baseline lipid oxidation rate (r = 0.39, p = 0.03), and baseline plasma free fatty acid concentration (r = 0.36, p = 0.04). In conclusion, maternal physical activity may reduce inflammation during pregnancy in obese women. Maternal lipid metabolism is related to systemic inflammation.

  15. Maternal obesity and the developmental programming of hypertension: a role for leptin.

    PubMed

    Taylor, P D; Samuelsson, A-M; Poston, L

    2014-03-01

    Mother-child cohort studies have established that both pre-pregnancy body mass index (BMI) and gestational weight gain are independently associated with cardio-metabolic risk factors in young adult offspring, including systolic and diastolic blood pressure. Animal models in sheep and non-human primates provide further evidence for the influence of maternal obesity on offspring cardiovascular function, whilst recent studies in rodents suggest that perinatal exposure to the metabolic milieu of maternal obesity may permanently change the central regulatory pathways involved in blood pressure regulation. Leptin plays an important role in the central control of appetite, is also involved in activation of efferent sympathetic pathways to both thermogenic and non-thermogenic tissues, such as the kidney, and is therefore implicated in obesity-related hypertension. Leptin is also thought to have a neurotrophic role in the development of the hypothalamus, and altered neonatal leptin profiles secondary to maternal obesity are associated with permanently altered hypothalamic structure and function. In rodent studies, maternal obesity confers persistent sympathoexcitatory hyper-responsiveness and hypertension acquired in the early stages of development. Experimental neonatal hyperleptinaemia in naive rat pups provides further evidence of heightened sympathetic tone and proof of principle that hyperleptinaemia during a critical window of hypothalamic development may directly lead to adulthood hypertension. Insight from these animal models raises the possibility that early-life exposure to leptin in humans may lead to early onset essential hypertension. Ongoing mother-child cohort and intervention studies in obese pregnant women provide a unique opportunity to address associations between maternal obesity and offspring cardiovascular function. The goal of the review is to highlight the potential importance of leptin in the developmental programming of hypertension in obese

  16. Maternal obesity drives functional alterations in uterine NK cells

    PubMed Central

    Perdu, Sofie; Castellana, Barbara; Kim, Yoona; Chan, Kathy; DeLuca, Lauren; Beristain, Alexander G.

    2016-01-01

    Over one-fifth of North American women of childbearing age are obese, putting these women at risk for a variety of detrimental chronic diseases. In addition, obesity increases the risk for developing major complications during pregnancy. The mechanisms by which obesity contributes to pregnancy complications and loss remain unknown. Increasing evidence indicates that obesity results in major changes to adipose tissue immune cell composition and function; whether or not obesity also affects immune function in the uterus has not been explored. Here we investigated the effect of obesity on uterine natural killer (uNK) cells, which are essential for uterine artery remodeling and placental development. Using a cohort of obese or lean women, we found that obesity led to a significant reduction in uNK cell numbers accompanied with impaired uterine artery remodeling. uNK cells isolated from obese women had altered expression of genes and pathways associated with extracellular matrix remodeling and growth factor signaling. Specifically, uNK cells were hyper-responsive to PDGF, resulting in overexpression of decorin. Functionally, decorin strongly inhibited placental development by limiting trophoblast survival. Together, these findings establish a potentially new link between obesity and poor pregnancy outcomes, and indicate that obesity-driven changes to uterine-resident immune cells critically impair placental development. PMID:27699222

  17. [A survival analysis approach to assess the association between maternal smoking during pregnancy and childhood obesity].

    PubMed

    Suzuki, Kohta; Sato, Miri; Ando, Daisuke; Kondo, Naoki; Yamagata, Zentaro

    2012-08-01

    It has been suggested that maternal smoking during pregnancy has an effect on childhood obesity. We previously clarified the association between maternal lifestyle habits practiced during pregnancy, including smoking, and childhood obesity and overweight at 9-10 years of age. In this study, we aimed to demonstrate this association through survival analysis. This study was based on an on-going community-based prospective cohort study initiated in the fetal stage called Project Koshu. The study population comprised of the participants of Project Koshu, who were children born in a rural Japanese area between 1991 and 1999 and their mothers. In this project, maternal smoking status during pregnancy was collected through a questionnaire and childhood anthropometric data were measured at annual medical check-ups from 3 years of age to 9-10 years of age. Using these data, we performed a survival analysis using the Kaplan-Meier method to compare the cumulative rate of childhood obesity and overweight between those with mothers who smoked during pregnancy and those who did not. Subsequently, we calculated the hazard ratio (HR) of the effect of maternal smoking during pregnancy on childhood obesity using the Cox proportional hazard model. In the survival analysis of childhood obesity, we analyzed the data of 1428 children and their mothers (follow-up rate: 87.7%). Of these, 290 children (20.3%) became overweight and 92 children (6.4%) became obese between 3 years of age and 9-10 years of age. This shows that the cumulative rate of childhood obesity was significantly different between mothers with and without smoking habits (P < 0.001). Using the Cox proportional hazard model, we analyzed the data of 1204 children and their mothers (follow-up rate: 74.0%). Of these, 255 children (21.2%) became overweight and 76 children (6.3%) became obese between 3 years of age and 9-10 years of age. Maternal smoking during pregnancy was found to be associated with childhood obesity (HR, 2

  18. 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

  19. Maternal Exposure to Synthetic Chemicals and Obesity in the Offspring: Recent Findings.

    PubMed

    Liu, Yun; Peterson, Karen E

    2015-12-01

    Experimental studies suggest perinatal exposures to synthetic chemicals may be associated with early onset obesity, although this hypothesis has not been extensively examined in humans. This article summarizes the evidence relating maternal perinatal exposure to common persistent organic compounds (polychlorinated biphenyl, dichlorodiphenyldichloroethylene, dichlorodiphenyltrichloroethane, hexachlorobenzene, hexachlorocyclohexane), perfluoroalkyls, perfluorooctane sulfonate, polybrominated diphenyl ethers and tributyltin, and nonpersistent compounds (phthalates, bisphenol A) on child obesity during sensitive developmental periods. Twenty-two epidemiologic studies published from 2011 to 2015 offer inconsistent support for the obesogenic effects of most substances and are limited by relatively small sample sizes and indirect measures of adiposity. The clearest findings suggest an influence of maternal dichlorodiphenyldichloroethylene exposure on offspring overweight and obesity. Recommendations for future epidemiological research include longer follow-up of effects of pre- and postnatal exposures in large samples; utilization of direct measures of adiposity; and consideration of effect modification by sex, birth weight, dietary fat, and maternal weight status.

  20. Maternal Nutrition and Risk of Obesity in Offspring: The Trojan Horse of Developmental Plasticity

    PubMed Central

    Parlee, Sebastian D.; MacDougald, Ormond A.

    2013-01-01

    Mammalian embryos have evolved to adjust their organ and tissue development in response to an atypical environment. This adaptation, called phenotypic plasticity, allows the organism to thrive in the anticipated environment in which the fetus will emerge. Barker and colleagues proposed that if the environment in which the fetus emerges differs from that in which it develops, phenotypic plasticity may provide an underlying mechanism for disease. Epidemiological studies have shown that humans born small- or large-for-gestational-age, have a higher likelihood of developing obesity as adults. The amount and quality of food that the mother consumes during gestation influences birth weight, and therefore susceptibility of progeny to disease in later life. Studies in experimental animals support these observations, and find that obesity occurs as a result of maternal nutrient-restriction during gestation, followed by rapid compensatory growth associated with ad libitum food consumption. Therefore, obesity associated with maternal nutritional restriction has a developmental origin. Based on this phenomenon, one might predict that gestational exposure to a westernized diet would protect against future obesity in offspring. However, evidence from experimental models indicates that, like maternal dietary restriction, maternal consumption of a westernized diet during gestation and lactation interacts with an adult obesogenic diet to induce further obesity. Mechanistically, restriction of nutrients or consumption of a high fat diet during gestation may promote obesity in progeny by altering hypothalamic neuropeptide production and thereby increasing hyperphagia in offspring. In addition to changes in food intake these animals may also direct energy from muscle towards storage in adipose tissue. Surprisingly, generational inheritance studies in rodents have further indicated that effects on body length, body weight, and glucose tolerance appear to be propagated to subsequent

  1. Rat Maternal Obesity and High Fat Diet Program Offspring Metabolic Syndrome

    PubMed Central

    DESAI, Mina; JELLYMAN, Juanita K.; HAN, Guan; BEALL, Marie; LANE, Robert H.; ROSS, Michael G.

    2014-01-01

    Objective We determined the potential programming effects of maternal obesity and high fat (HF) diet during pregnancy and/or lactation on offspring metabolic syndrome. Study Design A rat model of maternal obesity was created using a HF diet prior to and throughout pregnancy and lactation. At birth, pups were cross fostered thereby generating four 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. Results Maternal phenotype during pregnancy and the end of lactation evidenced markedly elevated body fat and plasma corticosterone levels in HF dams. In the offspring, maternal HF diet during pregnancy alone programmed increased offspring adiposity, though with normal body weight, whereas maternal HF diet during lactation increased both body weight and adiposity. Metabolic disturbances, particularly that of hyperglycemia, were apparent in all groups exposed to maternal HF diet (during pregnancy and/or lactation), though differences were apparent in the manifestation of insulin resistant versus 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 as offspring that experienced in utero HF exposure had increased corticosterone levels. Conclusion Maternal obesity/HF diet markedly impact offspring body composition and the risk of metabolic syndrome dependent upon period of exposure during pregnancy and/or lactation. PMID:24631702

  2. 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.

  3. Maternal and Fetal Lipid and Adipokine Profiles and Their Association with Obesity

    PubMed Central

    Solis-Paredes, Mario; Espino y Sosa, Salvador; Estrada-Gutierrez, Guadalupe; Nava-Salazar, Sonia; Ortega-Castillo, Veronica; Rodriguez-Bosch, Mario; Bravo-Flores, Eyerahi; Espejel-Nuñez, Aurora; Tolentino-Dolores, Maricruz; Gaona-Estudillo, Rubí; Martinez-Bautista, Nancy; Perichart-Perera, Otilia

    2016-01-01

    Background. Maternal metabolic changes impact fetal metabolism resulting in a higher risk for developing chronic diseases later in life. The aim of this study was to assess the association between maternal and fetal adipokine and lipid profiles, as well as the influence of maternal weight on this association. Methods. Healthy pregnant women at term who delivered by C-section were enrolled. Maternal and fetal glucose, lipid profile, adiponectin, leptin, and resistin levels were analyzed by obesity and maternal weight gain. Statistics included descriptives, correlations, and mean differences (SPSS v20.0). Results. Adiponectin and resistin concentrations were higher in fetal blood, while leptin was lower (p < 0.05). A significant inverse association between maternal resistin and fetal LDL-cholesterol (LDL-C) (r = −0.327; p = 0.022) was observed. A positive correlation was found between maternal and fetal resistin (r = 0.358; p = 0.013). Women with excessive weight gain had higher leptin levels and their fetuses showed higher LDL-C levels (p < 0.05). Conclusions. Maternal resistin showed an inverse association with fetal LDL-C, suggesting that maternal adiposity status may play an active role in the regulation of fetal lipid profile and consequently, in fetal programming. Excessive maternal weight gain during pregnancy may exert an effect over metabolic mediators in both mother and newborn. PMID:27190514

  4. 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

  5. Maternal caffeine intake during pregnancy and risk of obesity in offspring: a prospective cohort study.

    PubMed

    Li, D-K; Ferber, J R; Odouli, R

    2015-04-01

    In-utero exposures through adverse fetal programming are emerging as an important contributing factor to the epidemic of childhood obesity. This study examines the impact of in-utero exposure to caffeine on the risk of childhood obesity in offspring. A prospective study of pregnant women with 15 years follow-up of their offspring was conducted to examine the impact of in-utero exposure to caffeine on the risk of childhood obesity. Maternal caffeine intake was prospectively ascertained during pregnancy and outcome measures (body mass index (BMI)) were ascertained from medical charts, with 17 BMI measurements per child, on average, during the follow-up period. Potential confounders including known perinatal risk factors for childhood obesity were adjusted for using the generalized estimating equations model with repeated measurements. After controlling for potential confounders, compared with those without caffeine exposure, in-utero exposure to caffeine overall is associated with 87% increased risk of childhood obesity: odds ratio (OR) =1.87, 95% confidence interval (CI): 1.12-3.12. This association demonstrated a dose-response relationship: OR=1.77 (1.05-3.00) for maternal daily caffeine intake <150 mg per day, OR=2.37 (1.24-4.52) for caffeine intake ⩾150 mg per day during pregnancy, respectively. We also observed a linear relationship: every one unit increase (log10 scale) in the amount of maternal caffeine intake was associated with 23% increased risk of obesity in offspring. The dose-response relationship appears stronger for persistent obesity than for transitory obesity (occasional high BMI), and for girls than for boys. We observed an association of in-utero exposure to caffeine with increased risk of childhood obesity. If this observation is further replicated in other studies, the finding will contribute to the understanding of fetal programming of childhood diseases and development of intervention strategy to prevent childhood obesity.

  6. Maternal obesity has little effect on the immediate offspring but impacts on the next generation.

    PubMed

    King, Vicky; Dakin, Rachel S; Liu, Lincoln; Hadoke, Patrick W F; Walker, Brian R; Seckl, Jonathan R; Norman, Jane E; Drake, Amanda J

    2013-07-01

    Maternal obesity during pregnancy has been linked to an increased risk of obesity and cardiometabolic disease in the offspring, a phenomenon attributed to developmental programming. Programming effects may be transmissible across generations through both maternal and paternal inheritance, although the mechanisms remain unclear. Using a mouse model, we explored the effects of moderate maternal diet-induced obesity (DIO) on weight gain and glucose-insulin homeostasis in first-generation (F1) and second-generation offspring. DIO was associated with insulin resistance, hyperglycemia and dyslipidemia before pregnancy. Birth weight was reduced in female offspring of DIO mothers (by 6%, P = .039), and DIO offspring were heavier than controls at weaning (males by 47%, females by 27%), however there were no differences in glucose tolerance, plasma lipids, or hepatic gene expression at 6 months. Despite the relative lack of effects in the F1, we found clear fetal growth restriction and persistent metabolic changes in otherwise unmanipulated second-generation offspring with effects on birth weight, insulin levels, and hepatic gene expression that were transmitted through both maternal and paternal lines. This suggests that the consequences of the current dietary obesity epidemic may also have an impact on the descendants of obese individuals, even when the phenotype of the F1 appears largely unaffected.

  7. 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.

  8. A pilot study on the prevalence of maternal obesity in selected Greek counties.

    PubMed

    Grammatikopoulou, Maria G; Pritsa, Agathi A; Badeka, Sophia; Aggelaki, Irini; Giantsiou, Ioanna; Houta, Assimina; Zeibekoglou, Vasiliki; Kyriazi, Maria; Papanastasiou, Polykseni; Perdiki, Eleni; Gkipatidou, Despoina; Tsigga, Maria

    2013-11-01

    To report a pilot prevalence of maternal overweight, obesity and underweight in selected Greek counties. A total of 441 adult childbearing women were recruited from maternity clinics in 6 Greek counties for this cross-sectional study. Pre-gravid weight status was defined according to the WHO cut-offs and gravid weight status was diagnosed with the Mardones and Rosso weight gain chart. During gestation the majority of the participants were of normal body weight (BW) (34.0%), obesity was apparent in 25.6% of the sample, 23.8% of the participants were underweight, and the remaining 16.6% were overweight. Overall, pregnancy tripled the prevalence of underweight, increased the prevalence of obesity (by 388.0%) and decreased the number of participants in the normal BW category (p≤0.001 for all). The majority of participants classified in each pre-gravid weight-category remained in the same weight category during their gestation. All the pre-gravidly obese women were also obese during pregnancy. Underweight was more prevalent in Kavala (37.5%) and obesity was more frequent in Thessaloniki (30.8%). Women who were overweight prior to conception were highly likely to be overweight/obese during pregnancy (OR: 23.8, CI: 11.1-51.0). The results indicate a high prevalence of overweight, obesity and underweight among pregnant women in Greece. Copyright © 2012 SEEN. Published by Elsevier Espana. All rights reserved.

  9. Maternal pre-pregnancy obesity and the risk of shoulder dystocia: a meta-analysis.

    PubMed

    Zhang, C; Wu, Y; Li, S; Zhang, D

    2017-08-02

    Results from epidemiological studies about the association between maternal pre-pregnancy obesity and the risk of shoulder dystocia are inconsistent. To evaluate the effect of maternal pre-pregnancy obesity on the risk of shoulder dystocia. We searched PubMed and Web of Science database for all relevant studies up to 5 August 2016 and reviewed the reference lists of identified articles. Observational studies that investigated the association between pre-pregnancy obesity and the risk of shoulder dystocia were included. A total of 20 articles involving 2 153 898 participants were included in this meta-analysis. A random effects model was used to calculate the pooled relative risks (RRs) with 95% confidence intervals (CIs). For obese versus non-obese, the pooled RR of shoulder dystocia was 1.63 (95% CI 1.33-1.99). The findings remained significant in the cohort studies (RR = 1.59, 95% CI 1.28-1.97) and case-control studies (RR = 1.92, 95% CI 1.03-3.57). With regard to the subgroup of continents, there was significant association between obesity and the risk of shoulder dystocia in Europe (RR = 1.51, 95% CI 1.18-1.92) and Asia (RR = 2.59, 95% CI 1.15-5.83). The result from the sensitivity analysis for studies adjusted for gestational diabetes was significant (RR = 1.61, 95% CI 1.05-2.47). The pooled RRs for obesity classes I, II and III versus non-obese were 1.29 (95% CI 1.06-1.57), 1.94 (95% CI 1.26-2.98) and 2.47(95% CI 1.56-3.93), respectively. This meta-analysis suggests that maternal pre-pregnancy obesity is associated with increased risk of shoulder dystocia. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.

  10. 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.

  11. 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.

  12. Maternal obesity modulates intracellular lipid turnover in the human term placenta.

    PubMed

    Hirschmugl, B; Desoye, G; Catalano, P; Klymiuk, I; Scharnagl, H; Payr, S; Kitzinger, E; Schliefsteiner, C; Lang, U; Wadsack, C; Hauguel-de Mouzon, S

    2017-02-01

    Obesity before pregnancy is associated with impaired metabolic status of the mother and the offspring later in life. These adverse effects have been attributed to epigenetic changes in utero, but little is known about the role of placental metabolism and its contribution to fetal development. We examined the impact of maternal pre-pregnancy obesity on the expression of genes involved in placental lipid metabolism in lean and obese women. Seventy-three lean and obese women with healthy pregnancy were recruited at term elective cesarean delivery. Metabolic parameters were measured on maternal venous blood samples. Expression of 88 genes involved in lipid metabolism was measured in whole placenta tissue. Proteins of genes differently expressed in response to maternal obesity were quantified, correlated with maternal parameters and immunolocalized in placenta sections. Isolated primary trophoblasts were used for in vitro assays. Triglyceride (TG) content was increased in placental tissue of obese (1.10, CI 1.04-1.24 mg g(-1), P<0.05) vs lean (0.84, CI 0.72-1.02 mg g(-1)) women. Among target genes examined, six showed positive correlation (P<0.05) with maternal pre-pregnancy BMI, namely ATGL (PNPLA2), FATP1 (SLC27A1), FATP3 (SLC27A3), PLIN2, PPARG and CGI-58 (ABHD5). CGI-58 protein abundance was twofold higher (P<0.001) in placentas of obese vs lean women. CGI-58 protein levels correlated positively with maternal insulin levels and pre-pregnancy body mass index (R=0.63, P<0.001 and R=0.64, P<0.001, respectively). CGI-58 and PLIN2 were primarily located in the syncytiotrophoblast and, were upregulated (1.38- and 500-fold, respectively) upon oleic acid and insulin treatment of cultured trophoblast cells. Pre-gravid obesity significantly modifies the expression of placental genes related to transport and storage of neutral lipids. We propose that the upregulation of CGI-58, a master regulator of TG hydrolysis, contributes to the turnover of intracellular lipids in

  13. Maternal obesity modulates intracellular lipid turnover in the human term placenta

    PubMed Central

    Hirschmugl, B; Desoye, G; Catalano, P; Klymiuk, I; Scharnagl, H; Payr, S; Kitzinger, E; Schliefsteiner, C; Lang, U; Wadsack, C; Hauguel-de Mouzon, S

    2017-01-01

    Background: Obesity before pregnancy is associated with impaired metabolic status of the mother and the offspring later in life. These adverse effects have been attributed to epigenetic changes in utero, but little is known about the role of placental metabolism and its contribution to fetal development. Objectives: We examined the impact of maternal pre-pregnancy obesity on the expression of genes involved in placental lipid metabolism in lean and obese women. Subjects/Methods: Seventy-three lean and obese women with healthy pregnancy were recruited at term elective cesarean delivery. Metabolic parameters were measured on maternal venous blood samples. Expression of 88 genes involved in lipid metabolism was measured in whole placenta tissue. Proteins of genes differently expressed in response to maternal obesity were quantified, correlated with maternal parameters and immunolocalized in placenta sections. Isolated primary trophoblasts were used for in vitro assays. Results: Triglyceride (TG) content was increased in placental tissue of obese (1.10, CI 1.04–1.24 mg g−1, P<0.05) vs lean (0.84, CI 0.72–1.02 mg g−1) women. Among target genes examined, six showed positive correlation (P<0.05) with maternal pre-pregnancy BMI, namely ATGL (PNPLA2), FATP1 (SLC27A1), FATP3 (SLC27A3), PLIN2, PPARG and CGI-58 (ABHD5). CGI-58 protein abundance was twofold higher (P<0.001) in placentas of obese vs lean women. CGI-58 protein levels correlated positively with maternal insulin levels and pre-pregnancy body mass index (R=0.63, P<0.001 and R=0.64, P<0.001, respectively). CGI-58 and PLIN2 were primarily located in the syncytiotrophoblast and, were upregulated (1.38- and 500-fold, respectively) upon oleic acid and insulin treatment of cultured trophoblast cells. Conclusion: Pre-gravid obesity significantly modifies the expression of placental genes related to transport and storage of neutral lipids. We propose that the upregulation of CGI-58, a master regulator of TG

  14. A post-weaning obesogenic diet exacerbates the detrimental effects of maternal obesity on offspring insulin signaling in adipose tissue

    PubMed Central

    de Almeida Faria, Juliana; Duque-Guimarães, Daniella; Carpenter, Asha A. M.; Loche, Elena; Ozanne, Susan E.

    2017-01-01

    Previous studies have shown that maternal diet-induced obesity leads to increased risk of type 2 diabetes in offspring. The current study investigated if weaning onto an obesogenic diet exaggerated the detrimental effects of maternal diet-induced obesity in adipose tissue. Maternal obesity and offspring obesity led to reduced expression of key insulin signalling proteins, including insulin receptor substrate-1 (IRS-1). The effects of maternal obesity and offspring obesity were, generally, independent and additive. Irs1 mRNA levels were similar between all four groups of offspring, suggesting that in both cases post-transcriptional regulation was involved. Maternal diet-induced obesity increased miR-126 expression however levels of this miR were not influenced by a post-weaning obesogenic diet. In contrast, a post-weaning obesogenic diet was associated with increased levels of suppressor of cytokine signaling-1, implicating increased degradation of IRS-1 as an underlying mechanism. Our results suggest that whilst programmed reductions in IRS-1 are associated with increased levels of miR-126 and consequently reduced translation of Irs1 mRNA, the effects of a post-weaning obesogenic diet on IRS-1 are mediated by miR-126 independent mechanisms, including increased IRS-1 protein degradation. These divergent mechanisms explain why the combination of maternal obesity and offspring obesity leads to the most pronounced effects on offspring metabolism. PMID:28338072

  15. A post-weaning obesogenic diet exacerbates the detrimental effects of maternal obesity on offspring insulin signaling in adipose tissue.

    PubMed

    de Almeida Faria, Juliana; Duque-Guimarães, Daniella; Carpenter, Asha A M; Loche, Elena; Ozanne, Susan E

    2017-03-24

    Previous studies have shown that maternal diet-induced obesity leads to increased risk of type 2 diabetes in offspring. The current study investigated if weaning onto an obesogenic diet exaggerated the detrimental effects of maternal diet-induced obesity in adipose tissue. Maternal obesity and offspring obesity led to reduced expression of key insulin signalling proteins, including insulin receptor substrate-1 (IRS-1). The effects of maternal obesity and offspring obesity were, generally, independent and additive. Irs1 mRNA levels were similar between all four groups of offspring, suggesting that in both cases post-transcriptional regulation was involved. Maternal diet-induced obesity increased miR-126 expression however levels of this miR were not influenced by a post-weaning obesogenic diet. In contrast, a post-weaning obesogenic diet was associated with increased levels of suppressor of cytokine signaling-1, implicating increased degradation of IRS-1 as an underlying mechanism. Our results suggest that whilst programmed reductions in IRS-1 are associated with increased levels of miR-126 and consequently reduced translation of Irs1 mRNA, the effects of a post-weaning obesogenic diet on IRS-1 are mediated by miR-126 independent mechanisms, including increased IRS-1 protein degradation. These divergent mechanisms explain why the combination of maternal obesity and offspring obesity leads to the most pronounced effects on offspring metabolism.

  16. 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

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

    PubMed

    Vega, C C; Reyes-Castro, L A; Bautista, C J; Larrea, F; Nathanielsz, P W; Zambrano, E

    2015-04-01

    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. MO produces metabolic and endocrine dysfunction, increases maternal and offspring glucocorticoid exposure, oxidative stress and adverse offspring outcomes by postnatal day (PND) 36. MEx in part prevents these outcomes. F0 female rats ate either control or obesogenic diet from weaning through lactation. Half of each group wheel ran (from day 90 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. 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 increases glucose, insulin, cholesterol and oxidative stress. 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. MEx before and during pregnancy has beneficial effects on the maternal and offspring metabolism and endocrine function occurring with no weight change in mothers and offspring indicating the importance

  18. 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...

  19. Enhanced Adipogenic and Lipogenic Signatures in White Adipose Tissue of Offspring Exposed to Maternal Obesity In Utero

    USDA-ARS?s Scientific Manuscript database

    The risk of obesity throughout life is subject to programming beginning early in development. Exposure to maternal obesity (MO) at conception and during gestation increases the risk of obesity in adult-life. MO was induced in female Sprague Dawley rats via overfeeding of liquid diets (30% excess cal...

  20. 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...

  1. 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

  2. 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...

  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 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...

  5. Charting the Maternal and Infant Microbiome: What Is the Role of Diabetes and Obesity in Pregnancy?

    PubMed

    Singh, Sirtaj; Karagas, Margaret R; Mueller, Noel T

    2017-02-01

    The purpose of this review is to summarize the evidence on whether diabetes, obesity, and related metabolic derangements during pregnancy are associated with the maternal and infant microbiomes, and to identify gaps in the literature and offer guidance on future research on this topic. We found circumstantial evidence from four observational studies that the maternal gut microbiome was associated with either pre-pregnancy body mass index, gestational weight gain, gestational diabetes, and/or related metabolic biomarkers in pregnancy; we did not identify any studies that examined whether the vaginal microbiome varied according to these metabolic parameters. Maternal diabetes (in one study) and pregnancy weight status (in three studies) were found to be associated with the infant offspring gut microbiome, although some associations only appeared in certain cohort strata. Patterns of association across both maternal and infant microbiome studies, however, lacked consistency, which may owe to biologic or technical differences, or to the lack of control for important confounders or effect modifiers (e.g., delivery mode in infant microbiome studies). Metabolic diseases in pregnancy, such as diabetes and obesity, may be associated with the maternal and infant microbiomes, but there is a need for large prospective studies of mother-child dyads from diverse racial and ethnic backgrounds to determine the direction and potential causal nature of these associations. These studies should include serially collected biospecimens, standardized workflows that conserve microbial DNA and RNA, and rich data on clinical outcomes and environmental, lifestyle, and genetic risk factors for obesity and diabetes.

  6. 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.

  7. 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.

  8. 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.

  9. 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.

  10. 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.

  11. 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.

  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. 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.

  14. Independent and joint effects of prenatal maternal smoking and maternal exposure to second-hand smoke on the development of adolescent obesity: a longitudinal study.

    PubMed

    Wang, Liang; Mamudu, Hadii M; Alamian, Arsham; Anderson, James L; Brooks, Billy

    2014-11-01

    To examine associations of prenatal maternal smoking and second-hand smoke (SHS) exposure with the development of adolescent obesity. Longitudinal data (1991-2007) from National Institute of Child Health and Human Development Study of Early Child Care and Youth Development involving mothers that smoked and or exposed to SHS during the year before birth were analysed. Adolescent obesity in ages 12.0-15.9 years was defined as a BMI ≥ 95th percentile. Generalised estimating equations (GEE) were used for the analyses. Obesity was more prevalent among adolescents whose mothers smoked or had SHS exposure than those that did not smoke or exposed to SHS. After adjusting for maternal and child factors, GEE models showed that odds of adolescent obesity increased with prenatal maternal smoking (OR = 1.57, 95% CI = 1.03-2.39) and SHS exposure (OR = 1.53, 95% CI = 1.04-2.27). The odds for obesity increased more than two times among adolescents exposed to both maternal smoking and SHS (OR = 2.10, 95% CI = 1.24, 3.56) compared with those without exposure. Additionally, not breastfeeding, maternal obesity, and longer screen viewing hours per day were associated with increased odds of obesity. There is possibly a long-term joint effect of prenatal maternal smoke (smoking and SHS) exposure on obesity among adolescent offspring, and the effect is independent of birthweight. These findings suggest that adolescent obesity could possibly be curtailed with the development and promotion of smoking cessation programmes for families during the year before birth. © 2014 The Authors. Journal of Paediatrics and Child Health © 2014 Paediatrics and Child Health Division (Royal Australasian College of Physicians).

  15. The impact of preconceptional obesity on trajectories of maternal lipids during gestation

    PubMed Central

    Bozkurt, Latife; Göbl, Christian S.; Hörmayer, Anna-Theresa; Luger, Anton; Pacini, Giovanni; Kautzky-Willer, Alexandra

    2016-01-01

    Growing challenges of maternal obesity necessitate to focus metabolic management on alternative factors than glycaemia. The objective is to assess longitudinal changes in lipids and inflammatory parameters during pregnancies stratified by pregestational BMI. Therefore, 222 pregnant women (normal-weight BMI < 25: n = 91 (41%), overweight BMI 25–29.9: n = 69 (31%), obese BMI ≥ 30: n = 62 (28%)) underwent a detailed metabolic characterization including fasting lipids and glucometabolic parameters at <21st gestational week (GW) with follow-up assessments at further three visits (24–28th GW, 32–34th GW, >36th GW). Overweight and obesity was related to dyslipidemia already at baseline, i.e. elevated triglycerides (TG, p < 0.001), decreased high-density-lipoprotein-C (p = 0.009) and increased ultrasensitive-c-reactive-protein (usCRP, p < 0.001) independent of gestational diabetes prevalence. Trajectories of lipids during pregnancy progress revealed an unexpected less pronounced increase in TG, low-density-lipoprotein-C and total-cholesterol in overweight/obese women. usCRP remained associated with higher BMI throughout pregnancy showing no time-dependent longitudinal changes. Newborns of obese/overweight women were affected by higher birth-weight percentiles. Regarding lipids only maternal TG showed tendency for relation to prevalence of large-for-gestational-age offspring, particularly at the end of pregnancy (p = 0.048). Overweight and obese women show significant differences in trajectories of lipids during pregnancy that distinguish them from normal-weight women. Further studies should evaluate if targeting lipid metabolism could improve clinical management of maternal obesity. PMID:27436227

  16. Maternal inflammation during late pregnancy is lower in physically active compared to inactive obese women

    PubMed Central

    Tinius, Rachel A.; Cahill, Alison G.; Strand, Eric A.; Todd Cade, W.

    2016-01-01

    Purpose The primary purpose of this study was to compare maternal plasma inflammation between physically active and inactive obese women during late pregnancy. The secondary purpose was to examine the relationships between maternal plasma inflammation and lipid metabolism and maternal and neonatal metabolic health in these women. Methods A cross-sectional, observational study design was performed in 16 obese-inactive ((OBI) age: 25.0 ± 4.8 years, pre-pregnancy BMI: 36.3 ± 4.3kg/m2, body fat percentage in late gestation: 37.7 ± 3.5%) and 16 obese-active ((OBA) age: 28.9 ± 4.8 years, pre-pregnancy BMI: 34.0±3.7kg/m2, body fat in late gestation: 36.6 ± 3.8%) women during the third trimester of pregnancy. Maternal plasma inflammation (C -reactive protein (CRP)) and insulin resistance (Homeostatic Model Assessment-Insulin Resistance (HOMA-IR)) were measured at rest. Plasma lipid concentration and metabolism (lipid oxidation and lipolysis) were measured at rest, during a 30-minute bout of low-intensity (40% VO2peak) exercise, and during a resting recovery period using indirect calorimetry. Umbilical cord blood was collected for measurement of neonatal plasma insulin resistance, inflammation, and lipid concentration. Neonatal body composition was measured via air displacement plethysmography. Results Maternal plasma CRP concentration was significantly higher in OBI compared to OBA women (9.1 ± 4.0 mg/L versus 6.3 ±2.5mg/L, p=0.02). Maternal plasma CRP concentration was significantly associated with maternal lipolysis (r=0.43, p=0.02), baseline lipid oxidation rate (r=0.39, p=0.03), and baseline plasma free fatty acid concentration (r=0.36, p=0.04). Conclusions Maternal physical activity may reduce inflammation during pregnancy in obese women. Maternal lipid metabolism is related to systemic inflammation. PMID:26799789

  17. 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.

  18. Pregnancy, obesity and insulin resistance: maternal overnutrition and the target windows of fetal development.

    PubMed

    Muhlhausler, Beverly S; Gugusheff, Jessica R; Ong, Zhi Yi; Vithayathil, Mini A

    2013-09-01

    A substantial body of literature has demonstrated that the nutritional environment an individual experiences before birth or in early infancy is a key determinant of their health outcomes across the life course. This concept, the developmental origins of health and disease (DOHaD) hypothesis, was initially focused on the adverse consequences of exposure to a suboptimal nutrient supply and provided evidence that maternal undernutrition, fetal growth restriction, and low birth weight were associated with heightened risk of central adiposity, insulin resistance, and cardiovascular disease. More recently, the epidemic rise in the incidence of maternal obesity has seen the attention of the DOHaD field turn toward identifying the impact on the offspring of exposure to an excess nutrient supply in early life. The association between maternal obesity and increased risk of obesity in the offspring has been documented in human populations worldwide, and animal models have provided critical insights into the biological mechanisms that drive this relationship. This review will discuss the important roles that programming of the adipocyte and programming of the central neural networks which control appetite and reward play in the early life programming of metabolic disease by maternal overnutrition. It will also highlight the important research gaps and challenges that remain to be addressed and provide a personal perspective on where the field should be heading in the coming 5-10 years.

  19. Associations of maternal obesity and excessive weight gain during pregnancy with subcutaneous fat mass in infancy.

    PubMed

    Jharap, Varsha V; Santos, Susana; Steegers, Eric A P; Jaddoe, Vincent W V; Gaillard, Romy

    2017-05-01

    Not much is known about the associations of maternal obesity and excessive gestational weight gain with body fat in infancy. To examine the associations of maternal pre-pregnancy body mass index and gestational weight gain with infant subcutaneous fat. In a population-based prospective cohort study among 845 mothers and their infants, we obtained maternal pre-pregnancy body mass index and measured maternal weight during pregnancy. At 1.5, 6 and 24months, we estimated infant total subcutaneous fat (sum of biceps, triceps, suprailiacal and subscapular skinfold thicknesses) and central-to-total subcutaneous fat ratio (sum of suprailiacal and subscapular skinfold thicknesses/total subcutaneous fat). Maternal body mass index was positively associated with higher infant body mass index from 6months onwards. Maternal body mass index was not associated with infant subcutaneous fat measures at 1.5 or 6months. A 1-standard deviation scores (SDS) higher maternal body mass index was associated with a 0.09 (95% Confidence Interval 0.01, 0.17) SDS higher infant total subcutaneous fat at 24months, but not with central-to-total subcutaneous fat ratio. No associations were present for maternal total or period-specific gestational weight gain with infant fat. Maternal body mass index was positively associated with infant body mass index and total subcutaneous fat in late infancy. Maternal total and period-specific gestational weight gain were not associated with infant body fat mass measures. Copyright © 2017 Elsevier B.V. All rights reserved.

  20. 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.

  1. Toddlers' bias to look at average versus obese figures relates to maternal anti-fat prejudice.

    PubMed

    Ruffman, Ted; O'Brien, Kerry S; Taumoepeau, Mele; Latner, Janet D; Hunter, John A

    2016-02-01

    Anti-fat prejudice (weight bias, obesity stigma) is strong, prevalent, and increasing in adults and is associated with negative outcomes for those with obesity. However, it is unknown how early in life this prejudice forms and the reasons for its development. We examined whether infants and toddlers might display an anti-fat bias and, if so, whether it was influenced by maternal anti-fat attitudes through a process of social learning. Mother-child dyads (N=70) split into four age groups participated in a preferential looking paradigm whereby children were presented with 10 pairs of average and obese human figures in random order, and their viewing times (preferential looking) for the figures were measured. Mothers' anti-fat prejudice and education were measured along with mothers' and fathers' body mass index (BMI) and children's television viewing time. We found that older infants (M=11months) had a bias for looking at the obese figures, whereas older toddlers (M=32months) instead preferred looking at the average-sized figures. Furthermore, older toddlers' preferential looking was correlated significantly with maternal anti-fat attitudes. Parental BMI, education, and children's television viewing time were unrelated to preferential looking. Looking times might signal a precursor to explicit fat prejudice socialized via maternal anti-fat attitudes.

  2. 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.

  3. 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

  4. 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

  5. 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.

  6. 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

  7. From fatalism to mitigation: a conceptual framework for mitigating fetal programming of chronic disease by maternal obesity

    PubMed Central

    Boone-Heinonen, Janne; Messer, Lynne C.; Fortmann, Stephen P.; Wallack, Lawrence; Thornburg, Kent L.

    2015-01-01

    Prenatal development is recognized as a critical period in the etiology of obesity and cardiometabolic disease. Potential strategies to reduce maternal obesity-induced risk later in life have been largely overlooked. In this paper, we first propose a conceptual framework for the role of public health and preventive medicine in mitigating the effects of fetal programming. Second, we review a small but growing body of research (through August 2015) that examines interactive effects of maternal obesity and two public health foci – diet and physical activity – in the offspring. Results of the review support the hypothesis that diet and physical activity after early life can attenuate disease susceptibility induced by maternal obesity, but human evidence is scant. Based on the review, we identify major gaps relevant for prevention research, such as characterizing the type and dose response of dietary and physical activity exposures that modify the adverse effects of maternal obesity in the offspring. Third, we discuss potential implications of interactions between maternal obesity and postnatal dietary and physical activity exposures for interventions to mitigate maternal obesity-induced risk among children. Our conceptual framework, evidence review, and future research directions offer a platform to develop, test, and implement fetal programming mitigation strategies for the current and future generations of children. PMID:26522092

  8. From fatalism to mitigation: A conceptual framework for mitigating fetal programming of chronic disease by maternal obesity.

    PubMed

    Boone-Heinonen, Janne; Messer, Lynne C; Fortmann, Stephen P; Wallack, Lawrence; Thornburg, Kent L

    2015-12-01

    Prenatal development is recognized as a critical period in the etiology of obesity and cardiometabolic disease. Potential strategies to reduce maternal obesity-induced risk later in life have been largely overlooked. In this paper, we first propose a conceptual framework for the role of public health and preventive medicine in mitigating the effects of fetal programming. Second, we review a small but growing body of research (through August 2015) that examines interactive effects of maternal obesity and two public health foci - diet and physical activity - in the offspring. Results of the review support the hypothesis that diet and physical activity after early life can attenuate disease susceptibility induced by maternal obesity, but human evidence is scant. Based on the review, we identify major gaps relevant for prevention research, such as characterizing the type and dose response of dietary and physical activity exposures that modify the adverse effects of maternal obesity in the offspring. Third, we discuss potential implications of interactions between maternal obesity and postnatal dietary and physical activity exposures for interventions to mitigate maternal obesity-induced risk among children. Our conceptual framework, evidence review, and future research directions offer a platform to develop, test, and implement fetal programming mitigation strategies for the current and future generations of children.

  9. Maternal obesity, infertility and mitochondrial dysfunction: potential mechanisms emerging from mouse model systems

    PubMed Central

    Grindler, Natalia M.; Moley, Kelle H.

    2013-01-01

    Obesity is associated with ovulatory disorders, decreased rates of conception, infertility, early pregnancy loss and congenital abnormalities. Poor oocyte quality and reduced IVF success have also been reported in obese women. Recent attempts to understand the mechanism by which these defects occur have focused on mitochondria, essential organelles that are critical for oocyte maturation and subsequent embryo development. The oocyte relies on maternally supplied mitochondria until the resumption of mitochondrial replication in the peri-implantation period. Here we review current literature addressing the roles of mitochondria in oocyte function and how mitochondrial dysfunction can lead to fertility problems. The relationship between mitochondrial dysfunction and oocyte function is evaluated by examining the following examples of environmental exposures: tobacco smoke, aging, caloric restriction and hyperglycemia. Finally, we present new data from a mouse model of obesity that has demonstrated that oocyte mitochondria play a key role in obesity-associated reproductive disorders. PMID:23612738

  10. Over-expression of Stat5b confers protection against diabetes in the non-obese diabetic (NOD) mice via up-regulation of CD4{sup +}CD25{sup +} regulatory T cells

    SciTech Connect

    Jin, Yulan; Purohit, Sharad; Chen, Xueqin; Yi, Bing; She, Jin-Xiong

    2012-08-10

    Highlights: Black-Right-Pointing-Pointer This is the first study to provide direct evidence of the role of Stat5b in NOD mice. Black-Right-Pointing-Pointer Over-expression of wild type Stat5b transgene protects NOD mice against diabetes. Black-Right-Pointing-Pointer This protection may be mediated by the up-regulation of CD4{sup +}CD25{sup +} Tregs. -- Abstract: The signal transducers and activators of transcription (STAT) family of proteins play a critical role in cytokine signaling required for fine tuning of immune regulation. Previous reports showed that a mutation (L327M) in the Stat5b protein leads to aberrant cytokine signaling in the NOD mice. To further elaborate the role of Stat5b in diabetes, we established a NOD transgenic mouse that over-expresses the wild type Stat5b gene. The incidences of spontaneous diabetes as well as cyclophosphamide-induced diabetes were significantly reduced and delayed in the Stat5b transgenic NOD mice compared to their littermate controls. The total cell numbers of CD4{sup +} T cells and especially CD8{sup +} T cells in the spleen and pancreatic lymph node were increased in the Stat5b transgenic NOD mice. Consistent with these findings, CD4{sup +} and CD8{sup +} T cells from the Stat5b transgenic NOD mice showed a higher proliferation capacity and up-regulation of multiple cytokines including IL-2, IFN-{gamma}, TNF-{alpha} and IL-10 as well as anti-apoptotic gene Bcl-xl. Furthermore, the number and proportion of CD4{sup +}CD25{sup +} regulatory T cells were significantly increased in transgenic mice although in vitro suppression ability of the regulatory T-cells was not affected by the transgene. Our results suggest that Stat5b confers protection against diabetes in the NOD mice by regulating the numbers and function of multiple immune cell types, especially by up-regulating CD4{sup +}CD25{sup +} regulatory T cells.

  11. Maternal nutrition and risk of obesity in offspring: the Trojan horse of developmental plasticity.

    PubMed

    Parlee, Sebastian D; MacDougald, Ormond A

    2014-03-01

    Mammalian embryos have evolved to adjust their organ and tissue development in response to an atypical environment. This adaptation, called phenotypic plasticity, allows the organism to thrive in the anticipated environment in which the fetus will emerge. Barker and colleagues proposed that if the environment in which the fetus emerges differs from that in which it develops, phenotypic plasticity may provide an underlying mechanism for disease. Epidemiological studies have shown that humans born small- or large-for-gestational-age, have a higher likelihood of developing obesity as adults. The amount and quality of food that the mother consumes during gestation influences birth weight, and therefore susceptibility of progeny to disease in later life. Studies in experimental animals support these observations, and find that obesity occurs as a result of maternal nutrient-restriction during gestation, followed by rapid compensatory growth associated with ad libitum food consumption. Therefore, obesity associated with maternal nutritional restriction has a developmental origin. Based on this phenomenon, one might predict that gestational exposure to a westernized diet would protect against future obesity in offspring. However, evidence from experimental models indicates that, like maternal dietary restriction, maternal consumption of a westernized diet during gestation and lactation interacts with an adult obesogenic diet to induce further obesity. Mechanistically, restriction of nutrients or consumption of a high fat diet during gestation may promote obesity in progeny by altering hypothalamic neuropeptide production and thereby increasing hyperphagia in offspring. In addition to changes in food intake these animals may also direct energy from muscle toward storage in adipose tissue. Surprisingly, generational inheritance studies in rodents have further indicated that effects on body length, body weight, and glucose tolerance appear to be propagated to subsequent

  12. Maternal obesity alters feto-placental cytochrome P4501A1 activity.

    PubMed

    DuBois, B N; O'Tierney-Ginn, P; Pearson, J; Friedman, J E; Thornburg, K; Cherala, G

    2012-12-01

    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 530/590 nm. 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 indicate 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. Copyright © 2012 Elsevier Ltd. All rights

  13. 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

  14. Maternal caffeine intake during pregnancy and risk of obesity in offspring: a prospective cohort study

    PubMed Central

    Li, D-K; Ferber, J R; Odouli, R

    2015-01-01

    Background/Objectives: In-utero exposures through adverse fetal programming are emerging as an important contributing factor to the epidemic of childhood obesity. This study examines the impact of in-utero exposure to caffeine on the risk of childhood obesity in offspring. Subjects/Methods: A prospective study of pregnant women with 15 years follow-up of their offspring was conducted to examine the impact of in-utero exposure to caffeine on the risk of childhood obesity. Maternal caffeine intake was prospectively ascertained during pregnancy and outcome measures (body mass index (BMI)) were ascertained from medical charts, with 17 BMI measurements per child, on average, during the follow-up period. Potential confounders including known perinatal risk factors for childhood obesity were adjusted for using the generalized estimating equations model with repeated measurements. Results: After controlling for potential confounders, compared with those without caffeine exposure, in-utero exposure to caffeine overall is associated with 87% increased risk of childhood obesity: odds ratio (OR) =1.87, 95% confidence interval (CI): 1.12–3.12. This association demonstrated a dose–response relationship: OR=1.77 (1.05–3.00) for maternal daily caffeine intake <150 mg per day, OR=2.37 (1.24–4.52) for caffeine intake ⩾150 mg per day during pregnancy, respectively. We also observed a linear relationship: every one unit increase (log10 scale) in the amount of maternal caffeine intake was associated with 23% increased risk of obesity in offspring. The dose–response relationship appears stronger for persistent obesity than for transitory obesity (occasional high BMI), and for girls than for boys. Conclusions: We observed an association of in-utero exposure to caffeine with increased risk of childhood obesity. If this observation is further replicated in other studies, the finding will contribute to the understanding of fetal programming of childhood diseases and

  15. 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

  16. Programming of fetal insulin resistance in pregnancies with maternal obesity by ER stress and inflammation.

    PubMed

    Westermeier, Francisco; Sáez, Pablo J; Villalobos-Labra, Roberto; Sobrevia, Luis; 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.

  17. 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.

  18. A systems approach to reducing maternal obesity: The Health in Preconception, Pregnancy and Postbirth (HIPPP) Collaborative.

    PubMed

    Skouteris, Helen; Huang, Terry; Millar, Lynne; Kuhlberg, Jill; Dodd, Jodie; Callaway, Leonie; Forster, Della; Collins, Clare; Hills, Andrew; Harrison, Paul; Nagle, Cate; Moodie, Marj; Teede, Helena

    2015-08-01

    Obesity in our childbearing population has increased to epidemic proportions in developed countries; efforts to address this issue need to focus on prevention. The Health in Preconception, Pregnancy and Postbirth (HIPPP) Collaborative - a group of researchers, practitioners, policymakers and end-users - was formed to take up the challenge to address this issue as a partnership. Application of systems thinking, participatory systems modelling and group model building was used to establish research questions aiming to optimise periconception lifestyle, weight and health. Our goal was to reduce the burden of maternal obesity through systems change.

  19. 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.

  20. 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

  1. 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.

  2. 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.

  3. 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...

  4. Developmental ORIgins of Healthy and Unhealthy AgeiNg: the role of maternal obesity--introduction to DORIAN.

    PubMed

    Iozzo, Patricia; Holmes, Megan; Schmidt, Mathias V; Cirulli, Francesca; Guzzardi, Maria Angela; Berry, Alessandra; Balsevich, Georgia; Andreassi, Maria Grazia; Wesselink, Jan-Jaap; Liistro, Tiziana; Gómez-Puertas, Paulino; Eriksson, Johan G; Seckl, Jonathan

    2014-01-01

    Europe has the highest proportion of elderly people in the world. Cardiovascular disease, type 2 diabetes, sarcopenia and cognitive decline frequently coexist in the same aged individual, sharing common early risk factors and being mutually reinforcing. Among conditions which may contribute to establish early risk factors, this review focuses on maternal obesity, since the epidemic of obesity involves an ever growing number of women of reproductive age and children, calling for appropriate studies to understand the consequences of maternal obesity on the offspring's health and for developing effective measures and policies to improve people's health before their conception and birth. Though the current knowledge suggests that the long-term impact of maternal obesity on the offspring's health may be substantial, the outcomes of maternal obesity over the lifespan have not been quantified, and the molecular changes induced by maternal obesity remain poorly characterized. We hypothesize that maternal insulin resistance and reduced placental glucocorticoid catabolism, leading to oxidative stress, may damage the DNA, either in its structure (telomere shortening) or in its function (via epigenetic changes), resulting in altered gene expression/repair, disease during life, and pathological ageing. This review illustrates the background to the EU-FP7-HEALTH-DORIAN project. © 2014 S. Karger GmbH, Freiburg.

  5. 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.

  6. [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.

  7. 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

  8. Maternal obesity and labour complications following induction of labour in prolonged pregnancy.

    PubMed

    Arrowsmith, S; Wray, S; Quenby, S

    2011-04-01

    To investigate the effect of maternal obesity on mode of delivery following induction of labour (IOL) for prolonged pregnancy and subsequent intrapartum and neonatal complications. Retrospective (historical) cohort study. Liverpool Women's Hospital NHS Foundation Trust, UK. A total of 29, 224 women with singleton pregnancies between 2004 and 2008 of whom 3076 had a prolonged pregnancy (defined as ≥290 days or 41(+3) weeks of gestation) and received IOL. Kruskal-Wallis test, chi-square test and multivariable logistic regression. Mode of delivery and risk of delivery and neonatal complications in obese verses non-obese women following IOL. Obese women had a significantly higher rate of IOL ending in caesarean section compared with women of normal weight following IOL (38.7% versus 23.8% primiparous; 9.9% versus 7.9% multiparous women, respectively); however, length of labour, incidence of postpartum haemorrhage and third-degree tear, rate of low cord blood pH, low Apgar scores and shoulder dystocia were similar in all body mass index categories. Complications included a higher incidence of fetal macrosomia and second-degree, but not third-degree, tear in primiparous women. Higher maternal body mass index at booking is associated with an increased risk of prolonged pregnancy and increased rate of IOL. Despite this, more than 60% of obese primiparous and 90% of multiparous women with prolonged pregnancies who were induced achieved vaginal delivery and labour complications in the obese women with prolonged pregnancies were largely comparable to those of normal weight women with prolonged pregnancies. Our data suggest that IOL for prolonged pregnancy in obese women is a reasonable and safe management option. © 2011 The Authors Journal compilation © RCOG 2011 BJOG An International Journal of Obstetrics and Gynaecology.

  9. Maternal obesity and labour complications following induction of labour in prolonged pregnancy

    PubMed Central

    Arrowsmith, S; Wray, S; Quenby, S

    2011-01-01

    Objective To investigate the effect of maternal obesity on mode of delivery following induction of labour (IOL) for prolonged pregnancy and subsequent intrapartum and neonatal complications. Design Retrospective (historical) cohort study. Setting Liverpool Women's Hospital NHS Foundation Trust, UK. Population A total of 29 224 women with singleton pregnancies between 2004 and 2008 of whom 3076 had a prolonged pregnancy (defined as ≥290 days or 41+3 weeks of gestation) and received IOL. Methods Kruskal–Wallis test, chi-square test and multivariable logistic regression. Main outcome measures Mode of delivery and risk of delivery and neonatal complications in obese verses non-obese women following IOL. Results Obese women had a significantly higher rate of IOL ending in caesarean section compared with women of normal weight following IOL (38.7% versus 23.8% primiparous; 9.9% versus 7.9% multiparous women, respectively); however, length of labour, incidence of postpartum haemorrhage and third-degree tear, rate of low cord blood pH, low Apgar scores and shoulder dystocia were similar in all body mass index categories. Complications included a higher incidence of fetal macrosomia and second-degree, but not third-degree, tear in primiparous women. Conclusions Higher maternal body mass index at booking is associated with an increased risk of prolonged pregnancy and increased rate of IOL. Despite this, more than 60% of obese primiparous and 90% of multiparous women with prolonged pregnancies who were induced achieved vaginal delivery and labour complications in the obese women with prolonged pregnancies were largely comparable to those of normal weight women with prolonged pregnancies. Our data suggest that IOL for prolonged pregnancy in obese women is a reasonable and safe management option. PMID:21265999

  10. Influence of Maternal Obesity and Gestational Weight Gain on Maternal and Foetal Lipid Profile

    PubMed Central

    Cinelli, Giulia; Fabrizi, Marta; Ravà, Lucilla; Ciofi degli Atti, Marta; Vernocchi, Pamela; Vallone, Cristina; Pietrantoni, Emanuela; Lanciotti, Rosalba; Signore, Fabrizio; Manco, Melania

    2016-01-01

    Fatty acids (FAs) are fundamental for a foetus’s growth, serving as an energy source, structural constituents of cellular membranes and precursors of bioactive molecules, as well as being essential for cell signalling. Long-chain polyunsaturated FAs (LC-PUFAs) are pivotal in brain and visual development. It is of interest to investigate whether and how specific pregnancy conditions, which alter fatty acid metabolism (excessive pre-pregnancy body mass index (BMI) or gestational weight gain (GWG)), affect lipid supply to the foetus. For this purpose, we evaluated the erythrocyte FAs of mothers and offspring (cord-blood) at birth, in relation to pre-pregnancy BMI and GWG. A total of 435 mothers and their offspring (237 males, 51%) were included in the study. Distribution of linoleic acid (LA) and α-linolenic acid (ALA), and their metabolites, arachidonic acid, dihomogamma linoleic (DGLA) and ecosapentanoic acid, was significantly different in maternal and foetal erythrocytes. Pre-pregnancy BMI was significantly associated with maternal percentage of MUFAs (Coeff: −0.112; p = 0.021), LA (Coeff: −0.033; p = 0.044) and DHA (Coeff. = 0.055; p = 0.0016); inadequate GWG with DPA (Coeff: 0.637; p = 0.001); excessive GWG with docosaexahenoic acid (DHA) (Coeff. = −0.714; p = 0.004). Moreover, pre-pregnancy BMI was associated with foetus percentage of PUFAs (Coeff: −0.172; p = 0.009), omega 6 (Coeff: −0.098; p = 0.015) and DHA (Coeff: −0.0285; p = 0.036), even after adjusting for maternal lipids. Our findings show that maternal GWG affects maternal but not foetal lipid profile, differently from pre-pregnancy BMI, which influences both. PMID:27314385

  11. Maternal obesity impairs hippocampal BDNF production and spatial learning performance in young mouse offspring.

    PubMed

    Tozuka, Yusuke; Kumon, Mami; Wada, Etsuko; Onodera, Masafumi; Mochizuki, Hideki; Wada, Keiji

    2010-10-01

    Maternal obesity may affect the child's long-term development and health, increasing the risk of diabetes and metabolic syndrome. In addition to the metabolic and endocrine systems, recent reports have indicated that maternal obesity also modulates neural circuit formation in the offspring. However, this not yet been fully investigated. Here, we examined the effect of diet-induced maternal obesity on hippocampal development and function in the mouse offspring. Adult female mice were fed either a normal diet (ND, 4% fat) or a high-fat diet (HFD, 32% fat) before mating and throughout pregnancy and lactation. After weaning, all offspring were fed with a normal diet. We found that HFD offspring showed increased lipid peroxidation in the hippocampus during early postnatal development. HFD offspring had less brain-derived neurotrophic factor (BDNF) in the hippocampus than ND offspring. BDNF has been shown to play crucial roles in neuronal differentiation, plasticity and hippocampus-dependent cognitive functions such as spatial learning and memory. Using retroviral labeling, we demonstrated that dendritic arborization of new hippocampal neurons was impaired in the young HFD offspring. Finally, we evaluated cognitive function in these offspring using hippocampus-dependent behavioral tasks. The Barnes maze test demonstrated that HFD offspring showed impaired acquisition of spatial learning in the young but not adult period. This study, using a mouse model, indicates that diet-induced maternal obesity impairs hippocampal BDNF production and spatial cognitive function in young offspring, possibly due to their metabolic and oxidative changes. (c) 2010 Elsevier Ltd. All rights reserved.

  12. ENDOCANNABINOID CROSSTALK BETWEEN PLACENTA AND MATERNAL FAT IN A BABOON MODEL (Papio spp.) OF OBESITY

    PubMed Central

    Brocato, Brian; Zoerner, Alexander A; Janjetovic, Zorica; Skobowiat, Cezary; Gupta, Sonali; Moore, Bob; Slominski, Andrzej; Zhang, Jie; Schenone, Mauro; Phinehas, Ramona; Ferry, Robert J.; Dick, Edward; Hubbard, Gene B.; Mari, Giancarlo; Schlabritz-Loutsevitch, Natalia

    2013-01-01

    Introduction Maternal obesity (MO) remains a serious obstetric problem with acute and chronic morbidities for both mothers and offspring. The mechanisms underlying these adverse consequences of MOremain unknown. Endocannabinoids (ECB) are neuromodulatory lipids derived from adipocytes. Metabolic crosstalk between placenta and adipocytes may mediate sequelae of MO. The goal of this study was to elucidate placental and systemic ECBs in MO. Material and methods Placentas, serum, and subcutaneous fat were collected at Cesarean sections performed near term (0.9 G) in four non-obese (nOB) and four obese (OB) baboons (Papio spp.). Concentrations of anandamide (AEA) and 2-arachidonoylglycerol (2-AG) were measured by liquid chromatography coupled to tandem mass spectrometry. AEA and 2-AG pathways were characterized in placentas by Q-RT-PCR, Western blot, and immunohistochemistry. Results Placental 2-AG levels were lower and maternal fat AEA levels were higher in OB (1254.1 ± 401.3 nmol/kg and 17.3 ± 4 nmol/kg ) vs. nOB (3124.2 ± 557.3 nmol/kg and 3.1 ± 0.6 nmol/kg) animals. Concentrations of 2-AG correlated positively between maternal fat and placenta (r=0.82, p=0.013), but correlated negatively with maternal leptin concentrations (r=−0.72, p=0.04 and r=−0.83, p=0.01, respectively). Conclusion This is the first study to demonstrate differential ECB pathway regulation in maternal fat and placenta in MO. Differential regulation and function exist for AEA and 2-AG as the major ECB pathways in placenta. PMID:24008071

  13. Endocannabinoid crosstalk between placenta and maternal fat in a baboon model (Papio spp.) of obesity.

    PubMed

    Brocato, B; Zoerner, A A; Janjetovic, Z; Skobowiat, C; Gupta, S; Moore, B M; Slominski, A; Zhang, J; Schenone, M; Phinehas, R; Ferry, R J; Dick, E; Hubbard, G B; Mari, G; Schlabritz-Loutsevitch, N

    2013-11-01

    Maternal obesity (MO) remains a serious obstetric problem with acute and chronic morbidities for both mothers and offspring. The mechanisms underlying these adverse consequences of MO remain unknown. Endocannabinoids (ECB) are neuromodulatory lipids released from adipocytes and other tissues. Metabolic crosstalk between placenta and adipocytes may mediate sequelae of MO. The goal of this study was to elucidate placental and systemic ECB in MO. Placentas, sera, and subcutaneous fat were collected at Cesarean sections performed near term (0.9 G) in four non-obese (nOB) and four obese (OB) baboons (Papio spp.). Concentrations of anandamide (AEA) and 2-arachidonoylglycerol (2-AG) were measured by liquid chromatography coupled to tandem mass spectrometry. AEA and 2-AG pathways were characterized in placentas by Q-RT-PCR, Western blot and immunohistochemistry. Placental 2-AG levels were lower and maternal fat AEA levels were higher in OB (1254.1 ± 401.3 nmol/kg and 17.3 ± 4 nmol/kg) vs. nOB (3124.2 ± 557.3 nmol/kg and 3.1 ± 0.6 nmol/kg) animals. Concentrations of 2-AG correlated positively between maternal fat and placenta (r = 0.82, p = 0.013), but correlated negatively with maternal leptin concentrations (r = -0.72, p = 0.04 and r = -0.83, p = 0.01, respectively). This is the first study to demonstrate differential ECB pathway regulation in maternal fat and placenta in MO. Differential regulation and function exist for AEA and 2-AG as the major ECB pathways in placenta. Copyright © 2013 Elsevier Ltd. All rights reserved.

  14. 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.

  15. Developmental programming by maternal obesity in 2015: Outcomes, mechanisms, and potential interventions.

    PubMed

    Penfold, Naomi C; Ozanne, Susan E

    2015-11-01

    This article is part of a Special Issue "SBN 2014". Obesity in women of child-bearing age is a growing problem in developed and developing countries. Evidence from human studies indicates that maternal BMI correlates with offspring adiposity from an early age and predisposes to metabolic disease in later life. Thus the early life environment is an attractive target for intervention to improve public health. Animal models have been used to investigate the specific physiological outcomes and mechanisms of developmental programming that result from exposure to maternal obesity in utero. From this research, targeted intervention strategies can be designed. In this review we summarise recent progress in this field, with a focus on cardiometabolic disease and central control of appetite and behaviour. We highlight key factors that may mediate programming by maternal obesity, including leptin, insulin, and ghrelin. Finally, we explore potential lifestyle and pharmacological interventions in humans and the current state of evidence from animal models. Copyright © 2015 Elsevier Inc. All rights reserved.

  16. Population Attributable Risk Fractions of Maternal Overweight and Obesity for Adverse Perinatal Outcomes.

    PubMed

    MacInnis, Natasha; Woolcott, Christy G; McDonald, Sarah; Kuhle, Stefan

    2016-03-10

    The objective of the current study was to determine the proportion of adverse perinatal outcomes that could be potentially prevented if maternal obesity were to be reduced or eliminated (population attributable risk fractions, PARF); and the number needed to treat (NNT) of overweight or obese women to prevent one case of adverse perinatal outcome. Data from the Atlee Perinatal Database on 66,689 singleton infants born in Nova Scotia, Canada, between 2004 and 2014, and their mothers were used. Multivariable-adjusted PARFs and NNTs of maternal pre-pregnancy weight status were determined for various perinatal outcomes under three scenarios: If all overweight and obese women were to i) become normal weight before pregnancy; ii) shift down one weight class; or iii) lose 10% of their body weight, significant relative reductions would be seen for gestational diabetes mellitus (GDM, 57/33/15%), hypertensive disorders of pregnancy (HDP, 26/16/6%), caesarean section (CS, 18/10/3%), and large for gestational age births (LGA, 24/14/3%). The NNT were lowest for the outcomes GDM, induction of labour, CS, and LGA, where they ranged from 13 to 73. The study suggests that a substantial proportion of adverse perinatal outcomes may be preventable through reductions in maternal pre-pregnancy weight.

  17. 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

  18. Maternal obesity support services: a qualitative study of the perspectives of women and midwives

    PubMed Central

    2011-01-01

    Background Twenty percent of pregnant women in the UK are obese (BMI ≥ 30 kg/m2), reflecting the growing public health challenge of obesity in the 21st century. Obesity increases the risk of adverse outcomes during pregnancy and birth and has significant cost implications for maternity services. Gestational weight management strategies are a high priority; however the evidence for effective, feasible and acceptable weight control interventions is limited and inconclusive. This qualitative study explored the experiences and perceptions of pregnant women and midwives regarding existing support for weight management in pregnancy and their ideas for service development. Methods A purposive sample of 6 women and 7 midwives from Doncaster, UK, participated in two separate focus groups. Transcripts were analysed thematically. Results Two overarching themes were identified, 'Explanations for obesity and weight management' and 'Best care for pregnant women'. 'Explanations' included a lack of knowledge about weight, diet and exercise during pregnancy; self-talk messages which excused overeating; difficulties maintaining motivation for a healthy lifestyle; the importance of social support; stigmatisation; and sensitivity surrounding communication about obesity between midwives and their clients. 'Best care' suggested that weight management required care which was consistent and continuous, supportive and non-judgemental, and which created opportunities for interaction and mutual support between obese pregnant women. Conclusions Women need unambiguous advice regarding healthy lifestyles, diet and exercise in pregnancy to address a lack of knowledge and a tendency towards unhelpful self-talk messages. Midwives expressed difficulties in communicating with their clients about their weight, given awareness that obesity is a sensitive and potentially stigmatising issue. This indicates more could be done to educate and support them in their work with obese pregnant women

  19. Maternal obesity influences hepatic gene expression and genome-wide DNA methylation in offspring liver at weaning

    USDA-ARS?s Scientific Manuscript database

    Offspring from obese rat dams gain greater body weight and fat mass when fed HFD. Here we examine hepatic gene expression related to systemic energy expenditure and alterations in genome-wide DNA methylation. Maternal obesity was produced in rats prior to conception via overfeeding of diets. At PND2...

  20. Maternal pregravid obesity changes gene expression profiles toward greater inflammation and reduced insulin sensitivity in umbilical cord

    USDA-ARS?s Scientific Manuscript database

    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 gestationa...

  1. Sirt3 prevents maternal obesity-associated oxidative stress and meiotic defects in mouse oocytes.

    PubMed

    Zhang, Liang; Han, Longsen; Ma, Rujun; Hou, Xiaojing; Yu, Yang; Sun, Shaochen; Xu, Yinxue; Schedl, Tim; Moley, Kelle H; Wang, Qiang

    2015-01-01

    Maternal obese environment has been reported to induce oxidative stress and meiotic defects in oocytes, however the underlying molecular mechanism remains unclear. Here, using mice fed a high fat diet (HFD) as an obesity model, we first detected enhanced reactive oxygen species (ROS) content and reduced Sirt3 expression in HFD oocytes. We further observed that specific depletion of Sirt3 in control oocytes elevates ROS levels while Sirt3 overexpression attenuates ROS production in HFD oocytes, with significant suppression of spindle disorganization and chromosome misalignment phenotypes that have been reported in the obesity model. Candidate screening revealed that the acetylation status of lysine 68 on superoxide dismutase (SOD2K68) is dependent on Sirt3 deacetylase activity in oocytes, and acetylation-mimetic mutant SOD2K68Q results in almost threefold increase in intracellular ROS. Moreover, we found that acetylation levels of SOD2K68 are increased by ~80% in HFD oocytes and importantly, that the non-acetylatable-mimetic mutant SOD2K68R is capable of partially rescuing their deficient phenotypes. Together, our data identify Sirt3 as an important player in modulating ROS homeostasis during oocyte development, and indicate that Sirt3-dependent deacetylation of SOD2 plays a protective role against oxidative stress and meiotic defects in oocytes under maternal obese conditions.

  2. Sirt3 prevents maternal obesity-associated oxidative stress and meiotic defects in mouse oocytes

    PubMed Central

    Zhang, Liang; Han, Longsen; Ma, Rujun; Hou, Xiaojing; Yu, Yang; Sun, Shaochen; Xu, Yinxue; Schedl, Tim; Moley, Kelle H; Wang, Qiang

    2015-01-01

    Maternal obese environment has been reported to induce oxidative stress and meiotic defects in oocytes, however the underlying molecular mechanism remains unclear. Here, using mice fed a high fat diet (HFD) as an obesity model, we first detected enhanced reactive oxygen species (ROS) content and reduced Sirt3 expression in HFD oocytes. We further observed that specific depletion of Sirt3 in control oocytes elevates ROS levels while Sirt3 overexpression attenuates ROS production in HFD oocytes, with significant suppression of spindle disorganization and chromosome misalignment phenotypes that have been reported in the obesity model. Candidate screening revealed that the acetylation status of lysine 68 on superoxide dismutase (SOD2K68) is dependent on Sirt3 deacetylase activity in oocytes, and acetylation-mimetic mutant SOD2K68Q results in almost threefold increase in intracellular ROS. Moreover, we found that acetylation levels of SOD2K68 are increased by ∼80% in HFD oocytes and importantly, that the non-acetylatable-mimetic mutant SOD2K68R is capable of partially rescuing their deficient phenotypes. Together, our data identify Sirt3 as an important player in modulating ROS homeostasis during oocyte development, and indicate that Sirt3-dependent deacetylation of SOD2 plays a protective role against oxidative stress and meiotic defects in oocytes under maternal obese conditions. PMID:25790176

  3. Obesity and Endocrine Dysfunction Programmed by Maternal Smoking in Pregnancy and Lactation

    PubMed Central

    Lisboa, Patricia Cristina; de Oliveira, Elaine; de Moura, Egberto Gaspar

    2012-01-01

    Obesity is a global epidemic, and maternal smoking has been shown to be associated with the development of childhood obesity. Overall, approximately 40% of children worldwide are exposed to tobacco smoke at home. It is well known that environmental changes within a critical window of development, such as gestation or lactation, can initiate permanent alterations in metabolism that lead to diseases in adulthood, a phenomenon called programming. It is known that programming is based on epigenetic alterations (changes in DNA methylation, histone acetylation, or small interfering RNA expression) that change the expression pattern of several genes. However, little is known concerning the mechanisms by which smoke exposure in neonatal life programs the adipose tissue and endocrine function. Here, we review several epidemiological and experimental studies that confirm the association between maternal nicotine or tobacco exposure during gestation or lactation and the development of obesity and endocrine dysfunction. For example, a positive correlation was demonstrated in rodents between increased serum leptin in the neonatal period and exposure of the mothers to nicotine during lactation, and the further development of leptin and insulin resistance, and thyroid and adrenal dysfunction, in adulthood in the same offspring. Thus, a smoke-free environment during the lactation period is essential to improving health outcomes in adulthood and reducing the risk for future diseases. An understanding of the pathophysiological mechanisms underlying the effects of smoking on programming can provide new insights into therapeutic strategies for obesity. PMID:23181022

  4. 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.

  5. Maternal testosterone and reproductive outcome in a rat model of obesity.

    PubMed

    Arnon, Liat; Hazut, Noa; Tabachnik, Tzlil; Weller, Aron; Koren, Lee

    2016-09-01

    Global sex differences in obesity rates are persistent, suggesting the involvement of sex steroids. In addition, adipose tissue is a metabolic site for steroidogenesis. Here, we compared female reproductive parameters in a rat model of obesity, with the same parameters in its lean control strain, and tested for an association with integrated measures of corticosterone and testosterone. Steroids were extracted and quantified from 17 Otsuka Long Evans Tokushima Fatty (OLETF; an animal model for obesity) and 13 Long Evans Tokushima Otsuka (LETO; the lean control strain) hair samples that were collected after weaning offspring. The obese OLETF mothers had higher hair testosterone levels than the control LETO strain. Overall, testosterone, but not corticosterone, predicted litter sex ratios. Younger mothers with large litters and older mothers with small litters tended to have the highest sex ratios (i.e., male-biased litters). In the lean LETO strain, but not in the obese OLETF, maternal testosterone was positively associated with litter size and number of male pups. Corticosterone did not differ between the two strains and was not associated with testosterone or with reproductive parameters. This study suggests that long-term circulating testosterone is associated with female reproduction in multiple ways. The possible trade-off between litter size and sex ratio may be mediated by testosterone and influenced by body fat and composition, which influence the individual's well-being. Exploring the multiple roles of testosterone in females may also help explain the complex relationship between obesity and reproduction.

  6. 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

  7. Maternal obesity and attention-related symptoms in the preterm offspring.

    PubMed

    van der Burg, Jelske W; Jensen, Elizabeth T; van de Bor, Margot; Joseph, Robert M; O'Shea, T Michael; Kuban, Karl; Allred, Elizabeth N; Scott, Megan; Hunter, Scott; Hooper, Stephen R; Dammann, Olaf; Leviton, Alan

    2017-08-17

    Maternal pre-pregnancy obesity, in term-born children, is associated with an increased risk of attention problems, however this relationship has not been explored among children born extremely preterm. To estimate the risk of attention problems at age 10years in children born very preterm to overweight (i.e., body mass index (BMI) 25-29kg/m(2)) and obese (i.e., BMI≥30kg/m(2)) women relative to the risk among children born to women who were neither overweight nor obese (i.e. BMI<25kg/m(2)). Multi-center prospective cohort study. A total of 764 children born before the 28th week of gestation and whose mother's pre-pregnancy height and pre-pregnancy weight were obtained at birth had an IQ≥70 at age 10years when parents and teachers completed Child Symptom Inventory-4 questionnaires that included items about the presence of ADHD. Compared to children whose mother's pre-pregnancy weight was in the normal range (BMI<25kg/m(2)), children were at increased risk of parent-identified ADHD behaviors if their mother was overweight (odds ratio (OR)=1.9; 95% confidence interval (CI): 1.1, 3.3), or obese (OR=2.3; 95% CI: 1.4, 3.9). They were not at increased risk of teacher-identified ADHD characteristics if their mother was overweight before her pregnancy (OR=1.0; 95% CI: 0.6, 1.8), or obese (OR=1.0; 95% CI: 0.6, 1.6). Maternal overweight and obesity are associated with increased risk of parent-identified ADHD characteristics at 10years of age in children born extremely preterm. Copyright © 2017. Published by Elsevier B.V.

  8. Of the bugs that shape us: maternal obesity, the gut microbiome, and long-term disease risk.

    PubMed

    Gohir, Wajiha; Ratcliffe, Elyanne M; Sloboda, Deborah M

    2015-01-01

    Chronic disease risk is inextricably linked to our early-life environment, where maternal, fetal, and childhood factors predict disease risk later in life. Currently, maternal obesity is a key predictor of childhood obesity and metabolic complications in adulthood. Although the mechanisms are unclear, new and emerging evidence points to our microbiome, where the bacterial composition of the gut modulates the weight gain and altered metabolism that drives obesity. Over the course of pregnancy, maternal bacterial load increases, and gut bacterial diversity changes and is influenced by pre-pregnancy- and pregnancy-related obesity. Alterations in the bacterial composition of the mother have been shown to affect the development and function of the gastrointestinal tract of her offspring. How these microbial shifts influence the maternal-fetal-infant relationship is a topic of hot debate. This paper will review the evidence linking nutrition, maternal obesity, the maternal gut microbiome, and fetal gut development, bringing together clinical observations in humans and experimental data from targeted animal models.

  9. 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.

  10. 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 (PM2.5) 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 PM2.5 programs offspring obesity, female C57Bl/6j mice were exposed to filtered air (FA) or concentrated ambient PM2.5 (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 PM2.5 programs obesity in male offspring probably through alterations in the methylation of the promoter region of the leptin gene.

  11. 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.

  12. 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.

  13. 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.

  14. 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.

  15. 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

  16. Oxidative stress and altered lipid homeostasis in the programming of offspring fatty liver by maternal obesity.

    PubMed

    Alfaradhi, Maria Z; Fernandez-Twinn, Denise S; Martin-Gronert, Malgorzata S; Musial, Barbara; Fowden, Abigail; Ozanne, Susan E

    2014-07-01

    Changes in the maternal nutritional environment during fetal development can influence offspring's metabolic risk in later life. Animal models have demonstrated that offspring of diet-induced obese dams develop metabolic complications, including nonalcoholic fatty liver disease. In this study we investigated the mechanisms in young offspring that lead to the development of nonalcoholic fatty liver disease (NAFLD). Female offspring of C57BL/6J dams fed either a control or obesogenic diet were studied at 8 wk of age. We investigated the roles of oxidative stress and lipid metabolism in contributing to fatty liver in offspring. There were no differences in body weight or adiposity at 8 wk of age; however, offspring of obese dams were hyperinsulinemic. Oxidative damage markers were significantly increased in their livers, with reduced levels of the antioxidant enzyme glutathione peroxidase-1. Mitochondrial complex I and II activities were elevated, while levels of mitochondrial cytochrome c were significantly reduced and glutamate dehydrogenase was significantly increased, suggesting mitochondrial dysfunction. Offspring of obese dams also had significantly greater hepatic lipid content, associated with increased levels of PPARγ and reduced triglyceride lipase. Liver glycogen and protein content were concomitantly reduced in offspring of obese dams. In conclusion, offspring of diet-induced obese dams have disrupted liver metabolism and develop NAFLD prior to any differences in body weight or body composition. Oxidative stress may play a mechanistic role in the progression of fatty liver in these offspring.

  17. 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.

  18. The Impact of Maternal Diabetes, Obesity and Race on Infant Birth Weights in South Dakota.

    PubMed

    Halvorson, Kari L; Vogt, H Bruce; Kightlinger, Lon; Stevens, Dennis

    2017-02-01

    Maternal obesity, high gestational weight gain and diabetes mellitus during pregnancy are known risk factors that correlate with high infant birth weight and the mother's race. Previous studies have focused on low birth weight, prematurity and infant mortality. This study examined the interaction between race, maternal risk factors and high infant birth weights at the population level in South Dakota to identify factors contributing to the high Native American infant birth weights. We hypothesized that high infant birth weights were associated with maternal diabetes, obesity and high gestational weight gain, and that Native American infants' higher birth weights were related to the prevalence of diabetes and obesity. De-identified birth certificate data was provided by the South Dakota Department of Health. We used data for live infant births to South Dakota resident mothers from 2006 through 2011. The mothers were categorized as Native American or white by the mother's self-reported primary race. Infants were excluded from the study population for missing data, birth weight less than 350 g or gestational age less than 24 weeks or greater than 45 weeks. The study population included 11,416 Native American infants and 59,263 white infants for a total study population of 70,679 infants. Maternal variables (race, pre-pregnancy weight and body mass index [BMI], gestational weight gain, pre-pregnancy diabetes mellitus [DM], gestational diabetes [GDM] and delivery BMI) and infant variables (gestational age and birth weight) were analyzed using SPSS software. The mean birth weight (BW) of Native American (NA) infants (3377 g) was significantly greater than the mean BW of white (W) infants (3315 g) even though NA infants had a younger mean gestational age (p = 0.006). More NA infants were categorized as high birth weight (HBW) (11.8 percent) than W infants (8.5 percent). Both DM and GDM were significantly more common among NA mothers. Infants of NA mothers with GDM had a

  19. Modulation of fatty acid transport and metabolism by maternal obesity in the human full-term placenta.

    PubMed

    Dubé, Evemie; Gravel, Ariane; Martin, Coralie; Desparois, Guillaume; Moussa, Issa; Ethier-Chiasson, Maude; Forest, Jean-Claude; Giguère, Yves; Masse, André; Lafond, Julie

    2012-07-01

    Knowledge of the consequences of maternal obesity in human placental fatty acids (FA) transport and metabolism is limited. Animal studies suggest that placental uptake of maternal FA is altered by maternal overnutrition. We hypothesized that high maternal body mass index (BMI) affects human placental FA transport by modifying expression of key transporters. Full-term placentas were obtained by vaginal delivery from normal weight (BMI, 18.5-24.9 kg/m(2)) and obese (BMI > 30 kg/m(2)) women. Blood samples were collected from the mother at each trimester and from cord blood at delivery. mRNA and protein expression levels were evaluated with real-time RT-PCR and Western blotting. Lipoprotein lipase (LPL) activity was evaluated using enzyme fluorescence. In vitro linoleic acid transport was studied with isolated trophoblasts. Our results demonstrated that maternal obesity is associated with increased placental weight, decreased gestational age, decreased maternal high-density lipoprotein (HDL) levels during the first and third trimesters, increased maternal triglyceride levels during the second and third trimesters, and increased maternal T3 levels during all trimesters, and decreased maternal cholesterol (CHOL) and low-density lipoprotein (LDL) levels during the third trimester; and increased newborn CHOL, LDL, apolipoprotein B100, and T3 levels. Increases in placental CD36 mRNA and protein expression levels, decreased SLC27A4 and FABP1 mRNA and protein and FABP3 protein expression, and increased LPL activity and decreased villus cytotrophoblast linoleic acid transport were also observed. No changes were seen in expression of PPARA, PPARD, or PPARG mRNA and protein. Overall this study demonstrated that maternal obesity impacts placental FA uptake without affecting fetal growth. These changes, however, could modify the fetus metabolism and its predisposition to develop diseases later in life.

  20. 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.

  1. Maternal hypothyroxinaemia in pregnancy is associated with obesity and adverse maternal metabolic parameters

    PubMed Central

    Knight, Bridget A; Shields, Beverley M; Hattersley, Andrew T; Vaidya, Bijay

    2016-01-01

    Objective Subclinical hypothyroidism and isolated hypothyroxinaemia in pregnancy have been associated with an increased risk of gestational diabetes. We aimed to ascertain if these women have a worse metabolic phenotype than euthyroid pregnant women. Design, subjects and methods We recruited 956 healthy Caucasian women with singleton, non-diabetic pregnancies from routine antenatal clinics. Detailed anthropometric measurements (including BMI and skinfold thickness) and fasting blood samples (for TSH, free thyroxine (FT4), free triiodothyronine (FT3), HbA1c, lipid profile, plasma glucose and insulin resistance (HOMA-IR) analysis) were obtained at 28 weeks gestation. Results In comparison to euthyroid women (n=741), women with isolated hypothyroxinaemia (n=82) had significantly increased BMI (29.5 vs 27.5 kg/m2, P<0.001), sum of skinfolds (57.5 vs 51.3 mm, P=0.002), fasting plasma glucose (4.5 vs 4.3 mmol/l, P=0.01), triglycerides (2.3 vs 2.0 mmol/l, P<0.001) and HOMA-IR (2.0 vs 1.3, P=0.001). Metabolic parameters in women with subclinical hypothyroidism (n=133) were similar to those in euthyroid women. Maternal FT4 was negatively associated with BMI (r=−0.22), HbA1c (r=−0.14), triglycerides (r=−0.17), HOMA-IR (r=−0.15) but not total/HDL cholesterol ratio (r=−0.03). Maternal FT3:FT4 ratio was positively associated with BMI (r=0.4), HbA1c (r=0.21), triglycerides (r=0.2), HOMA–IR (r=0.33) and total/HDL cholesterol ratio (r=0.07). TSH was not associated with the metabolic parameters assessed. Conclusions Isolated hypothyroxinaemia, but not subclinical hypothyroidism, is associated with adverse metabolic phenotype in pregnancy, as is decreasing maternal FT4 and increasing FT3:FT4 ratio. These associations may be a reflection of changes in the thyroid hormone levels secondary to increase in BMI rather than changes in thyroid hormone levels affecting body weight and related metabolic parameters. PMID:26586839

  2. 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

  3. 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...

  4. CELL BIOLOGY SYMPOSIUM: Impacts of maternal obesity on placental and gut inflammation and health.

    PubMed

    Zhu, M J; Du, M; Ford, S P

    2014-05-01

    Obesity in pregnant women is a growing public health concern that negatively affects fetal development and has long-term impacts on offspring health. The placenta plays an essential role in nutrient transport to the fetus and supports fetal growth and development. Maternal obesity (MO) induces an exacerbated proinflammatory milieu in the placenta providing an inflammatory environment for fetuses. The gut is one of the largest immune organs and mainly develops during the fetal stage. Maternal obesity and the corresponding inflammatory uteroplacental environment affect gut development, incurring inflammatory responses in the fetal intestine that further prime or program the offspring gut to enhance inflammation and impair intestinal barrier integrity. This review summarizes the impact of MO on inflammatory responses in placenta and fetal intestine and the long-term effects on offspring intestinal health. Because "leaky gut" is one of the main etiological factors for a number of common diseases, including inflammatory bowel diseases, type I diabetes, and related autoimmune diseases, the adverse effect of MO on the overall health of progeny is further discussed.

  5. Maternal obesity and breast-feeding practices among white and black women.

    PubMed

    Liu, Jihong; Smith, Michael G; Dobre, Mirela A; Ferguson, James E

    2010-01-01

    Despite the increase in obesity among women of reproductive ages, few studies have considered maternal obesity as a risk factor for breast-feeding success. We tested the hypothesis that women who are obese (BMI = 30-34.9) and very obese (BMI >or=35) before pregnancy are less likely to initiate and maintain breast-feeding than are their normal-weight counterparts (BMI = 18.5-24.9) among white and black women. Data from 2000 to 2005 South Carolina Pregnancy Risk Assessment Monitoring System (PRAMS) were used. The overall response rate was 71.0%; there were 3,517 white and 2,846 black respondents. Black women were less likely to initiate breast-feeding and breast-fed their babies for a shorter duration than white women. Compared to normal-weight white women, very obese white women were less likely to initiate breast-feeding (odds ratio: 0.63; 95% confidence interval (CI) = 0.42, 0.94) and more likely to discontinue breast-feeding within the first 6 months (hazard ratio (HR) = 1.89; 95% CI: 1.39, 2.58). Among black women, prepregnancy BMI was neither associated with breast-feeding initiation nor with breast-feeding continuation within the first 6 months. Because very obese white women are less likely to initiate or continue breast-feeding than other white women, health professionals should be aware that very obese white women need additional breast-feeding support. Lower rates of breast-feeding among black women suggest that they should continue to be the focus of the programs and policies aimed at breast-feeding promotion in the United States.

  6. Influence of Maternal Obesity on Insulin Sensitivity and Secretion in Offspring

    PubMed Central

    Mingrone, Geltrude; Manco, Melania; Valera Mora, Maria Elena; Guidone, Caterina; Iaconelli, Amerigo; Gniuli, Donatella; Leccesi, Laura; Chiellini, Chiara; Ghirlanda, Giovanni

    2008-01-01

    OBJECTIVE—The purpose of this study was to clarify the effects of maternal obesity on insulin sensitivity and secretion in offspring. RESEARCH DESIGN AND METHODS—Fifty-one offspring of both sexes of obese (Ob group) and 15 offspring of normal-weight (control group) mothers were studied. Plasma glucose, insulin, and C-peptide were measured during an oral glucose tolerance test (OGTT). Insulin sensitivity was calculated using the oral glucose insulin sensitivity index, and insulin secretion and β-cell glucose sensitivity were computed by a mathematical model. Fasting leptin and adiponectin were also measured. Body composition was assessed by dual-X-ray absorptiometry. RESULTS—No birth weight statistical difference was observed in the two groups. Of the Ob group, 69% were obese and 19% were overweight. The Ob group were more insulin resistant than the control group (398.58 ± 79.32 vs. 513.81 ± 70.70 ml−1 · min−1 · m−2 in women, P < 0.0001; 416.42 ± 76.17 vs. 484.242 ± 45.76 ml−1 · min−1 · m−2 in men, P < 0.05). Insulin secretion after OGTT was higher in Ob group than in control group men (63.94 ± 21.20 vs. 35.71 ± 10.02 nmol · m−2, P < 0.01) but did not differ significantly in women. β-Cell glucose sensitivity was not statistically different between groups. A multivariate analysis of variance showed that maternal obesity and offspring sex concurred together with BMI and β-cell glucose sensitivity to determine the differences in insulin sensitivity and secretion observed in offspring. CONCLUSIONS—Obese mothers can give birth to normal birth weight babies who later develop obesity and insulin resistance. The maternal genetic/epigenetic transmission shows a clear sexual dimorphism, with male offspring having a higher value of insulin sensitivity (although not statistically significant) associated with significantly higher insulin secretion than female offspring. PMID:18535193

  7. 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.

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

    PubMed Central

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

    2015-01-01

    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. PMID:26692415

  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. Influences of Gestational Obesity on Associations between Genotypes and Gene Expression Levels in Offspring following Maternal Gastrointestinal Bypass Surgery for Obesity

    PubMed Central

    Guénard, Frédéric; Lamontagne, Maxime; Bossé, Yohan; Deshaies, Yves; Cianflone, Katherine; Kral, John G.; Marceau, Picard; Vohl, Marie-Claude

    2015-01-01

    Maternal obesity and excess gestational weight gain with compromised metabolic fitness predispose offspring to lifelong obesity and its comorbidities. We demonstrated that compared to offspring born before maternal gastrointestinal bypass surgery (BMS) those born after (AMS) were less obese, with less cardiometabolic risk reflected in the expression and methylation of diabetes, immune and inflammatory pathway genes. Here we examine relationships between gestational obesity and offspring gene variations on expression levels. Methods Whole-genome genotyping and gene expression analyses in blood of 22 BMS and 23 AMS offspring from 19 mothers were conducted using Illumina HumanOmni-5-Quad and HumanHT-12 v4 Expression BeadChips, respectively. Using PLINK we analyzed interactions between offspring gene variations and maternal surgical status on offspring gene expression levels. Altered biological functions and pathways were identified and visualized using DAVID and Ingenuity Pathway Analysis. Results Significant interactions (p ≤ 1.22x10-12) were found for 525 among the 16,060 expressed transcripts: 1.9% of tested SNPs were involved. Gene function and pathway analysis demonstrated enrichment of transcription and of cellular metabolism functions and overrepresentation of cellular stress and signaling, immune response, inflammation, growth, proliferation and development pathways. Conclusion We suggest that impaired maternal gestational metabolic fitness interacts with offspring gene variations modulating gene expression levels, providing potential mechanisms explaining improved cardiometabolic risk profiles of AMS offspring related to ameliorated maternal lipid and carbohydrate metabolism. PMID:25603303

  11. Short inter-pregnancy intervals, parity, excessive pregnancy weight gain and risk of maternal obesity

    PubMed Central

    Davis, Esa M.; Babineau, Denise C.; Wang, Xuelei; Zyzanski, Stephen; Abrams, Barbara; Bodnar, Lisa; Horwitz, Ralph

    2013-01-01

    Objective To investigate the relationship among parity, length of the inter-pregnancy intervals and excessive pregnancy weight gain in the first pregnancy and the risk of obesity. Methods Using a prospective cohort study of 3422 non-obese, non-pregnant U.S. women aged 14–22 years at baseline, adjusted Cox models were used to estimate the association among parity, inter-pregnancy intervals, and excessive pregnancy weight gain in the first pregnancy and the relative hazard rate (HR) of obesity. Results Compared to nulliparous women, primiparous women with excessive pregnancy weight gain in the first pregnancy had a HR of obesity of 1.79 (95% CI: 1.40, 2.29); no significant difference was seen between primiparous without excessive pregnancy weight gain in the first pregnancy and nulliparous women. Among women with the same pregnancy weight gain in the first pregnancy and the same number of inter-pregnancy intervals (12 and 18 months or ≥ 18 months), the HR of obesity increased 2.43-fold (95% CI: (1.21, 4.89); p=0.01) for every additional inter-pregnancy interval of < 12 months; no significant association was seen for longer inter-pregnancy intervals. Among women with the same parity and inter-pregnancy interval pattern, women with excessive pregnancy weight gain in the first pregnancy had an HR of obesity 2.41 times higher (95% CI: (1.81, 3.21); p<0.001) than women without. Conclusions Primiparous and nulliparous women had similar obesity risk unless the primiparous women had excessive pregnancy weight gain in the first pregnancy, then their risk of obesity was greater. Multiparous women with the same excessive pregnancy weight gain in the first pregnancy and at least one additional short inter-pregnancy interval had a significant risk of obesity after childbirth. Perinatal interventions that prevent excessive pregnancy weight gain in the first pregnancy or lengthen the inter-pregnancy interval are necessary for reducing maternal obesity. PMID:23595566

  12. Effects of Maternal Linseed Oil Supplementation on Metabolic Parameters in Cafeteria Diet-induced Obese Rats.

    PubMed

    Benaissa, Nawel; Merzouk, Hafida; Merzouk, Sid Ahmed; Narce, Michel

    2015-04-01

    Because linseed oil may influence maternal and fetal metabolisms, we investigated its role in the modulation of lipid metabolism in cafeteria diet-induced obese rats and their offspring. Female Wistar rats were fed control or cafeteria food, which were either supplemented or not supplemented with linseed oil (5%) for 1 month before and during gestation. At parturition, serum and tissue lipids and enzyme activities were analyzed. Cafeteria diet induced adverse metabolic alterations in both mothers and offspring. Linseed oil improved metabolic status. In conclusion, linseed oil displayed health benefits by modulating tissue enzyme activities in both obese mothers and their newborns. Copyright © 2015 The Editorial Board of Biomedical and Environmental Sciences. Published by China CDC. All rights reserved.

  13. 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

  14. Maternal Obesity and Excessive Gestational Weight Gain Are Associated with Components of Child Cognition123

    PubMed Central

    Richardson, Gale A; Hutcheon, Jennifer A; Himes, Katherine P; Brooks, Maria M; Day, Nancy L; Bodnar, Lisa M

    2015-01-01

    Background: Maternal overweight and obesity affect two-thirds of women of childbearing age and may increase the risk of impaired child cognition. Objective: 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. Methods: 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. Results: 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

  15. Association of childhood obesity with maternal exposure to ambient air polycyclic aromatic hydrocarbons during pregnancy.

    PubMed

    Rundle, Andrew; Hoepner, Lori; Hassoun, Abeer; Oberfield, Sharon; Freyer, Greg; Holmes, Darrell; Reyes, Marilyn; Quinn, James; Camann, David; Perera, Frederica; Whyatt, Robin

    2012-06-01

    There are concerns that prenatal exposure to endocrine-disrupting chemicals increases children's risk of obesity. African-American and Hispanic children born in the Bronx or Northern Manhattan, New York (1998-2006), whose mothers underwent personal air monitoring for polycyclic aromatic hydrocarbon (PAH) exposure during pregnancy, were followed up to ages 5 (n = 422) and 7 (n = 341) years. At age 5 years, 21% of the children were obese, as were 25% of those followed to age 7 years. After adjustment for child's sex, age at measurement, ethnicity, and birth weight and maternal receipt of public assistance and prepregnancy obesity, higher prenatal PAH exposures were significantly associated with higher childhood body size. In adjusted analyses, compared with children of mothers in the lowest tertile of PAH exposure, children of mothers in the highest exposure tertile had a 0.39-unit higher body mass index z score (95% confidence interval (CI): 0.08, 0.70) and a relative risk of 1.79 (95% CI: 1.09, 2.96) for obesity at age 5 years, and they had a 0.30-unit higher body mass index z score (95% CI: 0.01, 0.59), a 1.93-unit higher percentage of body fat (95% CI: 0.33, 3.54), and a relative risk of 2.26 (95% CI: 1.28, 4.00) for obesity at age 7 years. The data indicate that prenatal exposure to PAHs is associated with obesity in childhood.

  16. Modulation of endothelial cell migration by ER stress and insulin resistance: a role during maternal obesity?

    PubMed

    Sáez, Pablo J; Villalobos-Labra, Roberto; Westermeier, Francisco; Sobrevia, Luis; Farías-Jofré, Marcelo

    2014-01-01

    Adverse microenvironmental stimuli can trigger the endoplasmic reticulum (ER) stress pathway, which initiates the unfolded protein response (UPR), to restore protein-folding homeostasis. Several studies show induction of ER stress during obesity. Chronic UPR has been linked to different mechanisms of disease in obese and diabetic individuals, including insulin resistance (IR) and impaired angiogenesis. Endothelial cell (EC) migration is an initial step for angiogenesis, which is associated with remodeling of existing blood vessels. EC migration occurs according to the leader-follower model, involving coordinated processes of chemotaxis, haptotaxis, and mechanotaxis. Thus, a fine-tuning of EC migration is necessary to provide the right timing to form the required vessels during angiogenesis. ER stress modulates EC migration at different levels, usually impairing migration and angiogenesis, although different effects may be observed depending on the tissue and/or microenvironment. In the context of pregnancy, maternal obesity (MO) induces IR in the offspring. Interestingly, several proteins associated with obesity-induced IR are also involved in EC migration, providing a potential link with the ER stress-dependent alterations observed in obese individuals. Different signaling cascades that converge on cytoskeleton regulation directly impact EC migration, including the Akt and/or RhoA pathways. In addition, ER is the main intracellular reservoir for Ca(2+), which plays a pivotal role during EC migration. Therefore, ER stress-related alterations in Ca(2+) signaling or Ca(2+) levels might also produce distorted EC migration. However, the above findings have been studied in the context of adult obesity, and no information has been reported regarding the effect of MO on fetal EC migration. Here we summarize the state of knowledge about the possible mechanisms by which ER stress and IR might impact EC migration and angiogenesis in fetal endothelium exposed to MO during

  17. Association of Childhood Obesity With Maternal Exposure to Ambient Air Polycyclic Aromatic Hydrocarbons During Pregnancy

    PubMed Central

    Rundle, Andrew; Hoepner, Lori; Hassoun, Abeer; Oberfield, Sharon; Freyer, Greg; Holmes, Darrell; Reyes, Marilyn; Quinn, James; Camann, David; Perera, Frederica; Whyatt, Robin

    2012-01-01

    There are concerns that prenatal exposure to endocrine-disrupting chemicals increases children’s risk of obesity. African-American and Hispanic children born in the Bronx or Northern Manhattan, New York (1998–2006), whose mothers underwent personal air monitoring for polycyclic aromatic hydrocarbon (PAH) exposure during pregnancy, were followed up to ages 5 (n = 422) and 7 (n = 341) years. At age 5 years, 21% of the children were obese, as were 25% of those followed to age 7 years. After adjustment for child’s sex, age at measurement, ethnicity, and birth weight and maternal receipt of public assistance and prepregnancy obesity, higher prenatal PAH exposures were significantly associated with higher childhood body size. In adjusted analyses, compared with children of mothers in the lowest tertile of PAH exposure, children of mothers in the highest exposure tertile had a 0.39-unit higher body mass index z score (95% confidence interval (CI): 0.08, 0.70) and a relative risk of 1.79 (95% CI: 1.09, 2.96) for obesity at age 5 years, and they had a 0.30-unit higher body mass index z score (95% CI: 0.01, 0.59), a 1.93-unit higher percentage of body fat (95% CI: 0.33, 3.54), and a relative risk of 2.26 (95% CI: 1.28, 4.00) for obesity at age 7 years. The data indicate that prenatal exposure to PAHs is associated with obesity in childhood. PMID:22505764

  18. Placental microRNA Expression Is Not Altered by Maternal Obesity and Fetal Overgrowth

    PubMed Central

    Ghaffari, Neda; Parry, Samuel; Elovitz, Michal A.; Durnwald, Celeste P.

    2016-01-01

    Objective The epigenetic mechanisms underlying fetal metabolic programming are poorly understood. We studied whether obesity is associated with alterations in placental miRNA expression. Study Design A cross-sectional study was performed, including (1) normal-weight women (BMI 20–24.9 kg/m2) and normal-birth-weight (BW) infants (2,700–3,500 g) (n = 20), (2) normal-weight and macrosomic infants (BW ≥ 4,000 g) (n = 10), (3) obese (BMI ≥ 35 kg/m2) and normal BW infants (n = 16), and (4) obese and macrosomic infants (n = 10). All had term deliveries (37–41 weeks) and normal glucose tolerance (1 hour GCT < 7.2 mmol/L [130 mg/dL]). The expression of 5,639 placental miRNAs was assessed using miRNA microarray. Differential miRNA expression was determined using two-way ANOVA and pairwise contrasts, with the Benjamini-Hochberg (BH) correction. MiRNAs with Z-scores ≥ 2 and false discovery rate (FDR) < 20% were considered significant. Results Principal components analysis demonstrated similar global miRNA expression profiles among groups. Of 5,639 miRNAs, only 5 were significantly different between obese and controls, which were not validated by quantitative polymerase reaction. Conclusion There was no difference in placental miRNA expression associated with obesity or overgrowth. Aberrant placental miRNA expression is an unlikely mechanism underlying fetal metabolic programming related to maternal obesity. PMID:28050331

  19. Maternal obesity, health status during pregnancy, and breastfeeding initiation and duration.

    PubMed

    Kitsantas, Panagiota; Pawloski, Lisa R

    2010-02-01

    The purpose of this study was to determine whether maternal prepregnancy overweight/obesity has independent effects on breastfeeding initiation and duration and whether these effects are different for women who experience medical problems during pregnancy or labor/delivery complications in comparison with those who have no medical or labor/delivery complications. We used the early childhood longitudinal study-birth cohort data. Kaplan-Meier survival functions, logistic, and Cox regression modeling were used in the analyses. Findings indicate that overweight/obese women with medical or labor/delivery complications were less likely to initiate breastfeeding in comparison with their counterparts of normal weight. We did not find an independent effect of prepregnancy overweight/obesity on breastfeeding initiation among women with no medical problems. This group of women, however, had an 11% increased risk of stopping breastfeeding with each additional month of breastfeeding duration in comparison to those of normal weight. It is important to evaluate the health history and pregnancy complications among overweight/obese mothers in developing interventions for successful initiation and duration of breastfeeding.

  20. Maternal obesity and contraction strength in the first stage of labor.

    PubMed

    Chin, Jeanette R; Henry, Erick; Holmgren, Calla M; Varner, Michael W; Branch, D Ware

    2012-08-01

    The purpose of this study was to determine whether maternal obesity is associated with cesarean delivery and decreased contraction strength in the first stage of labor. We studied a retrospective cohort of women who delivered within a single healthcare system from 2007-2009; we included 5410 women with an intrauterine pressure catheter during the last 2 hours of the first stage of labor and who either had a vaginal delivery or cesarean delivery for dystocia. Logistic regression was used to determine how body mass index was associated with cesarean delivery or mean Montevideo units of ≥200. Although obese women were at significantly greater odds of cesarean delivery than normal-weight women (odds ratio, 2.4; 95% confidence interval, 1.9-3.1), they were equally able to achieve Montevideo units of ≥200. Among women with a vaginal delivery, obese women had a longer first stage of labor compared with normal-weight women (597 vs 566 min; P = .003). Obese women have longer labors but are equally able to achieve adequate Montevideo units as normal-weight women. Copyright © 2012 Mosby, Inc. All rights reserved.

  1. 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

  2. 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...

  3. 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.

  4. 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

  5. Chronic maternal inflammation or high-fat-feeding programs offspring obesity in a sex-dependent manner.

    PubMed

    Dudele, A; Hougaard, K S; Kjølby, M; Hokland, M; Winther, G; Elfving, B; Wegener, G; Nielsen, A L; Larsen, A; Nøhr, M K; Pedersen, S B; Wang, T; Lund, S

    2017-09-01

    The current world-wide obesity epidemic partially results from a vicious circle whereby maternal obesity during pregnancy predisposes the offspring for accelerated weight gain and development of metabolic syndrome. Here we investigate whether low-grade inflammation, characteristic of the obese state, provides a causal role for this disastrous fetal programming in mice. We exposed pregnant and lactating C57BL/6JBom female mice to either high-fat diet (HFD), or continuous infusion of lipopolysaccharide (LPS), a potent trigger of innate immunity, and studied offspring phenotypes. Both maternal LPS or HFD treatments rendered the offspring hyperphagic and inept of coping with a HFD challenge during adulthood, increasing their adiposity and weight gain. The metabolic effects were more pronounced in female offspring, while exposed male offspring mounted a larger inflammatory response to HFD at adulthood. This supports our hypothesis and highlights the programming potential of inflammation in obese pregnancies.

  6. 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.

  7. 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

  8. Maternal Obesity Class as a Predictor of Induction Failure: A Practical Risk Assessment Tool.

    PubMed

    Ronzoni, Stefania; Rosen, Hadar; Melamed, Nir; Porat, Shay; Farine, Dan; Maxwell, Cynthia

    2015-12-01

    To assess the impact of body mass index (BMI) on the rate of cesarean section (rCS) in induction of labor (IOL). A total of 7,543 singleton term pregnancies undergoing IOL (cervical dilatation at admission, CDA ≤ 3 cm) were divided according to BMI: underweight (n = 325); normal weight (NW) (n = 4,633); overweight (OW) (n = 1,610); and obese (n = 975). Age, parity, macrosomia, gestational age (GA), gestational weight gain (GWG), CDA, and IOL indications were considered. A higher rate of macrosomia (15.0 vs. 11.1%; p < 0.0001), earlier induction (GA 39.7 ± 1.3 vs. 40.1 ± 1.3 weeks; p < 0.0001) for maternal indications (39.1 vs. 21.1%; p < 0.001), and lower CDA (≤1cm; 66.4 vs. 61.4%; p < 0.005) were observed in obese versus NW. The rate of weight gain above the recommended range was higher in obese (obese 70.6% vs. NW 43.9%; p < 0.001), despite a significantly lower mean GWG compared with NW (14 ± 7.5 vs. 16.5 ± 5.6 kg; p < 0.001). Compared with NW, OW and obese demonstrated a significantly higher rCS (OW 31.1% and obese 36.9% vs. NW 24.7%; p < 0.001). BMI represented an independent factor affecting the rCS (vs. NW; OW odds ratio [OR] 1.4; confidence interval [CI] 1.2-1.7; p < 0.001; obese OR 2.3; CI 1.9-2.7 p < 0.001). In the case of IOL, obesity represents an independent factor associated with a significant increase of CS to be considered during induction counselling. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

  9. Effect of maternal obesity on birthweight and neonatal fat mass: A prospective clinical trial

    PubMed Central

    Tanguy, Marie-Laure; Ciangura, Cécile; Lacorte, Jean-Marc; De Carne, Céline; Foix L’Hélias, Laurence; Chavatte-Palmer, Pascale; Charles, Marie-Aline; Dommergues, Marc

    2017-01-01

    Objective To discriminate the effect of maternal obesity and gestational diabetes on birth weight and adipose tissue of the newborn. Methods Normal BMI women (group N, n = 243; 18.5≤ BMI<25 kg/m2) and obese women (group Ob, n = 253; BMI≥30 kg/m2) were recruited in a prospective study between 15 and 18 weeks of gestation. All women were submitted to a 75g oral glucose tolerance test in the second and third trimester. First trimester fasting blood glucose was also obtained from Ob women. All women with one measurement above normal values were considered positive for gestational diabetes and first treated by dietary intervention. When dietary measures were not efficient, they were treated by insulin. Neonatal anthropometrics, sum of skinfolds and cord serum hormones were measured. Results 222 N and 226 Ob mothers and their newborns were included in the analysis. Diabetes was diagnosed in 20% and 45.2% of N and Ob women, respectively. Birth weight was not statistically different between groups (boys: 3456g±433 and 3392g±463; girls: 3316g±402 and 3391g±408 for N and Ob, respectively). Multivariate analysis demonstrated that skinfold thickness and serum leptin concentrations were significantly increased in girls born to women with obesity (18.0mm±0.6 versus 19.7mm±0.5, p = 0.004 and 11.3ng/mL±1.0 versus 15.3ng/mL±1.0, p = 0.02), but not in boys (18.4mm±0.6 versus 18.5mm±0.5, p = 0.9 and 9.3ng/mL±1.0 versus 9.0ng/mL±1.0, p = 0.9). Based on data from 136 N and 124 Ob women, maternal insulin resistance at 37 weeks was also positively related to skinfold in girls, only, with a 1-point increase in HOMA-IR corresponding to a 0.33mm±0.08 increase in skinfold (p<0.0001). Conclusions Regardless of gestational diabetes, maternal obesity and insulin resistance were associated with increased adiposity in girls only. Persistence of this sexual dimorphism remains to be explored during infancy. PMID:28750045

  10. Effect of maternal obesity on birthweight and neonatal fat mass: A prospective clinical trial.

    PubMed

    Mitanchez, Delphine; Jacqueminet, Sophie; Nizard, Jacky; Tanguy, Marie-Laure; Ciangura, Cécile; Lacorte, Jean-Marc; De Carne, Céline; Foix L'Hélias, Laurence; Chavatte-Palmer, Pascale; Charles, Marie-Aline; Dommergues, Marc

    2017-01-01

    To discriminate the effect of maternal obesity and gestational diabetes on birth weight and adipose tissue of the newborn. Normal BMI women (group N, n = 243; 18.5≤ BMI<25 kg/m2) and obese women (group Ob, n = 253; BMI≥30 kg/m2) were recruited in a prospective study between 15 and 18 weeks of gestation. All women were submitted to a 75g oral glucose tolerance test in the second and third trimester. First trimester fasting blood glucose was also obtained from Ob women. All women with one measurement above normal values were considered positive for gestational diabetes and first treated by dietary intervention. When dietary measures were not efficient, they were treated by insulin. Neonatal anthropometrics, sum of skinfolds and cord serum hormones were measured. 222 N and 226 Ob mothers and their newborns were included in the analysis. Diabetes was diagnosed in 20% and 45.2% of N and Ob women, respectively. Birth weight was not statistically different between groups (boys: 3456g±433 and 3392g±463; girls: 3316g±402 and 3391g±408 for N and Ob, respectively). Multivariate analysis demonstrated that skinfold thickness and serum leptin concentrations were significantly increased in girls born to women with obesity (18.0mm±0.6 versus 19.7mm±0.5, p = 0.004 and 11.3ng/mL±1.0 versus 15.3ng/mL±1.0, p = 0.02), but not in boys (18.4mm±0.6 versus 18.5mm±0.5, p = 0.9 and 9.3ng/mL±1.0 versus 9.0ng/mL±1.0, p = 0.9). Based on data from 136 N and 124 Ob women, maternal insulin resistance at 37 weeks was also positively related to skinfold in girls, only, with a 1-point increase in HOMA-IR corresponding to a 0.33mm±0.08 increase in skinfold (p<0.0001). Regardless of gestational diabetes, maternal obesity and insulin resistance were associated with increased adiposity in girls only. Persistence of this sexual dimorphism remains to be explored during infancy.

  11. Maternal obesity is associated with ovarian inflammation and upregulation of early growth response factor 1.

    PubMed

    Ruebel, Meghan; Shankar, Kartik; Gaddy, Dana; Lindsey, Forrest; Badger, Thomas; Andres, Aline

    2016-07-01

    Obesity impairs reproductive functions through multiple mechanisms, possibly through disruption of ovarian function. We hypothesized that increased adiposity will lead to a proinflammatory gene signature and upregulation of Egr-1 protein in ovaries from obese (OB; n = 7) compared with lean (LN; n = 10) female Sprague-Dawley rats during the peri-implantation period at 4.5 days postcoitus (dpc). Obesity was induced by overfeeding (40% excess calories for 28 days) via total enteral nutrition prior to mating. OB dams had higher body weight (P < 0.001), greater fat mass (P < 0.001), and reduced lean mass (P < 0.05) and developed metabolic dysfunction with elevated serum lipids, insulin, leptin, and CCL2 (P < 0.05) compared with LN dams. Microarray analyses identified 284 differentially expressed genes between ovaries from LN vs. OB dams (±1.3 fold, P < 0.05). RT-qPCR confirmed a decrease in expression of glucose transporters GLUT4 and GLUT9 and elevation of proinflammatory genes, including CCL2, CXCL10, CXCL11, CCR2, CXCR1, and TNFα in ovaries from OB compared with LN (P < 0.05). Protein levels of PI3K and phosphorylated Akt were significantly decreased (P < 0.05), whereas nuclear levels of Egr-1 (P < 0.05) were increased in OB compared with LN ovaries. Moreover, Egr-1 was localized to granulosa cells, with the highest expression in cumulus cells of preovulatory follicles. mRNA expression of VCAN, AURKB, and PLAT (P < 0.05) correlated with %visceral fat weight (r = 0.51, -0.77, and -0.57, respectively, P ≤ 0.05), suggesting alterations in ovarian function with obesity. In summary, maternal obesity led to an upregulation of inflammatory genes and Egr-1 expression in peri-implantation ovarian tissue and a concurrent downregulation of GLUTs and Akt and PI3K protein levels.

  12. The sex of the foetus affects maternal blood glucose concentrations in overweight and obese pregnant women.

    PubMed

    Seneviratne, Sumudu N; Derraik, José G B; Jiang, Yannan; McCowan, Lesley M E; Gusso, Silmara; Cutfield, Wayne S; Hofman, Paul L

    2016-12-26

    There is increasing evidence that the sex of the foetus may alter the maternal metabolic milieu during pregnancy. Following a randomized controlled trial of exercise in overweight and obese pregnant women, we assessed whether the sex of the foetus was associated with changes in maternal metabolism. Data were analysed on 74 randomized participants who completed the trial, including 38 mothers carrying males and 36 mothers carrying females. At 19 weeks of gestation, mothers carrying boys had higher blood glucose concentrations than those carrying girls (5.4 vs 4.9 mmol/l; p = .046). At 36 weeks of gestation, differences were more marked, with blood glucose concentrations 15% higher in mothers carrying females (5.7 vs 5.0 mmol/l; p = .004). In addition, mothers carrying girls had higher concentrations of hs-CRP across pregnancy (5.0 vs 3.6 mg/l; p = .029). Our findings provide further evidence that the sex of the foetus appears to influence maternal metabolism.

  13. 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.

  14. 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.

  15. 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

  16. 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.

  17. Maternal obesity caused by overnutrition exposure leads to reversal learning deficits and striatal disturbance in rats.

    PubMed

    Wu, Ting; Deng, Shining; Li, Wei-Guang; Yu, Yongguo; Li, Fei; Mao, Meng

    2013-01-01

    Maternal obesity caused by overnutrition during pregnancy increases susceptibility to metabolic risks in adulthood, such as obesity, insulin resistance, and type 2 diabetes; however, whether and how it affects the cognitive system associated with the brain remains elusive. Here, we report that pregnant obesity induced by exposure to excessive high fatty or highly palatable food specifically impaired reversal learning, a kind of adaptive behavior, while leaving serum metabolic metrics intact in the offspring of rats, suggesting a much earlier functional and structural defects possibly occurred in the central nervous system than in the metabolic system in the offspring born in unfavorable intrauterine nutritional environment. Mechanically, we found that above mentioned cognitive inflexibility might be associated with significant striatal disturbance including impaired dopamine homeostasis and disrupted leptin signaling in the adult offspring. These collective data add a novel perspective of understanding the adverse postnatal sequelae in central nervous system induced by developmental programming and the related molecular mechanism through which priming of risk for developmental disorders may occur during early life.

  18. Maternal Obesity Caused by Overnutrition Exposure Leads to Reversal Learning Deficits and Striatal Disturbance in Rats

    PubMed Central

    Wu, Ting; Deng, Shining; Li, Wei-Guang; Yu, Yongguo; Li, Fei; Mao, Meng

    2013-01-01

    Maternal obesity caused by overnutrition during pregnancy increases susceptibility to metabolic risks in adulthood, such as obesity, insulin resistance, and type 2 diabetes; however, whether and how it affects the cognitive system associated with the brain remains elusive. Here, we report that pregnant obesity induced by exposure to excessive high fatty or highly palatable food specifically impaired reversal learning, a kind of adaptive behavior, while leaving serum metabolic metrics intact in the offspring of rats, suggesting a much earlier functional and structural defects possibly occurred in the central nervous system than in the metabolic system in the offspring born in unfavorable intrauterine nutritional environment. Mechanically, we found that above mentioned cognitive inflexibility might be associated with significant striatal disturbance including impaired dopamine homeostasis and disrupted leptin signaling in the adult offspring. These collective data add a novel perspective of understanding the adverse postnatal sequelae in central nervous system induced by developmental programming and the related molecular mechanism through which priming of risk for developmental disorders may occur during early life. PMID:24223863

  19. A methyl-seq analyses of rat offspring liver reveals maternal obesity-induced alterations in dna methylation status at weaning

    USDA-ARS?s Scientific Manuscript database

    Exposure to maternal obesity (MO) increases the risk of obesity in adult-life. MO was induced in rats by overfeeding via total enteral nutrition. Male offspring from obese rats gain greater body weight, fat mass and develop insulin resistance when fed high fat diets. However the mechanisms underlyin...

  20. Maternal obesity leads to increased proliferation and numbers of astrocytes in the developing fetal and neonatal mouse hypothalamus.

    PubMed

    Kim, Dong Won; Glendining, Kelly A; Grattan, David R; Jasoni, Christine L

    2016-10-01

    Maternal obesity during pregnancy is associated with chronic maternal, placental, and fetal inflammation; and it elevates the risk for offspring obesity. Changes in the development of the hypothalamus, a brain region that regulates body weight and energy balance, are emerging as important determinants of offspring risk, but such changes are only beginning to be defined. Here we focused on the hypothesis that the pathological exposure of developing hypothalamic astrocytes to cytokines would alter their development. A maternal high-fat diet (mHFD) mouse model was used to investigate changes in hypothalamic astrocytes in the fetus during late gestation and in early neonates by using immunochemistry, confocal microscopy, and qPCR. The number of astrocytes and the proportion of proliferating astrocytes was significantly higher in the arcuate nucleus (ARC) and the supraoptic nucleus (SON) of the hypothalamus at both ages compared to control offspring from normal weight pregnancies. Supplemental to this we found that cultured fetal hypothalamic astrocytes proliferated significantly in response to IL6 (10ng/ml), one of the cytokines significantly elevated in fetuses of obese dams, via the JAK/STAT3 signaling pathway. Thus, maternal obesity during pregnancy stimulated the proliferation and thereby increased numbers of astrocytes in the fetal as well as early neonatal hypothalamus, which may be driven, during fetal life, by IL6. Copyright © 2016 ISDN. Published by Elsevier Ltd. All rights reserved.

  1. Gestational exposure to maternal obesity decreases mitochondrial SIRT3 and components of oxidative phosphorylation in offspring liver

    USDA-ARS?s Scientific Manuscript database

    Exposure to maternal overweight (OW) during development influences the risk of obesity in adult-life. We reported that by postnatal day (PND) 120 male offspring from OW rat dams have greater body weight and fat mass (p<0.005), and develop insulin resistance when fed high-fat diets (HFD, 45% fat). OW...

  2. 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.

  3. Maternal Obesity, Uterine Activity, and the Risk of Spontaneous Preterm Birth

    PubMed Central

    Ehrenberg, Hugh M.; Iams, Jay D.; Goldenberg, Robert L.; Newman, Roger B.; Weiner, Steven J.; Sibai, Baha M.; Caritis, Steve N.; Miodovnik, Menachem; Dombrowski, Mitchell P.

    2009-01-01

    OBJECTIVE To assess the associations between maternal obesity, uterine contraction frequency, and spontaneous preterm birth in at-risk women. METHODS In a secondary analysis, we analyzed data from 253 at-risk women (prior spontaneous preterm birth, vaginal bleeding) enrolled in a multi-center observational study of home uterine activity monitoring at 11 centers. All women wore a uterine activity monitor twice daily from 22 through 34 weeks of gestation. Mean and maximal contractions/hour at 22-24, 25-26, 27-28, 29-30, 31-32, and at or after 33 weeks of gestation were compared between overweight/obese women (a BMI at 22-24 weeks greater than 25 kg/m2) and normal/underweight women (a BMI of at least 25 kg/m2) at each gestational age interval. Multivariable analysis evaluated the influences of BMI, contractions, fetal fibronectin and transvaginal cervical length on spontaneous preterm birth before 35 weeks. RESULTS Obese/overweight women (n=156) were significantly less likely to experience spontaneous preterm birth before 35 weeks (8.3 vs 21.7%, p<0.01). For each gestational age interval before 32 weeks, obese/overweight women had fewer mean contractions/hour (P<0.01 for each) and maximal contractions/hour (p<0.01 for each) than normal/underweight women, although their mean cervical lengths (34.3 vs 33.1 mm, p=0.25), and fetal fibronectin levels (7.1% vs. 7.2% ≥50 ng/mL, p=0.97) were similar at study enrollment. Obese/overweight status was associated with a lower risk of spontaneous preterm birth before 35 weeks after controlling for contraction frequency and other factors evaluated at 22-24 and 31-32 weeks, but not at later time periods. CONCLUSION Obese/overweight women at risk for spontaneous preterm birth exhibit less uterine activity and less frequent spontaneous preterm birth before 35 weeks of gestation than normal/underweight women. PMID:19104359

  4. [Impact of maternal overnutrition on the periconceptional period].

    PubMed

    Velázquez, Miguel Abraham

    2015-05-01

    Overnutrition may lead to obesity. Maternal obesity may affect fertility not only via anovulation, but also through direct effects on oocytes and preimplantation embryos, indicating that the periconceptional period is sensitive to conditions of overnutrition. The periconceptional period includes from folliculogenesis to implantation. Animal model studies suggest that oocytes derived from obese females usually have a small size and mitochondrial abnormalities. These disruptions are probably induced by changes in the components of the ovarian follicular fluid. Experimental evidence also suggests that obesity may affect the microenvironment in oviducts and uterus, resulting in development of preimplantation embryos with reduced cell numbers and up-regulation of proinflammatory genes. However, further research is needed for in-depth characterization of the effects of maternal obesity during the periconceptional period. Copyright © 2014 SEEN. Published by Elsevier España, S.L.U. All rights reserved.

  5. Relationship between maternal obesity and prenatal, metabolic syndrome, obstetrical and perinatal complications of pregnancy in Indiana, 2008-2010.

    PubMed

    Feresu, Shingairai A; Wang, Yi; Dickinson, Stephanie

    2015-10-16

    Obesity is a serious medical condition affecting more than 30% of Indiana, and 25% of Unites States pregnant women. Obesity is related to maternal complications, and significantly impacts the health of pregnant women. The objective of this study was to describe the relationship between maternal complications and pre-pregnancy maternal weight. Using logistic regression models, we analyzed 2008 to 2010 birth certificate data, for 255,773 live births abstracted from the Indiana Vital Statistics registry. We examined the risk of reproductive factors, obstetrical complications and perinatal (intrapartum) complications for underweight, healthy weight, overweight and obese women for this population. Women who received prenatal care were more likely to be obese [adjusted odds ratio (AOR) = 1.82 (1.56-2.13)]. While women with parity of zero (0) were less likely to be obese [AOR = 0.89, 95% CI (0.86-0.91)]. Women giving birth to twins [AOR = 1.25, 95% CI (1.17- 1.33)], women delivering by Caesarian section [AOR = 2.31, 95% CI ( 2.26-2.37)], and women who previously had a Caesarian section [AOR = 1.95, 95% CI (1.88-2.02)] were more likely to be obese. There was evidence of metabolic like complication in this population, due to obesity. Obesity was significantly associated with obstetrical conditions of the metabolic syndrome, including pre-pregnancy diabetes, gestational diabetes, pre-pregnancy hypertension, pregnancy-induced hypertension and eclampsia [AOR = 5.12, 95% CI (4.47-5.85); AOR = 3.87, 95% CI (3.68-4.08); AOR = 7.66, 95% CI (6.77-8.65); AOR = 3.23, 95% CI (3.07-3.39); and AOR = 1.77, 95% CI (1.31-2.40), respectively. Maternal obesity modestly increased the risk of induction, epidural, post-delivery bleeding, and prolonged labor [AOR = 1.26, 95% CI (1.23-1.29); AOR = 1.15, 95% CI (1.13-1.18); AOR = 1.20, 95% CI (1.12-1.28); and AOR = 1.44, 95% CI (1.30-1.61)], respectively. Obese women were less likely to have blood transfusions [AOR

  6. Maternal nutrient restriction during early fetal kidney development attenuates the renal innate inflammatory response in obese young adult offspring.

    PubMed

    Sharkey, Don; Gardner, David S; Symonds, Michael E; Budge, Helen

    2009-11-01

    Obesity is an independent risk factor for developing chronic kidney disease. Toll-like receptor 4 (TLR4), interleukin (IL)-18, and uncoupling protein 2 (UCP2) are important components of the innate immune system mediating inflammatory renal damage. Early to midgestation maternal nutrient restriction appears to protect the kidney from the deleterious effects of early onset obesity, although the mechanisms remain unclear. We examined the combined effects of gestational maternal nutrient restriction during early fetal kidney development and early onset obesity on the renal innate immune response in offspring. Pregnant sheep were randomly assigned to a normal (control, 100%) or nutrient-restricted (NR, 50%) diet from days 30 to 80 gestation and 100% thereafter. Offspring were killed humanely at 7 days or, following rearing in an obesogenic environment, at 1 yr of age, and renal tissues were collected. IL-18 and TLR4 expression were strongly correlated irrespective of intervention. Seven-day NR offspring had significantly lower relative renal mass and IL-18 mRNA expression. At 1 yr of age, obesity resulted in increased mRNA abundance of TLR4, IL-18, and UCP2, coupled with tubular atrophy and greater immunohistological staining of glomerular IL-6 and medullary tumor necrosis factor (TNF)-alpha. NR obese offspring had a marked reduction of TLR4 abundance and renal IL-6 staining. In conclusion, maternal nutrient restriction during early fetal kidney development attenuates the effects of early onset obesity-related nephropathy, in part, through the downregulation of the innate inflammatory response. A better understanding of maternal nutrition and the in utero nutritional environment may offer therapeutic strategies aimed at reducing the burden of later kidney disease.

  7. 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

  8. 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

    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.

  9. Maternal obesity and offspring body composition by indirect methods: a systematic review and meta-analysis.

    PubMed

    Castillo-Laura, Helen; Santos, Iná S; Quadros, Lenice C M; Matijasevich, Alicia

    2015-10-01

    This study reviewed the evidence that assessed the association between maternal pre-pregnancy body mass index (BMI) and/or gestational weight gain and offspring body composition in childhood. A systematic review was conducted. Cohort studies, case-control studies and randomized controlled trials measuring offspring body composition by indirect methods were included. Meta-analyses of the effect of pre-pregnancy BMI on offspring fat-free mass, body fat percent, and fat mass were conducted through random-effects models. 20 studies were included, most of which reported a positive association of pre-pregnancy BMI with offspring body fat. Standardized mean differences in body fat percent, fat mass and fat-free mass between infants of women with normal pre-pregnancy BMI and those of overweight/obese women were 0.31 percent points (95%CI: 0.19; 0.42), 0.38 kg (95%CI: 0.26; 0.50), and 0.18 kg (95%CI: -0.07; 0.42), respectively. Evidence so far suggests that pre-pregnancy maternal overweight is associated with higher offspring adiposity.

  10. 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

  11. 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

  12. Longitudinal association of maternal attempt to lose weight during the postpartum period and child obesity at age 3 years.

    PubMed

    Sonneville, Kendrin R; Rifas-Shiman, Sheryl L; Oken, Emily; Peterson, Karen E; Gortmaker, Steven L; Gillman, Matthew W; Taveras, Elsie M

    2011-10-01

    The effect of maternal attempt to lose weight during the postpartum period on later child weight has not been explored. Among 1,044 mother-infant pairs in Project Viva, we estimated longitudinal associations of maternal attempt to lose weight during the postpartum period with child weight and adiposity at age 3 years and examined differences in associations by type of weight loss strategy used. Using covariate-adjusted linear and logistic regression models, we estimated associations before and after adjusting for maternal weight-related variables including prepregnancy BMI. At 6 months postpartum, 53% mothers were trying to lose weight. At age 3 years, mean (s.d.) child BMI z-score was 0.44 (1.01) and 8.9% of children were obese. Children whose mothers were trying to lose weight at 6 months postpartum had higher BMI z-scores (0.30 (95% confidence interval (CI) 0.18, 0.42)) and were more likely to be obese (3.0 (95% CI 1.6, 5.8)) at 3 years of age. Addition of maternal prepregnancy BMI to the models attenuated but did not eliminate the associations seen for BMI z-score (0.24 (95% CI 0.12, 0.36) and obesity (2.4 (95% CI 1.2, 4.7)). Attempting to lose weight by exercising alone was the only weight loss strategy that consistently predicted higher child BMI z-score (0.36 (95% CI 0.14, 0.58)) and odds of obesity (6.0 (95% CI 2.2, 16.5)) at age 3 years. In conclusion, we observed an association between maternal attempt to lose weight at 6 months postpartum, particularly through exercise alone, measured using a single item and child adiposity at age 3 years. This association should be thoroughly examined in future studies.

  13. 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.

  14. Increased risk of orofacial clefts associated with maternal obesity: case–control study and Monte Carlo-based bias analysis

    PubMed Central

    Stott-Miller, Marni; Heike, Carrie L.; Kratz, Mario; Starr, Jacqueline R.

    2010-01-01

    Summary Our objective was to evaluate whether infants born to obese or diabetic women are at higher risk of non-syndromic orofacial clefting. We conducted a population-based case–control study using Washington State birth certificate and hospitalisation data for the years 1987–2005. Cases were infants born with orofacial clefts (n = 2153) and controls infants without orofacial clefts (n = 18 070). The primary exposures were maternal obesity (body mass index ≥30) and diabetes (either pre-existing or gestational). We estimated adjusted odds ratios (ORs) to compare, for mothers of cases and controls, the proportions of obese vs. normal-weight women and diabetic vs. non-diabetic women. We additionally performed Monte Carlo-based simulation analysis to explore possible influences of biases. Obese women had a small increased risk of isolated orofacial clefts in their offspring compared with normal-body mass index women [adjusted OR 1.26; 95% confidence interval 1.03, 1.55]. Results were similar regardless of type of cleft. Bias analyses suggest that estimates may represent underlying ORs of stronger magnitude. Results for diabetic women were highly imprecise and inconsistent. We and others have observed weak associations of similar magnitude between maternal obesity and risk of nonsyndromic orofacial clefts. These results could be due to bias or residual confounding. However, it is also possible that these results represent a stronger underlying association. More precise exposure measurement could help distinguish between these two possibilities. PMID:20670231

  15. Maternal Obesity Management Using Mobile Technology: A Feasibility Study to Evaluate a Text Messaging Based Complex Intervention during Pregnancy

    PubMed Central

    Soltani, Hora; Duxbury, Alexandra M. S.; Arden, Madelynne A.; Dearden, Andy; Furness, Penny J.; Garland, Carolyn

    2015-01-01

    Background. Maternal obesity and excessive gestational weight gain (GWG) are on the rise with negative impact on pregnancy and birth outcomes. Research into managing GWG using accessible technology is limited. The maternal obesity management using mobile technology (MOMTech) study aimed at evaluating the feasibility of text messaging based complex intervention designed to support obese women (BMI ≥ 30) with healthier lifestyles and limit GWG. Methods. Participants received two daily text messages, supported by four appointments with healthy lifestyle midwife, diet and activity goal setting, and self-monitoring diaries. The comparison group were obese mothers who declined to participate but consented for their routinely collected data to be used for comparison. Postnatal interviews and focus groups with participants and the comparison group explored the intervention's acceptability and suggested improvements. Results. Fourteen women completed the study which did not allow statistical analyses. However, participants had lower mean GWG than the comparison group (6.65 kg versus 9.74 kg) and few (28% versus 50%) exceeded the Institute of Medicine's upper limit of 9 kg GWG for obese women. Conclusions. MOMTech was feasible within clinical setting and acceptable intervention to support women to limit GWG. Before further trials, slight modifications are planned to recruitment, text messages, and the logistics of consultation visits. PMID:25960889

  16. Polycystic ovary syndrome and maternal obesity affect oocyte size in in vitro fertilization/intracytoplasmic sperm injection cycles.

    PubMed

    Marquard, Kerri L; Stephens, Sahar M; Jungheim, Emily S; Ratts, Valerie S; Odem, Randall R; Lanzendorf, Susan; Moley, Kelle H

    2011-05-01

    To determine the impact of maternal metabolic state on oocyte development in women undergoing in vitro fertilization/intracytoplasmic sperm injection (IVF/ICSI), we retrospectively analyzed a cohort of women with PCOS undergoing IVF/ICSI from 2008-2009 in a university-based fertility center. We determined that women with PCOS and obesity have smaller oocytes than control subjects, and that when further subdivided by body mass index, both PCOS and obesity independently influence oocyte size. Copyright © 2011 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.

  17. Decreased basal insulin secretion from pancreatic islets of pups in a rat model of maternal obesity.

    PubMed

    Zambrano, Elena; Sosa-Larios, Tonantzin; Calzada, Lizbeth; Ibáñez, Carlos A; Mendoza-Rodríguez, Carmen A; Morales, Angélica; Morimoto, Sumiko

    2016-10-01

    Maternal obesity (MO) is a deleterious condition that enhances susceptibility of adult offspring to metabolic diseases such as type 2 diabetes. The objective is to study the effect of MO on in vitro insulin secretion and pancreatic cellular population in offspring. We hypothesize that a harmful antenatal metabolic environment due to MO diminishes the basal glucose-responsive secretory function of pancreatic beta cells in offspring. Mothers were fed a control (C) or high-fat diet from weaning through pregnancy (120 days) and lactation. At postnatal days (PNDs) 36 and 110, pups were killed, peripheral blood was collected and pancreatic islets were isolated. Basal insulin secretion was measured in vitro in islets for 60 min. It was found that blood insulin, glucose and homeostasis model assessment (HOMA) index were unaffected by maternal diet and age in females. However, male MO offspring at PND 110 showed hyperinsulinemia and insulin resistance compared with C. Body weight was not modified by MO, but fat content was higher in MO pups compared with C pups. Triglycerides and leptin concentrations were higher in MO than in C offspring in all groups except in females at PND 36. Pancreatic islet cytoarchitecture was unaffected by MO. At PND 36, islets of male and female C and MO offspring responded similarly to glucose, but at PND 110, male and female MO offspring islets showed a 50% decrease in insulin secretion. It was concluded that MO impairs basal insulin secretion of offspring with a greater impact on males than females, and this effect mainly manifests in adulthood.

  18. 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

  19. Activation of placental insulin and mTOR signaling in a mouse model of maternal obesity associated with fetal overgrowth.

    PubMed

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

    2016-01-01

    Fetal overgrowth is common in obese women and is associated with perinatal complications and increased risk for the child to develop metabolic syndrome later in life. Placental nutrient transport capacity has been reported to be increased in obese women giving birth to large infants; however, the underlying mechanisms are not well established. Obesity in pregnancy is characterized by elevated maternal serum insulin and leptin, hormones that stimulate placental amino acid transporters in vitro. We hypothesized that maternal obesity activates placental insulin/IGF-I/mTOR and leptin signaling pathways. We tested this hypothesis in a mouse model of obesity in pregnancy that is associated with fetal overgrowth. 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. Placentas were collected at embryonic day 18.5. Using Western blot analysis, placental mTOR activity was determined along with energy, inflammatory, leptin, and insulin signaling pathways (upstream modulators of mTOR). Phosphorylation of S6 ribosomal protein (S-235/236), 4E-BP1 (T-37/46), Insulin receptor substrate 1 (Y-608), Akt (T-308), and STAT-3 (Y-705) was increased in obese dams. In contrast, expression of placental caspase-1, IкBα, IL-1β, and phosphorylated-JNK(p46/54-T183/Y185) was unaltered. Fetal amino acid availability is a key determinant of fetal growth. We propose that activation of placental insulin/IGF-I/mTOR and leptin signaling pathways in obese mice stimulates placental amino acid transport and contributes to increased fetal growth. Copyright © 2016 the American Physiological Society.

  20. Causal relationship between obesity-related traits and TLR4-driven responses at the maternal-fetal interface.

    PubMed

    Yang, Xiaohua; Li, Ming; Haghiac, Maricela; Catalano, Patrick M; O'Tierney-Ginn, Perrie; Hauguel-de Mouzon, Sylvie

    2016-11-01

    Obesity triggers complex inflammatory networks within the innate immune system. During pregnancy, the placenta amplifies the low-grade inflammation through activation of Toll-like receptor 4 (TLR4) signalling pathways. The purpose of this study was to investigate the impact of obesity on placental TLR4 expression and inflammatory signals. The secondary aim was to analyse the placental cell type responsible for TLR4 activation. Thirty-nine women recruited at term-scheduled Caesarean section were grouped according to their pre-gravid BMI (<25 kg/m(2) and >30 kg/m(2)). Placenta, venous maternal and cord blood were obtained at delivery for analysis. Data were analysed with linear regression and Spearman's rank correlation coefficient analysis. TLR4, IL6 and IL8 expression was increased three- to ninefold (p < 0.001) in the placenta of obese vs lean women. There was a positive correlation between placental TLR4 and maternal systemic and placental IL6 and IL8 concentrations. Placental TLR4 expression was correlated with maternal pre-gravid BMI, insulin resistance index, plasma insulin and C-reactive protein (r = 0.57, 0.31, 0.35, 0.53, respectively; p < 0.001) but not with plasma glucose, maternal age, gestational age and gestational weight gain (r < 0.2; p > 0.1). TLR4 was located in both trophoblast and macrovascular endothelial cells lining fetal vasculature. Lipopolysaccharide-induced TLR4 activation was more robust in trophoblasts than in endothelial vascular cells (100-fold vs tenfold; p < 0.001). Trophoblastic TLR4 is strongly implicated in the propagation of placental inflammation. Placental inflammation is related to maternal metabolic conditions such as pre-gravid BMI, whilst gestational weight gain or gestational age are not. These results implicate the pre-gravid condition as a significant contributor to metabolic inflammation in late pregnancy.

  1. The impact of maternal obesity, age, pre-eclampsia and insulin dependent diabetes on severe maternal morbidity by mode of delivery-a register-based cohort study.

    PubMed

    Pallasmaa, Nanneli; Ekblad, Ulla; Gissler, Mika; Alanen, Anna

    2015-02-01

    To determine the rate of severe maternal morbidity related to delivery by delivery mode and to assess if the impact of studied risk factors varies by delivery mode. A register-based study including all women having singleton delivery in Finland in 2007-2011, n = 292,253, data derived from the Finnish Medical Birth Registry and Hospital Discharge Registry. Diagnoses and interventions indicating a severe maternal complication were searched and the mode of delivery was assessed by data linkage. The impact of obesity, maternal age 35 years or more, pre-eclampsia and insulin dependent diabetes on severe maternal morbidity (all severe complications, severe infections and severe) was studied in each mode of delivery and calculated as Odds ratios. The overall incidence of severe complications was 12.8/1,000 deliveries. The total complication rate was lowest in vaginal deliveries (VD) in all risk groups. Obesity increased the risk for all severe complications and severe infections in the total population, but not significantly in specific delivery modes. Age increased the risk of hemorrhage in VD. Pre-eclampsia increased the risk for hemorrhage in all deliveries except elective CS. In women with pre-eclampsia, overall morbidity was similar in VD, attempted VD and elective CS. The presence of any studied risk factor increased the risk for complications within the risk groups by the high proportion of emergency CS performed. An attempt of VD is the safest way to deliver even for high-risk women with the exception of women with pre-eclampsia, who had a similar risk in an attempt of VD and elective CS.

  2. 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…

  3. 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…

  4. Translation of fetal abdominal circumference-guided therapy of gestational diabetes complicated by maternal obesity to a clinical outpatient setting.

    PubMed

    Quevedo, Stephen F; Bovbjerg, Marit L; Kington, Randi L

    2017-06-01

    To evaluate the effectiveness of fetal abdominal circumference-guided therapy for gestational diabetes (GDM) in an outpatient population characterized by highly-prevalent maternal obesity. Data for this translational retrospective cohort study come from medical records. Fetal abdominal circumference was assessed by ultrasound in late second trimester, and sex- and gestational age-specific percentiles assigned. Taking fetal abdominal circumference percentile as a marker for adequacy of fetal growth, maternal glucose targets were set accordingly: loose, moderate or tight. Associations between mother's targets and neonatal outcomes (small for gestational age (SGA), large for gestational age (LGA), macrosomia, neonatal intensive care unit (NICU) admission, and neonatal hypoglycemia) were assessed using unconditional logistic regression, controlling for pre-gravid body mass index (BMI) and gestational weight gain. In 419 consecutive pregnancies complicated by GDM, neonatal outcomes compared favorably with previous randomized trials of intensive GDM management. Importantly, adverse outcomes were observed less often than might be expected in an obese GDM population. BMI did not have an independent effect on neonatal outcomes. Ultrasound-guided therapy of GDM, in general clinic use, can limit excess macrosomia and LGA, even in a population with significant maternal obesity.

  5. The effect of combined inositol supplementation on maternal metabolic profile in pregnancies complicated by metabolic syndrome and obesity.

    PubMed

    Ferrari, Francesca; Facchinetti, Fabio; Ontiveros, Alejandra E; Roberts, Robyn P; Saade, Mia M; Blackwell, Sean C; Sibai, Baha M; Refuerzo, Jerrie S; Longo, Monica

    2016-10-01

    Myoinositol and D-chiroinositol improve insulin resistance in women with obesity and gestational diabetes and in postmenopausal women with metabolic syndrome. We previously reported that offspring born to hypertensive dams lacking endothelial nitric oxide synthase and fed a high-fat diet develop metabolic-like syndrome phenotype. The objective of the study was to investigate the effect of a mixture of myoinositol/D-chiroinositol supplementation during pregnancy on the maternal metabolic profile in pregnancies complicated by the metabolic-like syndrome and obesity using a pregnant mouse model. Female heterozygous endothelial nitric oxide synthase(-/+) mice with moderate hypertension were placed on a high-fat diet for 4 weeks to induce a metabolic-like syndrome phenotype. Similarly, wild-type C57BL/6 mice were placed on a high-fat diet for 4 weeks to induce a murine obesity model. Mice were then bred with wild-type males. On gestational day 1, dams were randomly allocated to receive either a mixture of myoinositol/D-chiroinositol in water (7.2/0.18 mg/mL, respectively) or water as control (placebo). At term (gestational day 18), maternal weights, systolic blood pressure, and a glucose tolerance test were obtained. Dams were then killed; pups and placentas were weighed and maternal blood collected. Serum levels of metabolic biomarkers relevant to diabetes and obesity (ghrelin, gastric inhibitory peptide, glucagon-like peptide 1, glucagon, insulin, leptin, resistin) were measured by a multiplex enzyme-linked immunosorbent assay. Analysis was done comparing metabolic-like syndrome-myoinositol/D-chiroinositol-treated vs metabolic-like syndrome-nontreated mice and obese-myoinositol/D-chiroinositol-treated vs obese nontreated mice. Mean systolic blood pressure was lower in metabolic-like syndrome pregnant mice treated with myoinositol/D-chiroinositol compared with placebo (P = .04), whereas there was no difference in systolic blood pressure between treated and placebo

  6. High Fat Diet and In Utero Exposure to Maternal Obesity Disrupts Circadian Rhythm and Leads to Metabolic Programming of Liver in Rat Offspring

    PubMed Central

    Borengasser, Sarah J.; Kang, Ping; Faske, Jennifer; Gomez-Acevedo, Horacio; Blackburn, Michael L.; Badger, Thomas M.; Shankar, Kartik

    2014-01-01

    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 steatosis, and lipogenic gene expression in the liver at weaning. However, the precise underlying mechanisms leading to metabolic dysregulation in the offspring remains unclear. Using a rat model of overfeeding-induced obesity, we previously demonstrated that exposure to maternal obesity from pre-conception to birth, is sufficient to program increased obesity risk in the offspring. Offspring of obese rat dams gain greater body weight and fat mass when fed high fat diet (HFD) as compared to lean dam. Since, disruptions of diurnal circadian rhythm are known to detrimentally impact metabolically active tissues such as liver, we examined the hypothesis that maternal obesity leads to perturbations of core clock components and thus energy metabolism in offspring liver. Offspring from lean and obese dams were examined at post-natal day 35, following a short (2 wk) HFD challenge. Hepatic mRNA expression of circadian (CLOCK, BMAL1, REV-ERBα, CRY, PER) and metabolic (PPARα, SIRT1) genes were strongly suppressed in offspring exposed to both maternal obesity and HFD. Using a mathematical model, we identified two distinct biological mechanisms that modulate PPARα mRNA expression: i) decreased mRNA synthesis rates; and ii) increased non-specific mRNA degradation rate. Moreover, our findings demonstrate that changes in PPARα transcription were associated with epigenomic alterations in H3K4me3 and H3K27me3 histone marks near the PPARα transcription start site. Our findings indicated that offspring from obese rat dams have detrimental alternations to circadian machinery that may contribute to impaired liver metabolism in response to HFD, specifically via reduced PPARα expression prior to

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

    PubMed Central

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

    2013-01-01

    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. PMID:23922128

  8. 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%).

  9. 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...

  10. Global methylation in the placenta and umbilical cord blood from pregnancies with maternal gestational diabetes, preeclampsia, and obesity.

    PubMed

    Nomura, Yoko; 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.

  11. 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

  12. Maternal diet-induced obesity programs cardiovascular dysfunction in adult male mouse offspring independent of current body weight.

    PubMed

    Blackmore, Heather L; Niu, Youguo; Fernandez-Twinn, Denise S; Tarry-Adkins, Jane L; Giussani, Dino A; Ozanne, Susan E

    2014-10-01

    Obese pregnancies are not only associated with adverse consequences for the mother but also the long-term health of her child. Human studies have shown that individuals from obese mothers are at increased risk of premature death from cardiovascular disease (CVD), but are unable to define causality. This study aimed to determine causality using a mouse model of maternal diet-induced obesity. Obesity was induced in female C57BL/6 mice by feeding a diet rich in simple sugars and saturated fat 6 weeks prior to pregnancy and throughout pregnancy and lactation. Control females were fed laboratory chow. Male offspring from both groups were weaned onto chow and studied at 3, 5, 8, and 12 weeks of age for gross cardiac morphometry using stereology, cardiomyocyte cell area by histology, and cardiac fetal gene expression using qRT-PCR. Cardiac function was assessed by isolated Langendorff technology at 12 weeks of age and hearts were analyzed at the protein level for the expression of the β1 adrenergic receptor, muscarinic type-2 acetylcholine receptor, and proteins involved in cardiac contraction. Offspring from obese mothers develop pathologic cardiac hypertrophy associated with re-expression of cardiac fetal genes. By young adulthood these offspring developed severe systolic and diastolic dysfunction and cardiac sympathetic dominance. Importantly, cardiac dysfunction occurred in the absence of any change in corresponding body weight and despite the offspring eating a healthy low-fat diet. These findings provide a causal link to explain human observations relating maternal obesity with premature death from CVD in her offspring.

  13. Suboptimal maternal nutrition, during early fetal liver development, promotes lipid accumulation in the liver of obese offspring

    PubMed Central

    Hyatt, M A; Gardner, D S; Sebert, S; Wilson, V; Davidson, N; Nigmatullina, Y; Chan, L L Y; Budge, H; Symonds, M E

    2011-01-01

    Maternal nutrition during the period of early organ development can modulate the offspring's ability to metabolise excess fat as young adults when exposed to an obesogenic environment. This study examined the hypothesis that exposing offspring to nutrient restriction coincident with early hepatogenesis would result in endocrine and metabolic adaptations that subsequently lead to increased ectopic lipid accumulation within the liver. Pregnant sheep were fed either 50 or 100% of total metabolisable energy requirements from 30 to 80 days gestation and 100% thereafter. At weaning, offspring were made obese, and at ∼1 year of age livers were sampled. Lipid infiltration and molecular indices of gluconeogenesis, lipid metabolism and mitochondrial function were measured. Although hepatic triglyceride accumulation was not affected by obesity per se, it was nearly doubled in obese offspring born to nutrient-restricted mothers. This adaptation was accompanied by elevated gene expression for peroxisome proliferator-activated receptor γ (PPARG) and its co-activator PGC1α, which may be indicative of changes in the rate of hepatic fatty acid oxidation. In contrast, maternal diet had no influence on the stimulatory effect of obesity on gene expression for a range of proteins involved in glucose metabolism and energy balance including glucokinase, glucocorticoid receptors and uncoupling protein 2. Similarly, although gene expressions for the insulin and IGF1 receptors were suppressed by obesity they were not influenced by the prenatal nutritional environment. In conclusion, excess hepatic lipid accumulation with juvenile obesity is promoted by suboptimal nutrition coincident with early development of the fetal liver. PMID:21045167

  14. Effect of Maternal Age at Childbirth on Obesity in Postmenopausal Women

    PubMed Central

    We, Ji-Sun; Han, Kyungdo; Kwon, Hyuk-Sang; Kil, Kicheol

    2016-01-01

    Abstract The object of this study was to assess the obesity in postmenopausal women, according to age at childbirth. We analyzed the association between age at first childbirth, age at last childbirth, parity, and subject obesity status (general obesity; BMI >25 kg/m2, nongeneral obesity; BMI ≤25 kg/m2, abdominal obesity; waist circumference >85 cm, nonabdominal obesity; waist circumference ≤85 cm), using data from a nationwide population-based survey, the 2010 to 2012 Korean National Health and Nutrition Examination Survey. Data from a total of 4382 postmenopausal women were analyzed using multivariate regression analysis with complex survey design sampling. And, the subjects were subdivided into groups according to obesity or not. Age, smoking, alcohol consumption, exercise, education, income level, number of pregnancies, oral contraceptive uses, breast feeding experience were adjusted as the confounders. The prevalence of general obesity among Korean postmenopausal women was 37.08%. Women with general obesity and abdominal obesity were significantly younger at first childbirth compared with women with nongeneral obesity and no abdominal obesity (23.89 ± 0.1 vs. 23.22 ± 0.1, P <0.001). Age at first childbirth was inversely associated with obesity, while age at last childbirth was not associated with obesity or abdominal obesity. Women with a higher number of pregnancies were also more likely to have obesity and abdominal obesity. Age at first childbirth remained significantly associated with obesity, after adjusting for confounding factors. Obesity in postmenopausal women is associated with first childbirth at a young age, and higher parity. Further research is needed to clarify the association between obesity and reproductive characteristics. PMID:27175656

  15. Maternal obesity mediated predisposition to respiratory complications at birth and in later life: understanding the implications of the obesogenic intrauterine environment.

    PubMed

    McGillick, Erin V; Lock, Mitchell C; Orgeig, Sandra; Morrison, Janna L

    2017-01-01

    More women than not are entering pregnancy either overweight or obese. This presents a significant health care burden with respect to maternal morbidities and offspring complications at birth and in later life. In recent years it has also become clear that maternal obesity is an even greater global health problem than anticipated, because the effects are not limited to the mother but are also programmed in the fetus, known as the 'intergenerational cycle of obestiy'. Despite a large body of epidemiological evidence reporting outcomes of obese pregnancies, including offspring respiratory complications, much less is known about the molecular effects of maternal obesity on fetal lung development. This review focuses on the influence of altered substrate supply associated with the obesogenic intrauterine environment on fetal lung development. Understanding the molecular mechanisms contributing to altered fetal lung development will lead to improved respiratory outcomes for offspring at birth and in later life.

  16. 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

  17. Beneficial effects of exercise on offspring obesity and insulin resistance are reduced by maternal high-fat diet.

    PubMed

    Kasch, Juliane; Schumann, Sara; Schreiber, Saskia; Klaus, Susanne; Kanzleiter, Isabel

    2017-01-01

    We investigated the long-term effects of maternal high-fat consumption and post-weaning exercise on offspring obesity susceptibility and insulin resistance. 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. 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. 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.

  18. Maternal obesity and overnutrition increase oxidative stress in male rat offspring reproductive system and decrease fertility.

    PubMed

    Rodríguez-González, G L; Vega, C C; Boeck, L; Vázquez, M; Bautista, C J; Reyes-Castro, L A; Saldaña, O; Lovera, D; Nathanielsz, P W; Zambrano, E

    2015-04-01

    Increasing evidence exists that maternal obesity (MO) and overnutrition during pregnancy and lactation have long-lasting consequences for progeny metabolism, cardiovascular and endocrine function. Data on effects of MO on offspring reproduction are limited. We hypothesized that MO during pregnancy and lactation in founder F(0) rat mothers would increase testicular and sperm oxidative stress (OS) and adversely impact male fertility in their F(1) offspring. We induced pre-pregnancy MO by feeding F(0) females a high-fat diet from weaning through pregnancy and lactation. After weaning, all F(1) rats ate control (C) diet. We determined serum testosterone, malondialdehyde (MDA), reactive oxygen species (ROS) and superoxide dismutase (SOD) and glutathione peroxidase (GPx) activity in F(1) testes and sperm at postnatal days (PNDs) 110, 450 and 650. At PNDs 450 and 650, MO offspring had lower luteinizing hormone while testosterone levels were lower at all ages. Testicular MDA and ROS concentrations and SOD and GPx activity were higher in MO F(1) at all ages. Nitrotyrosine immunostaining was higher at all ages in MO F(1) testes than C F(1). At PNDs 450 and 650, MO F(1) spermatozoa showed higher MDA concentrations and lower SOD and GPx activity with reduced sperm concentration, viability and motility, and more sperm abnormalities. Fertility rate was not affected at PND 110 but was lower in MO F(1) at PNDs 450 and 650. We conclude that MO during pregnancy and lactation increases F(1) testicular and sperm OS leading to premature aging of reproductive capacity.

  19. 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

  20. The effects of morbid obesity on maternal and neonatal health outcomes: a systematic review and meta-analyses.

    PubMed

    Lutsiv, O; Mah, J; Beyene, J; McDonald, S D

    2015-07-01

    Morbidly obese (Class III, body mass index [BMI] ≥ 40 kg m(-2)) women constitute 8% of reproductive-aged women and are an increasing proportion; however, their pregnancy risks have not yet been well understood. Hence, we performed meta-analyses following the MOOSE (Meta-Analysis of Observational Studies in Epidemiology) guideline, searching Medline and Embase from their inceptions. To examine graded relationships, we compared Class III obesity to Class I and I/II, and separately to normal weight. We found important effects on all three primary outcomes in morbidly obese women: preterm birth <37 weeks was 31% higher compared with Class I (relative risk [RR] 1.31 [1.19, 1.43]) and 20% higher than Class I/II (RR 1.20 [1.13, 1.27]), large-for-gestational age was higher (RR 1.37 [1.29, 1.45] and RR 1.30 [1.24, 1.36] compared with Class I and I/II, respectively), while small-for-gestational age was lower (RR 0.89 [0.84, 0.93] compared with Class I, with nearly identical reductions for Class I/II). Morbidly obese women have higher risks of preterm birth, large-for-gestational age and numerous other adverse maternal and infant health outcomes, relative to not only normal weight but also Class I or I/II obese women. These findings have important implications for screening and care of morbidly obese pregnant women, to try to decrease adverse outcomes. © 2015 World Obesity.

  1. Sexual dimorphism in miR-210 expression and mitochondrial dysfunction in the placenta with maternal obesity

    PubMed Central

    Muralimanoharan, S; Guo, C; Myatt, L; Maloyan, A

    2015-01-01

    BACKGROUND Maternal obesity is a major problem in obstetrics, and the placenta is involved in obesity-related complications via its roles at the maternal–fetal interface. We have recently shown a causative role for micro(mi)RNA-210, a so called ‘hypoxamir’ regulated by HIF-1α, in mitochondrial dysfunction in placentas from women with preeclampsia. We also reported mitochondrial dysfunction in placentas with maternal obesity. Here we hypothesized that expression of miR-210 is dysregulated in the placentas with obesity. METHODS Placentas from uncomplicated pregnancies were collected at term from healthy weight or control (CTRL, pre-pregnancy body mass index (BMI)<25), overweight (OW, BMI = 25–24.9) and obese (OB, BMI>30) women following C-section with no labor. Expression of miRNA-210 and its target genes was measured by reverse transcription–PCR and Western Blot, respectively. Mitochondrial respiration was assessed by Seahorse Analyzer in syncytiotrophoblast (ST) 72 h after cytotrophoblast isolation. RESULTS Expression of miR-210 was significantly increased in placentas of OB and OW women with female but not male fetuses compared with CTRL placentas of females. However, expression of HIF-1α in these placentas remained unchanged. Levels of tumor-necrosis factor-alpha (TNFα) were increased in OW and OB placentas of females but not males, and in silico analysis suggested that activation of miR-210 expression in these placentas might be activated by NFκB1 (p50) signaling. Indeed, chromatin Immunoprecipitation assay showed that NFkB1 binds to placental miR-210 promoter in a fetal sex-dependent manner. Female but not male STs treated with TNFα showed overexpression of miR-210, reduction of mitochondrial target genes and decreased mitochondrial respiration. Pre-treatment of these STs with small interfering RNA to NFkB1 or antagomiR-210 prevented the TNFα-mediated inhibition of mitochondrial respiration. CONCLUSIONS Our data suggest that the inflammatory

  2. 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.

  3. Maternal obese-type gut microbiota differentially impact cognition, anxiety and compulsive behavior in male and female offspring in mice

    PubMed Central

    Fernandez-Kim, Sun-Ok; Townsend, R. Leigh; Kruger, Claudia; Carmouche, Richard; Newman, Susan; Salbaum, J. Michael; Berthoud, Hans-Rudolf

    2017-01-01

    Maternal obesity is known to predispose offspring to metabolic and neurodevelopmental abnormalities. While the mechanisms underlying these phenomena are unclear, high fat diets dramatically alter intestinal microbiota, and gut microbiota can impact physiological function. To determine if maternal diet-induced gut dysbiosis can disrupt offspring neurobehavioral function, we transplanted high fat diet- (HFD) or control low fat diet-associated (CD) gut microbiota to conventionally-housed female mice. Recipient mice were then bred and the behavioral phenotype of male and female offspring was tracked. While maternal behavior was unaffected, neonatal offspring from HFD dams vocalized less upon maternal separation than pups from CD dams. Furthermore, weaned male offspring from HFD dams had significant and selective disruptions in exploratory, cognitive, and stereotypical/compulsive behavior compared to male offspring from CD dams; while female offspring from HFD dams had increases in body weight and adiposity. 16S metagenomic analyses confirmed establishment of divergent microbiota in CD and HFD dams, with alterations in diversity and taxonomic distribution throughout pregnancy and lactation. Likewise, significant alterations in gut microbial diversity and distribution were noted in offspring from HFD dams compared to CD dams, and in males compared to females. Regression analyses of behavioral performance against differentially represented taxa suggest that decreased representation of specific members of the Firmicutes phylum predict behavioral decline in male offspring. Collectively, these data establish that high fat diet-induced maternal dysbiosis is sufficient to disrupt behavioral function in murine offspring in a sex-specific manner. Thus these data reinforce the essential link between maternal diet and neurologic programming in offspring and suggest that intestinal dysbiosis could link unhealthy modern diets to the increased prevalence of neurodevelopmental and

  4. Maternal obese-type gut microbiota differentially impact cognition, anxiety and compulsive behavior in male and female offspring in mice.

    PubMed

    Bruce-Keller, Annadora J; Fernandez-Kim, Sun-Ok; Townsend, R Leigh; Kruger, Claudia; Carmouche, Richard; Newman, Susan; Salbaum, J Michael; Berthoud, Hans-Rudolf

    2017-01-01

    Maternal obesity is known to predispose offspring to metabolic and neurodevelopmental abnormalities. While the mechanisms underlying these phenomena are unclear, high fat diets dramatically alter intestinal microbiota, and gut microbiota can impact physiological function. To determine if maternal diet-induced gut dysbiosis can disrupt offspring neurobehavioral function, we transplanted high fat diet- (HFD) or control low fat diet-associated (CD) gut microbiota to conventionally-housed female mice. Recipient mice were then bred and the behavioral phenotype of male and female offspring was tracked. While maternal behavior was unaffected, neonatal offspring from HFD dams vocalized less upon maternal separation than pups from CD dams. Furthermore, weaned male offspring from HFD dams had significant and selective disruptions in exploratory, cognitive, and stereotypical/compulsive behavior compared to male offspring from CD dams; while female offspring from HFD dams had increases in body weight and adiposity. 16S metagenomic analyses confirmed establishment of divergent microbiota in CD and HFD dams, with alterations in diversity and taxonomic distribution throughout pregnancy and lactation. Likewise, significant alterations in gut microbial diversity and distribution were noted in offspring from HFD dams compared to CD dams, and in males compared to females. Regression analyses of behavioral performance against differentially represented taxa suggest that decreased representation of specific members of the Firmicutes phylum predict behavioral decline in male offspring. Collectively, these data establish that high fat diet-induced maternal dysbiosis is sufficient to disrupt behavioral function in murine offspring in a sex-specific manner. Thus these data reinforce the essential link between maternal diet and neurologic programming in offspring and suggest that intestinal dysbiosis could link unhealthy modern diets to the increased prevalence of neurodevelopmental and

  5. 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

  6. Association between maternal intimate partner violence and incident obesity in preschool-aged children: results from the Fragile Families and Child Well-being Study.

    PubMed

    Boynton-Jarrett, Renée; Fargnoli, Jessica; Suglia, Shakira Franco; Zuckerman, Barry; Wright, Rosalind J

    2010-06-01

    To examine the impact of chronicity of maternal intimate partner violence (IPV) on obesity risk among preschool-aged children. Prospective cohort study. Several large US cities. A subsample of the Fragile Families and Child Well-being Study participants (n = 1595), who were children born between 1998 and 2000 and their parents interviewed at baseline and at 12, 36, and 60 months. Maternal report of restrictive, sexual, and physical abuse from an intimate partner. Chronic IPV was defined as any maternal IPV exposure during both pregnancy or infancy (0-12 months) and early childhood (36-60 months). Repeated measures of child body mass index. Among the 1595 children, 16.5% were obese at age 5 years and 49.4% of the mothers reported some form of IPV. Compared with those who had no IPV exposure, children whose mothers reported chronic IPV had an elevated risk for obesity at age 5 years (adjusted odds ratio = 1.80; 95% confidence interval, 1.24-2.61). Stratified analyses indicated increased risk for obesity among girls with a maternal history of chronic IPV (adjusted odds ratio = 2.21; 95% confidence interval, 1.30-3.75) compared with boys (adjusted odds ratio = 1.66; 95% confidence interval, 0.94-2.93) and a larger effect of any maternal IPV on obesity among children living in less safe neighborhoods (adjusted odds ratio = 1.56; 95% confidence interval, 1.03-2.36). Chronic maternal IPV is associated with increased risk of obesity among preschool-aged children. Preventing family violence and improving community safety may help reduce childhood obesity.

  7. Maternal obesity during pregnancy and premature mortality from cardiovascular event in adult offspring: follow-up of 1 323 275 person years

    PubMed Central

    Allan, Keith M; Raja, Edwin A; Bhattacharya, Sohinee; McNeill, Geraldine; Hannaford, Philip C; Sarwar, Nadeem; Lee, Amanda J; Bhattacharya, Siladitya; Norman, Jane E

    2013-01-01

    Objectives To determine whether maternal obesity during pregnancy is associated with increased mortality from cardiovascular events in adult offspring. Design Record linkage cohort analysis. Setting Birth records from the Aberdeen Maternity and Neonatal databank linked to the General Register of Deaths, Scotland, and the Scottish Morbidity Record systems. Population 37 709 people with birth records from 1950 to present day. Main outcome measures Death and hospital admissions for cardiovascular events up to 1 January 2012 in offspring aged 34-61. Maternal body mass index (BMI) was calculated from height and weight measured at the first antenatal visit. The effect of maternal obesity on outcomes in offspring was tested with time to event analysis with Cox proportional hazard regression to compare outcomes in offspring of mothers in underweight, overweight, or obese categories of BMI compared with offspring of women with normal BMI. Results All cause mortality was increased in offspring of obese mothers (BMI >30) compared with mothers with normal BMI after adjustment for maternal age at delivery, socioeconomic status, sex of offspring, current age, birth weight, gestation at delivery, and gestation at measurement of BMI (hazard ratio 1.35, 95% confidence interval 1.17 to 1.55). In adjusted models, offspring of obese mothers also had an increased risk of hospital admission for a cardiovascular event (1.29, 1.06 to 1.57) compared with offspring of mothers with normal BMI. The offspring of overweight mothers also had a higher risk of adverse outcomes. Conclusions Maternal obesity is associated with an increased risk of premature death in adult offspring. As one in five women in the United Kingdom is obese at antenatal booking, strategies to optimise weight before pregnancy are urgently required. PMID:23943697

  8. 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

  9. Maternal depression, stress and feeding styles: towards a framework for theory and research in child obesity

    USDA-ARS?s Scientific Manuscript database

    Against the background of rising rates of obesity in children and adults in the USA, and modest effect sizes for obesity interventions, the aim of the present narrative review paper is to extend the UNICEF care model to focus on childhood obesity and its associated risks with an emphasis on the emot...

  10. Early growth response protein-1 mediates lipotoxicity-associated placental inflammation: Role in maternal obesity

    USDA-ARS?s Scientific Manuscript database

    Obesity is associated with low-grade chronic inflammation, which contributes to cellular dysfunction promoting metabolic disease. Obesity during pregnancy leads to a pro-inflammatory milieu in the placenta; however, the underlying causes for obesity-induced placental inflammation remain unclear. H...

  11. 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...

  12. 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

  13. 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.

  14. RNA-seq Analysis of the Rat Placentation Site Reveals Maternal Obesity-Associated Changes in Placental and Offspring Thyroid Hormone Signaling

    PubMed Central

    Saben, Jessica; Kang, Ping; Zhong, Ying; Thakali, Keshari M.; Gomez-Acevedo, Horacio; Borengasser, Sarah J.; Andres, Aline; Badger, Thomas M.; Shankar, Kartik

    2014-01-01

    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 unknown. Methods Using a rat maternal obesity model, we conducted transcriptomic profiling of the utero-placental compartments and fetal liver (FL) at dpc 18.5, in conjunction with analyses of mRNA expression of key thyroid hormone (TH) signaling genes in the placenta, fetus and weanling offspring. Results and Discussion Gene expression analysis of placenta and offspring revealed that each utero-placental compartment responds distinctly to maternal OB with changes in inflammatory signaling, lipid metabolism and hormone stimulus being the predominant effects. OB-induced alterations in 17 genes were confirmed by qPCR, including reductions in thyrotropin-releasing hormone (Trh) in JZ. We further characterized mRNA and protein expression of TH signaling regulators including deiodinases (Dio), TH receptors (Tr), and downstream targets (uncoupling proteins (Ucp)). A concerted down-regulation of multiple facets of thyroid hormone signaling in the JZ and FL was observed. JZ expression of thyroid hormone signaling components Trh, Dio2, Trα, and Ucp2 were negatively associated with maternal leptin. mRNA expression of TRH, TRβ and UCP1 were also decreased in term placenta from OB women. Finally, our studies identified persistent impairments in expression of TH related genes in tissues from offspring of obese dams. Conclusions The role of lower placental thyroid expression is worthy of further study as a possible pathway that leads to low energy metabolism and obesity in animals born to obese mothers. PMID:25449029

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

    PubMed Central

    Borengasser, Sarah J.; Faske, Jennifer; Kang, Ping; Blackburn, Michael L.; Badger, Thomas M.

    2014-01-01

    The proportion of pregnant women who are obese at conception 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 maternally inherited, and we have previously shown impaired mitochondrial function in rat offspring exposed to maternal obesity in utero. Mitochondrial health is maintained by mitochondrial dynamics, or the processes of fusion and fission, which serve to repair damaged mitochondria, remove irreparable mitochondria, and maintain mitochondrial morphology. An imbalance between fusion and fission has been associated with obesity, insulin resistance, and reproduction complications. In the present study, we examined the influence of maternal obesity and postweaning high-fat diet (HFD) on key regulators of mitochondrial fusion and fission in rat offspring at important developmental milestones which included postnatal day (PND)35 (2 wk HFD) and PND130 (∼16 wk HFD). Our results indicate HFD-fed offspring had reduced mRNA expression of presenilin-associated rhomboid-like (PARL), optic atrophy (OPA)1, mitofusin (Mfn)1, Mfn2, fission (Fis)1, and nuclear respiratory factor (Nrf)1 at PND35, while OPA1 and Mfn2 remained decreased at PND130. Putative transcriptional regulators of mitochondrial dynamics were reduced in rat placenta and offspring liver and skeletal muscle [peroxisome proliferator-activated receptor gamma coactivator (PGC1)α, PGC1β, and estrogen-related receptor (ERR)α], consistent with indirect calorimetry findings revealing reduced energy expenditure and impaired fat utilization. Overall, maternal obesity detrimentally alters mitochondrial targets that may contribute to impaired mitochondrial health and increased obesity susceptibility in later life. PMID:25336449

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

    PubMed

    Borengasser, Sarah J; Faske, Jennifer; Kang, Ping; Blackburn, Michael L; Badger, Thomas M; Shankar, Kartik

    2014-12-01

    The proportion of pregnant women who are obese at conception 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 maternally inherited, and we have previously shown impaired mitochondrial function in rat offspring exposed to maternal obesity in utero. Mitochondrial health is maintained by mitochondrial dynamics, or the processes of fusion and fission, which serve to repair damaged mitochondria, remove irreparable mitochondria, and maintain mitochondrial morphology. An imbalance between fusion and fission has been associated with obesity, insulin resistance, and reproduction complications. In the present study, we examined the influence of maternal obesity and postweaning high-fat diet (HFD) on key regulators of mitochondrial fusion and fission in rat offspring at important developmental milestones which included postnatal day (PND)35 (2 wk HFD) and PND130 (∼16 wk HFD). Our results indicate HFD-fed offspring had reduced mRNA expression of presenilin-associated rhomboid-like (PARL), optic atrophy (OPA)1, mitofusin (Mfn)1, Mfn2, fission (Fis)1, and nuclear respiratory factor (Nrf)1 at PND35, while OPA1 and Mfn2 remained decreased at PND130. Putative transcriptional regulators of mitochondrial dynamics were reduced in rat placenta and offspring liver and skeletal muscle [peroxisome proliferator-activated receptor gamma coactivator (PGC1)α, PGC1β, and estrogen-related receptor (ERR)α], consistent with indirect calorimetry findings revealing reduced energy expenditure and impaired fat utilization. Overall, maternal obesity detrimentally alters mitochondrial targets that may contribute to impaired mitochondrial health and increased obesity susceptibility in later life.

  17. Maternal and Early Childhood Risk Factors for Overweight and Obesity among Low-Income Predominantly Black Children at Age Five Years: A Prospective Cohort Study

    PubMed Central

    Janjua, Naveed Zafar; Mahmood, Bushra; Islam, M. Aminul; Goldenberg, Robert L.

    2012-01-01

    Objective. To identify maternal and early childhood risk factors for obesity and overweight among children at age 5 in the state of Alabama. Methods. We recruited 740 mothers during early pregnancy from University of Alabama Prenatal Clinics in a prospective cohort study and followed them throughout pregnancy. We followed their children from birth until 5 years of age. The main outcome measure was obesity (BMI for age and sex ≥ 95th percentile) at 5 years of age. We used poisson regression with robust variance estimation to compute risk ratio (RR). Results. At the 5th year of followup, 71 (9.6%) of the children were obese and 85 (11.5%) were overweight (BMI ≥ 85th–<95th percentile). In multivariable analysis, maternal prepregnancy overweight (RR: 2.30, 95% CI: 1.29–4.11) and obesity (RR: 2.53, 95% CI: 1.49–4.31), and child's birth weight >85th percentile (RR: 2.04, 95% CI: 1.13–3.68) were associated with childhood obesity. Maternal prepregnancy BMI, birth weight, and maternal smoking were associated with the child being overweight 1–12 cigarettes/day versus 0 cigarettes/day (RR: 1.40, 95% CI: 1.02–1.91). Conclusion. Children of overweight and obese mothers, and children with higher birth weight, are more likely to be obese and overweight at age 5. Maternal smoking 1–12 cigarettes per day is associated with the child being overweight. PMID:23056928

  18. 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

  19. Maternal obesity programs offspring non-alcoholic fatty liver disease through disruption of 24-h rhythms in mice.

    PubMed

    Mouralidarane, A; Soeda, J; Sugden, D; Bocianowska, A; Carter, R; Ray, S; Saraswati, R; Cordero, P; Novelli, M; Fusai, G; Vinciguerra, M; Poston, L; Taylor, P D; Oben, J A

    2015-09-01

    Maternal obesity increases offspring propensity to metabolic dysfunctions and to non-alcoholic fatty liver disease (NAFLD), which may lead to cirrhosis or liver cancer. The circadian clock is a transcriptional/epigenetic molecular machinery synchronising physiological processes to coordinate energy utilisation within a 24-h light/dark period. Alterations in rhythmicity have profound effects on metabolic pathways, which we sought to investigate in offspring with programmed NAFLD. Mice were fed a standard or an obesogenic diet (OD), before and throughout pregnancy, and during lactation. Offspring were weaned onto standard or an OD at 3 weeks postpartum and housed in 12:12 light/dark conditions. Biochemical and histological indicators of NAFLD and fibrosis, analysis of canonical clock genes with methylation status and locomotor activity were investigated at 6 months. We show that maternal obesity interacts with an obesogenic post-weaning diet to promote the development of NAFLD with disruption of canonical metabolic rhythmicity gene expression in the liver. We demonstrate hypermethylation of BMAL-1 (brain and muscle Arnt like-1) and Per2 promoter regions and altered 24-h rhythmicity of hepatic pro-inflammatory and fibrogenic mediators. These data implicate disordered circadian rhythms in NAFLD and suggest that disruption of this system during critical developmental periods may be responsible for the onset of chronic liver disease in adulthood.

  20. Maternal obesity in females born small: Pregnancy complications and offspring disease risk.

    PubMed

    Mahizir, Dayana; Briffa, Jessica F; Hryciw, Deanne H; Wadley, Glenn D; Moritz, Karen M; Wlodek, Mary E

    2016-01-01

    Obesity is a major public health crisis, with 1.6 billion adults worldwide being classified as overweight or obese in 2014. Therefore, it is not surprising that the number of women who are overweight or obese at the time of conception is increasing. Obesity during pregnancy is associated with the development of gestational diabetes and preeclampsia. The developmental origins of health and disease hypothesis proposes that perturbations during critical stages of development can result in adverse fetal changes that leads to an increased risk of developing diseases in adulthood. Of particular concern, children born to obese mothers are at a greater risk of developing cardiometabolic disease. One subset of the population who are predisposed to developing obesity are children born small for gestational age, which occurs in 10% of pregnancies worldwide. Epidemiological studies report that these growth-restricted children have an increased susceptibility to type 2 diabetes, obesity, and hypertension. Importantly during pregnancy, growth-restricted females have a higher risk of developing cardiometabolic disease, indicating that they may have an exacerbated phenotype if they are also overweight or obese. Thus, the development of early pregnancy interventions targeted to obese mothers may prevent their children from developing cardiometabolic disease in adulthood. © 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

  1. 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.

  2. The effect of maternal obesity on the rate of failed induction of labor.

    PubMed

    Wolfe, Katherine B; Rossi, Rocco A; Warshak, Carri R

    2011-08-01

    The purpose of this study was to quantify the relationship between class of obesity and rate of failed induction of labor. Using the Ohio Department of Health's birth certificate database from January 1, 2006, through December 31, 2007, we performed a population-based cohort study that compared failed induction of labor rates between obese and normal-weight women. The rate of induction is associated with increasing body mass index from 28% in normal-weight women to 34% in class III obese women (body mass index, ≥40 kg/m2). Induction failure rates are also associated with increasing obesity class from 13% in normal-weight women to 29% in class III obese women. Women with class III obesity without a previous vaginal delivery and a macrosomic fetus had the highest rate of failed induction at 80%. Obesity is associated with an increased risk of failed labor induction that appears to be related directly to increasing class of obesity. Copyright © 2011 Mosby, Inc. All rights reserved.

  3. Maternal obesity and gestational weight gain are risk factors for infant death.

    PubMed

    Bodnar, Lisa M; Siminerio, Lara L; Himes, Katherine P; Hutcheon, Jennifer A; Lash, Timothy L; Parisi, Sara M; Abrams, Barbara

    2016-02-01

    Assessment of the joint and independent relationships of gestational weight gain and prepregnancy body mass index (BMI) on risk of infant mortality was performed. This study used Pennsylvania linked birth-infant death records (2003-2011) from infants without anomalies born to mothers with prepregnancy BMI categorized as underweight (n = 58,973), normal weight (n = 610,118), overweight (n = 296,630), grade 1 obesity (n = 147,608), grade 2 obesity (n = 71,740), and grade 3 obesity (n = 47,277). Multivariable logistic regression models stratified by BMI category were used to estimate dose-response associations between z scores of gestational weight gain and infant death after confounder adjustment. Infant mortality risk was lowest among normal-weight women and increased with rising BMI category. For all BMI groups except for grade 3 obesity, there were U-shaped associations between gestational weight gain and risk of infant death. Weight loss and very low weight gain among women with grades 1 and 2 obesity were associated with high risks of infant mortality. However, even when gestational weight gain in women with obesity was optimized, the predicted risk of infant death remained higher than that of normal-weight women. Interventions aimed at substantially reducing preconception weight among women with obesity and avoiding very low or very high gestational weight gain may reduce risk of infant death. © 2015 The Obesity Society.

  4. Impact of Restricted Maternal Weight Gain on Fetal Growth and Perinatal Morbidity in Obese Women With Type 2 Diabetes

    PubMed Central

    Ásbjörnsdóttir, Björg; Rasmussen, Signe S.; Kelstrup, Louise; Damm, Peter; Mathiesen, Elisabeth R.

    2013-01-01

    OBJECTIVE Since January 2008, obese women with type 2 diabetes were advised to gain 0–5 kg during pregnancy. The aim with this study was to evaluate fetal growth and perinatal morbidity in relation to gestational weight gain in these women. RESEARCH DESIGN AND METHODS A retrospective cohort comprised the records of 58 singleton pregnancies in obese women (BMI ≥30 kg/m2) with type 2 diabetes giving birth between 2008 and 2011. Birth weight was evaluated by SD z score to adjust for gestational age and sex. RESULTS Seventeen women (29%) gained ≤5 kg, and the remaining 41 gained >5 kg. The median (range) gestational weight gains were 3.7 kg (−4.7 to 5 kg) and 12.1 kg (5.5–25.5 kg), respectively. Prepregnancy BMI was 33.5 kg/m2 (30–53 kg/m2) vs. 36.8 kg/m2 (30–48 kg/m2), P = 0.037, and median HbA1c was 6.7% at first visit in both groups and decreased to 5.7 and 6.0%, P = 0.620, in late pregnancy, respectively. Gestational weight gain ≤5 kg was associated with lower birth weight z score (P = 0.008), lower rates of large-for-gestational-age (LGA) infants (12 vs. 39%, P = 0.041), delivery closer to term (268 vs. 262 days, P = 0.039), and less perinatal morbidity (35 vs. 71%, P = 0.024) compared with pregnancies with maternal weight gain >5 kg. CONCLUSIONS In this pilot study in obese women with type 2 diabetes, maternal gestational weight gain ≤5 kg was associated with a more proportionate birth weight and less perinatal morbidity. PMID:23248191

  5. Growth and obesity through the first 7 y of life in association with levels of maternal glycemia during pregnancy: a prospective cohort study12

    PubMed Central

    Zhu, Yeyi; Olsen, Sjurdur F; Mendola, Pauline; Yeung, Edwina H; Vaag, Allan; Bowers, Katherine; Liu, Aiyi; Bao, Wei; Li, Shanshan; Madsen, Camilla; Grunnet, Louise G; Granström, Charlotta; Hansen, Susanne; Martin, Kelly; Chavarro, Jorge E; Hu, Frank B; Langhoff-Roos, Jens; Damm, Peter; Zhang, Cuilin

    2016-01-01

    Background: Given the long-term adverse sequelae of childhood obesity, identification of early life factors related to fetal growth and childhood obesity is warranted. Investigation on growth and obesity in early life in association with intrauterine exposure to maternal hyperglycemia, a common metabolic pregnancy complication, is of public health significance and clinical implications. Objective: We investigated the association of fasting plasma glucose (FPG) concentrations during pregnancy with offspring growth and risk of overweight/obesity through age 7 y, after adjustment for confounders, including maternal prepregnancy obesity status. Design: FPG concentrations at 28 gestational weeks (IQR: 22–32 wk) were extracted from medical records for 661 pregnancies complicated by gestational diabetes mellitus in the Danish National Birth Cohort (1996–2002). Offspring’s ponderal index was derived from birth weight and length; age- and sex-specific body mass index (BMI) z scores at 5 mo, 12 mo, and 7 y were calculated based on WHO reference data. Relations between FPG and offspring growth and obesity were assessed by linear and Poisson regression with robust standard errors, adjusting for maternal prepregnancy BMI and sociodemographic and perinatal factors. Results: At birth, maternal FPG during pregnancy was significantly associated with offspring ponderal index (β = 0.46; 95% CI: 0.14, 0.78 per 1-mmol/L increase) and risk of macrosomia (birth weight >4000 g) (RR = 1.21; 95% CI: 1.07, 1.38 per 1-mmol/L increase). At 7 y, higher maternal FPG concentrations were significantly associated with increased BMI z scores (β = 0.20; 95% CI: 0.04, 0.36) and elevated risk of overweight/obesity (RR = 1.21; 95% CI: 1.01, 1.50). Additional adjustment for birth weight and childhood lifestyle factors did not appreciably alter results. No associations were observed at 5 or 12 mo. Conclusion: Among women with gestational diabetes mellitus, maternal FPG concentrations during

  6. 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.

  7. Delayed onset of lactogenesis among first-time mothers is related to maternal obesity and factors associated with ineffective breastfeeding.

    PubMed

    Nommsen-Rivers, Laurie A; Chantry, Caroline J; Peerson, Janet M; Cohen, Roberta J; Dewey, Kathryn G

    2010-09-01

    Delayed onset of lactogenesis (OL) is most common in primiparas and increases the risk of excess neonatal weight loss, formula supplementation, and early weaning. We examined variables associated with delayed OL among first-time mothers who delivered at term and initiated breastfeeding (n = 431). We conducted in-person interviews during pregnancy and at days 0, 3, and 7 postpartum and extracted obstetric and newborn information from medical records. We defined OL as delayed if it occurred after 72 h and used chi-square analysis to examine its association with potential risk factors across 6 dimensions: 1) prenatal characteristics, 2) maternal anthropometric characteristics, 3) labor and delivery experience, 4) newborn characteristics, 5) maternal postpartum factors, and 6) infant feeding variables. We examined independent associations by using multivariable logistic regression analysis. Median OL was 68.9 h postpartum; 44% of mothers experienced delayed OL. We observed significant bivariate associations between delayed OL and variables in all 6 dimensions (P < 0.05). In a multivariate model adjusted for prenatal feeding intentions, independent risk factors for delayed OL were maternal age > or =30 y, body mass index in the overweight or obese range, birth weight >3600 g, absence of nipple discomfort between 0-3 d postpartum, and infant failing to "breastfeed well" > or =2 times in the first 24 h. Postpartum edema was significant in an alternate model excluding body mass index (P < 0.05). The risk factors for delayed OL are multidimensional. Public health and obstetric and maternity care interventions are needed to address what has become an alarmingly common problem among primiparas.

  8. Maternal depression, stress and feeding styles: towards a framework for theory and research in child obesity.

    PubMed

    El-Behadli, Ana F; Sharp, Carla; Hughes, Sheryl O; Obasi, Ezemenari M; Nicklas, Theresa A

    2015-01-01

    Against the background of rising rates of obesity in children and adults in the USA, and modest effect sizes for obesity interventions, the aim of the present narrative review paper is to extend the UNICEF care model to focus on childhood obesity and its associated risks with an emphasis on the emotional climate of the parent-child relationship within the family. Specifically, we extended the UNICEF model by applying the systems approach to childhood obesity and by combining previously unintegrated sets of literature across multiple disciplines including developmental psychology, clinical psychology and nutrition. Specifically, we modified the extended care model by explicitly integrating new linkages (i.e. parental feeding styles, stress, depression and mother's own eating behaviour) that have been found to be associated with the development of children's eating behaviours and risk of childhood obesity. These new linkages are based on studies that were not incorporated into the original UNICEF model, but suggest important implications for childhood obesity. In all, this narrative review offers important advancements to the scientific understanding of familial influences on children's eating behaviours and childhood obesity.

  9. 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.

  10. Maternal obesity induced by a high fat diet causes altered cellular development in fetal brains suggestive of a predisposition of offspring to neurological disorders in later life.

    PubMed

    Stachowiak, Ewa K; Srinivasan, Malathi; Stachowiak, Michal K; Patel, Mulchand S

    2013-12-01

    Fetal development in an obese maternal intrauterine environment has been shown to predispose the offspring for a number of metabolic disorders in later life. The observation that a large percentage of women of child-bearing age in the US are overweight/obese during pregnancy is therefore a source of concern. A high fat (HF) diet-induced obesity in female rats has been used as a model for maternal obesity. The objective of this study was to determine cellular development in brains of term fetuses of obese rats fed a HF diet from the time of weaning. Fetal brains were dissected out on gestational day 21 and processed for immunohistochemical analysis in the hypothalamic as well as extra-hypothalamic regions. The major observation of this study is that fetal development in the obese HF female rat induced several alterations in the HF fetal brain. Marked increases were observed in orexigenic signaling and a significant decrease was observed for anorexigenic signaling in the vicinity of the 3rd ventricle in HF brains. Additionally, our results indicated diminished migration and maturation of stem-like cells in the 3rd ventricular region as well as in the brain cortex. The results from the present study indicate developmental alterations in the hypothalamic and extra-hypothalamic regions in the HF fetal brain suggestive of a predisposition for the development of obesity and possibly neurodevelopmental abnormalities in the offspring.

  11. 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

  12. 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

  13. Insatiable insecurity: maternal obesity as a risk factor for mother-child attachment and child weight.

    PubMed

    Keitel-Korndörfer, Anja; Sierau, Susan; Klein, Annette M; Bergmann, Sarah; Grube, Matthias; von Klitzing, Kai

    2015-01-01

    Childhood obesity has become a rising health problem, and because parental obesity is a basic risk factor for childhood obesity, biological factors have been especially considered in the complex etiology. Aspects of the family interaction, e.g., mother-child attachment, have not been the main focus. Our study tried to fill this gap by investigating whether there is a difference between children of obese and normal weight mothers in terms of mother-child attachment, and whether mother-child attachment predicts child's weight, in a sample of 31 obese and 31 normal weight mothers with children aged 19 to 58 months. Mother-child attachment was measured with the Attachment Q-Set. We found that (1) children of obese mothers showed a lower quality of mother-child attachment than children of normal weight mothers, which indicates that they are less likely to use their mothers as a secure base; (2) the attachment quality predicted child`s BMI percentile; and (3) the mother-child attachment adds incremental validity to the prediction of child's BMI beyond biological parameters (child's BMI birth percentile, BMI of the parents) and mother's relationship status. Implications of our findings are discussed.

  14. Effect of pre-existing maternal obesity, gestational diabetes and adipokines on the expression of genes involved in lipid metabolism in adipose tissue.

    PubMed

    Lappas, Martha

    2014-02-01

    To determine the effect of maternal obesity, gestational diabetes mellitus (GDM) and adipokines on the expression of genes involved in fatty acid uptake, transport, synthesis and metabolism. Human subcutaneous and omental adipose tissues were obtained from lean, overweight and obese normal glucose tolerant (NGT) women and women with GDM. Quantitative RT-PCR (qRT-PCR) was performed to determine the level of expression. Adipose tissue explants were performed to determine the effect of the adipokines TNFα, IL-1β and leptin on adipose tissue gene expression. Pre-existing maternal obesity and GDM are associated with decreased expression in genes involved in fatty acid uptake and intracellular transport (LPL, FATP2, FATP6, FABPpm and ASCL1), triacylglyceride (TAG) biosynthesis (MGAT1,7 MGAT2 and DGAT1), lipogenesis (FASN) and lipolysis (PNPLA2, HSL and MGLL). Decreased gene expression was also observed for the transcription factors involved in lipid metabolism (LXRα, PPARα, PPARδ, PPARγ, RXRα and SREBP1c). On the other hand, the gene expression of the adipokines TNFα, IL-1β and or leptin was increased in adipose tissue from obese and GDM women. Functional in vitro studies revealed that these adipokines decreased the gene expression of LPL, FATP2, FATP6, ASCL1, PNPLA2, PPARδ, PPARγ and RXRα. Pregnancies complicated by pre-existing maternal obesity and GDM are associated with abnormal adipose tissue lipid metabolism, which may play a role in the pathogenesis of these diseases. © 2014.

  15. Effects of an antenatal dietary intervention on maternal anthropometric measures in pregnant women with obesity

    PubMed Central

    Kannieappan, Lavern M.; Grivell, Rosalie M.; Deussen, Andrea R.; Moran, Lisa J.; Yelland, Lisa N.; Owens, Julie A.

    2015-01-01

    Objective The effect of providing antenatal dietary and lifestyle advice on secondary measures of maternal anthropometry was evaluated and their correlation with both gestational weight gain and infant birth weight was assessed. Methods In a multicenter, randomized controlled trial, pregnant women with BMI of ≥25 kg/m2 received either Lifestyle Advice or Standard Care. Maternal anthropometric outcomes included arm circumference, biceps, triceps, and subscapular skinfold thickness measurements (SFTM), percentage body fat (BF), gestational weight gain, and infant birth weight. The intention to treat principles were utilized by the analyses. Results The measurements were obtained from 807 (74.7%) women in the Lifestyle Advice Group and 775 (72.3%) women in the Standard Care Group. There were no statistically significant differences identified between the treatment groups with regards to arm circumference, biceps, triceps, and subscapular SFTM, or percentage BF at 36‐week gestation. Maternal anthropometric measurements were not significantly correlated with either gestational weight gain or infant birth weight. Conclusions Among pregnant women with a BMI of ≥25 kg/m2, maternal SFTM were not modified by an antenatal dietary and lifestyle intervention. Furthermore, maternal SFTM correlate poorly with both gestational weight gain and infant birth weight. PMID:26175260

  16. Maternal Obesity in Sheep Increases Fatty Acid Synthesis, Upregulates Nutrient Transporters, and Increases Adiposity in Adult Male Offspring after a Feeding Challenge

    PubMed Central

    Long, Nathan M.; Rule, Daniel C.; Tuersunjiang, Nuermaimaiti; Nathanielsz, Peter W.; Ford, Stephen P.

    2015-01-01

    Maternal obesity in women is increasing worldwide. The objective of this study was to evaluate differences in adipose tissue metabolism and function in adult male offspring from obese and control fed mothers subjected to an ad libitum feeding challenge. We developed a model in which obese ewes were fed 150% of feed provided for controls from 60 days before mating to term. All ewes were fed to requirements during lactation. After weaning, F1 male offspring were fed only to maintenance requirements until adulthood (control = 7, obese = 6), when they were fed ad libitum for 12 weeks with intake monitored. At the end of the feeding challenge offspring were given an intravenous glucose tolerance test (IVGTT), necropsied, and adipose tissue collected. During the feeding trial F1obese males consumed more (P < 0.01), gained more weight (P < 0.01) and became heavier (P < 0.05) than F1control males. During IVGTT, Obese F1 offspring were hyperglycemic and hypoinsulinemic (P < 0.01) compared to F1 control F1. At necropsy perirenal and omental adipose depots weights were 47% and 58% greater respectively and subcutaneous fat thickness 41% greater in F1obese vs F1control males (P < 0.05). Adipocyte diameters were greater (P ≤ 0.04) in perirenal, omental and subcutaneous adipose depots in F1obese males (11, 8 and 7% increase vs. control, respectively). When adipose tissue was incubated for 2 hrs with C-14 labeled acetate, subcutaneous, perirenal, and omental adipose tissue of F1 obese males exhibited greater incorporation (290, 83, and 90% increase vs. control, respectively P < 0.05) of acetate into lipids. Expression of fatty acid transporting, binding, and syntheses mRNA and protein was increased (P < 0.05) compared to F1 control offspring. Maternal obesity increased appetite and adiposity associated with increased adipocyte diameters and increased fatty acid synthesis in over-nourished adult male offspring. PMID:25875659

  17. Maternal undernutrition and fetal developmental programming of obesity: the glucocorticoid connection.

    PubMed

    Correia-Branco, Ana; Keating, Elisa; Martel, Fátima

    2015-02-01

    An adequate maternal nutrition during pregnancy is crucial for the health outcome of offspring in adulthood. Maternal undernutrition during critical periods of fetal development can program the fetus for metabolic syndrome (MetS) later in life, especially when postnatally challenged with a hypernutritive diet. Adipogenesis, which begins in utero and accelerates in neonatal life, is a major candidate for developmental programming. During fetal development, the hypothalamic-pituitary-adrenal (HPA) axis is extremely susceptible to programming, and the HPA tone is increased throughout life in undernourished conditions. As a consequence, an alteration in the expression and function of glucocorticoid (GC) receptors and of the major GC regulatory enzymes (11β-hydroxysteroid dehydrogenase 1 and -2) occurs. In this review, we will give insights into the role of maternoplacental adverse interactions under the specific context of maternal undernutrition, for later-in-life MetS development, with a special emphasis on the role of GCs. © The Author(s) 2014.

  18. The effect of maternal obesity on initiation and duration of breast-feeding in Greece: the GENESIS study.

    PubMed

    Manios, Yannis; Grammatikaki, Evangelia; Kondaki, Katerina; Ioannou, Elina; Anastasiadou, Anastasia; Birbilis, Manolis

    2009-04-01

    The current paper aims to describe the characteristics of mothers failing to initiate breast-feeding, provide information on the factors contributing to longer duration of breast-feeding and identify the association of maternal obesity with both initiation and duration of breast-feeding in the Greek population. Data from the cross-sectional GENESIS (Growth, Exercise and Nutrition Epidemiological Study In preSchoolers) study were used. Mothers were categorized by their pre-pregnancy BMI and their gestational weight gain according to guidelines from the Institute of Medicine. Preschool children aged 1-5 years in five counties in Greece. Preschoolers (n 2374) with full maternal anthropometric data before and during pregnancy and breast-feeding data. A higher percentage of mothers with increased pre-pregnancy BMI or high gestational weight gain failed to initiate breast-feeding compared with their normal-weight counterparts. Obese mothers were 2.86 times more likely to fail in initiating breast-feeding in a multiple logistic regression model. Multiple linear regression analysis showed that among women initiating breast-feeding, those who were either underweight before pregnancy or smoked at the third trimester of pregnancy breast-fed their children for about 1.5 weeks less than their normal-weight or non-smoking counterparts, respectively. Similarly, multiparous women breast-fed their children for about 7 weeks less than uniparous women. In women who initiated breast-feeding, no significant differences in breast-feeding duration were found between women of different gestational weight gains. Mothers with high pre-pregnancy BMI are less likely to initiate breast-feeding while high gestational weight gain has no effect on either the initiation or duration of breast-feeding in Greece.

  19. Maternal Pre-Pregnancy Obesity and Risk for Inattention and Negative Emotionality in Children

    ERIC Educational Resources Information Center

    Rodriguez, Alina

    2010-01-01

    Objective: 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. Methods: A Swedish population-based prospective pregnancy-offspring cohort was followed up when children were 5 years old (N = 1,714).…

  20. Maternal Pre-Pregnancy Obesity and Risk for Inattention and Negative Emotionality in Children

    ERIC Educational Resources Information Center

    Rodriguez, Alina

    2010-01-01

    Objective: 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. Methods: A Swedish population-based prospective pregnancy-offspring cohort was followed up when children were 5 years old (N = 1,714).…

  1. Maternal obesity in Europe: where do we stand and how to move forward?: A scientific paper commissioned by the European Board and College of Obstetrics and Gynaecology (EBCOG).

    PubMed

    Devlieger, Roland; Benhalima, Katrien; Damm, Peter; Van Assche, André; Mathieu, Chantal; Mahmood, Tahir; Dunne, Fidelma; Bogaerts, Annick

    2016-06-01

    Paralleling the global epidemic of obesity figures in the general population, the incidence of maternal obesity (BMI>30kg/m(2) at the start of pregnancy) has been rising over the last world. While most European countries do not systematically report obesity figures in their pregnant population, the prevalence of maternal obesity varies from 7 to 25% and seems strongly related to social and educational inequalities. Obesity during pregnancy represents an important preventable risk factor for adverse pregnancy outcomes and is associated with negative long-term health outcomes for both mothers and offspring. These effects are often aggravated by the high incidence of abnormal glucose tolerance and excessive gestational weight gain found in this group. The main controversies around the management of the obese pregnant women are related to (1) the value of repeated weighing during pregnancy, (2) the optimal gestational weight gain to advise and the lifestyle messages to deliver in order to achieve this, (3) the optimal strategy and timing of screening for gestational diabetes (GDM) and (4) the optimal timing and mode of delivery. These controversies are reviewed in this review, with the exception of screening for gestational diabetes that is discussed extensively elsewhere in this issue (Benhalima et al.). An agenda for research is proposed with the hope that it will catch the attention of policy-makers and funders and ultimately lead to the development of European-wide evidence-based guidelines for clinicians.

  2. Nutraceutical up-regulation of serotonin paradoxically induces compulsive behavior

    USDA-ARS?s Scientific Manuscript database

    The role of diet in either the etiology or treatment of complex mental disorder is highly controversial in psychiatry. However, physiological mechanisms by which diet can influence brain chemistry – particularly that of serotonin – are well established. Here we show that dietary up-regulation of br...

  3. 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.

  4. Differences in Obesity Rates Among Minority and White Women: The Latent Role of Maternal Stress.

    PubMed

    Patchen, Loral; Rebok, George; Astone, Nan M

    2016-07-01

    White and minority women experience different rates of obesity in the United States. Yet our understanding of the dynamics that give rise to this gap remains limited. This article presents a conceptual framework that considers pathways leading to these different rates. It draws upon the life-course perspective, allostatic load, and the weathering hypothesis to identify pathways linking childbearing, stress, and obesity. This conceptual framework extends prior work by identifying age at first birth as an important parameter that influences these pathways. Empirical evidence to test these pathways is needed.

  5. Women's and Midwives' Perspectives on the Design of a Text Messaging Support for Maternal Obesity Services: An Exploratory Study

    PubMed Central

    Soltani, H.; Furness, P. J.; Arden, M. A.; McSeveny, K.; Garland, C.; Sustar, H.; Dearden, A.

    2012-01-01

    This study was aimed to explore women's and midwives' views on the use of mobile technology in supporting obese pregnant women with healthy lifestyle choices. A purposive sample of 14 women and midwives participated in four focus groups in Doncaster, UK. A content analysis of the transcripts from the first focus group led to the emergence of three main constructs with associated subcategories including Benefits (“modernising,” “motivating,” “reminding,” and “reducing” the sense of isolation), Risks and Limitations (possibility of “being offensive,” “creating pressure or guilt,” and “being influenced by mood”), and Service Delivery (making it “available to all pregnant women,” giving attention to the “message tone” and development of “message content”). They also suggested the use of other modalities such as web-based services for weight management during pregnancy. Based on the above results a text messaging service was developed and presented to the 2nd focus group participants who confirmed the positive views from the first focus group on the use of the text messaging as being supportive and informative. The participants also welcomed “women's engagement and choice” in deciding the content, timing and frequency of messages. The results informed the development of a text messaging service to support maternal obesity management. The implementation and acceptability of this service requires further investigation. PMID:22900153

  6. Maternal obesity induces epigenetic modifications to facilitate Zfp423 expression and enhance adipogenic differentiation in fetal mice.

    PubMed

    Yang, Qi-Yuan; Liang, Jun-Fang; Rogers, Carl J; Zhao, Jun-Xing; Zhu, Mei-Jun; Du, Min

    2013-11-01

    Maternal obesity (MO) predisposes offspring to obesity and type 2 diabetes despite poorly defined mechanisms. Zfp423 is the key transcription factor committing cells to the adipogenic lineage, with exceptionally dense CpG sites in its promoter. We hypothesized that MO enhances adipogenic differentiation during fetal development through inducing epigenetic changes in the Zfp423 promoter and elevating its expression. Female mice were subjected to a control (Con) or obesogenic (OB) diet for 2 months, mated, and maintained on their diets during pregnancy. Fetal tissue was harvested at embryonic day 14.5 (E14.5), when the early adipogenic commitment is initiated. The Zfp423 expression was 3.6-fold higher and DNA methylation in the Zfp423 promoter was lower in OB compared with Con. Correspondingly, repressive histone methylation (H3K27me3) was lower in the Zfp423 promoter of OB fetal tissue, accompanied by reduced binding of enhancer of zeste 2 (EZH2). Gain- and loss-of-function analysis showed that Zfp423 regulates early adipogenic differentiation in fetal progenitor cells. In summary, MO enhanced Zfp423 expression and adipogenic differentiation during fetal development, at least partially through reducing DNA methylation in the Zfp423 promoter, which is expected to durably elevate adipogenic differentiation of progenitor cells in adult tissue, programming adiposity and metabolic dysfunction later in life.

  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 malformation and several

  8. Maternal Environmental Contribution to Adult Sensitivity and Resistance to Obesity in Long Evans Rats

    PubMed Central

    Schroeder, Mariana; Shbiro, Liat; Moran, Timothy H.; Weller, Aron

    2010-01-01

    Background The OLETF rat is an animal model of early onset hyperphagia induced obesity, presenting multiple pre-obese characteristics during the suckling period. In the present study, we used a cross-fostering strategy to assess whether interactions with obese dams in the postnatal environment contributed to the development of obesity. Methodology On postnatal Day (PND)-1 OLETF and control LETO pups were cross-fostered to same or opposite strain dams. An independent ingestion test was performed on PND11 and a nursing test on PND18. Rats were sacrificed at weaning or on PND90, and plasma leptin, insulin, cholesterol, triglycerides and alanine aminotransferase (ALT) were assayed. Fat pads were collected and weighed and adipocyte size and number were estimated. Body weight and intake, as well as the estrous cycle of the female offspring were monitored. Principal Findings During the suckling period, the pups' phenotype was almost completely determined by the strain of the mother. However, pups independently ingested food according to their genotype, regardless of their actual phenotype. At adulthood, cross fostered males of both strains and LETO females were affected in regard of their adiposity levels in the direction of the foster dam. On the other hand, OLETF females showed almost no alterations in adiposity but were affected by the strain of the dams in parameters related to the metabolic syndrome. Thus, OLETF females showed reduced liver adiposity and circulating levels of ALT, while LETO females presented a disrupted estrous cycle and increased cholesterol and triglycerides in the long term. Conclusions The present study provides further support for the early postnatal environment playing a sex-divergent role in programming later life phenotype. In addition, it plays a more central role in determining the functioning of mechanisms involved in energy balance that may provide protection from or sensitivity to later life obesity and pathologies related to the

  9. The impact of maternal obesity on intrapartum outcomes in otherwise low risk women: secondary analysis of the Birthplace national prospective cohort study

    PubMed Central

    Hollowell, J; Pillas, D; Rowe, R; Linsell, L; Knight, M; Brocklehurst, P

    2014-01-01

    Objectives To evaluate the impact of maternal BMI on intrapartum interventions and adverse outcomes that may influence choice of planned birth setting in healthy women without additional risk factors. Design Prospective cohort study. Setting Stratified random sample of English obstetric units. Sample 17 230 women without medical or obstetric risk factors other than obesity. Methods Multivariable log Poisson regression was used to evaluate the effect of BMI on risk of intrapartum interventions and adverse maternal and perinatal outcomes adjusted for maternal characteristics. Main outcome measures Maternal intervention or adverse outcomes requiring obstetric care (composite of: augmentation, instrumental delivery, intrapartum caesarean section, general anaesthesia, blood transfusion, 3rd/4th degree perineal tear); neonatal unit admission or perinatal death. Results In otherwise healthy women, obesity was associated with an increased risk of augmentation, intrapartum caesarean section and some adverse maternal outcomes but when interventions and outcomes requiring obstetric care were considered together, the magnitude of the increased risk was modest (adjusted RR 1.12, 95% CI 1.02–1.23, for BMI > 35 kg/m2 relative to low risk women of normal weight). Nulliparous low risk women of normal weight had higher absolute risks and were more likely to require obstetric intervention or care than otherwise healthy multiparous women with BMI > 35 kg/m2 (maternal composite outcome: 53% versus 21%). The perinatal composite outcome exhibited a similar pattern. Conclusions Otherwise healthy multiparous obese women may have lower intrapartum risks than previously appreciated. BMI should be considered in conjunction with parity when assessing the potential risks associated with birth in non-obstetric unit settings. PMID:24034832

  10. 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.

  11. 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

  12. Effect of maternal obesity with and without gestational diabetes on offspring subcutaneous and preperitoneal adipose tissue development from birth up to year-1

    PubMed Central

    2014-01-01

    Background Maternal obesity and gestational diabetes mellitus (GDM) may independently influence offspring fat mass and metabolic disease susceptibility. In this pilot study, body composition and fat distribution in offspring from obese women with and without GDM and lean women were assessed within the 1st year of life, and maternal and newborn plasma factors were related to offspring adipose tissue distribution. Methods Serum and plasma samples from pregnant obese women with (n = 16) or without (n = 13) GDM and normoglycemic lean women (n = 15) at 3rd trimester and offspring cord plasma were used for analyzing lipid profiles, insulin and adipokine levels. At week-1 and 6, month-4 and year-1, offspring anthropometrics and skinfold thickness (SFT) were measured and abdominal subcutaneous (SCA) and preperitoneal adipose tissue (PPA) were determined by ultrasonography. Results Cord insulin was significantly increased in the GDM group, whereas levels of cord leptin, total and high molecular weight (HMW) adiponectin were similar between the groups. Neonates of the GDM group showed significantly higher SFT and fat mass until week-6 and significantly increased SCA at week-1 compared to the lean group that persisted as strong trend at week-6. Interestingly, PPA in neonates of the GDM group was significantly elevated at week-1 compared to both the lean and obese group. At month-4 and year-1, significant differences in adipose tissue growth between the groups were not observed. Multiple linear regression analyses revealed that cord insulin levels are independently related to neonatal PPA that showed significant relation to PPA development at year-1. Maternal fasted C-peptide and HMW adiponectin levels at 3rd trimester emerged to be determinants for PPA at week-1. Conclusion Maternal pregravid obesity combined with GDM leads to newborn hyperinsulinemia and increased offspring fat mass until week-6, whereas pregravid obesity without GDM does not. This strongly

  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. 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.

  15. Diet-Induced Maternal Obesity Alters Insulin Signalling in Male Mice Offspring Rechallenged with a High-Fat Diet in Adulthood.

    PubMed

    Fante, Thaís de; Simino, Laís Angélica; Reginato, Andressa; Payolla, Tanyara Baliani; Vitoréli, Débora Cristina Gustavo; Souza, Monique de; Torsoni, Márcio Alberto; Milanski, Marciane; Torsoni, Adriana Souza

    2016-01-01

    Modern lifestyle has resulted in an increase in the prevalence of obesity and its comorbidities in pregnant women and the young population. It has been well established that the consumption of a high-fat diet (HFD) has many direct effects on glucose metabolism. However, it is important to assess whether maternal consumption of a HFD during critical periods of development can lead to metabolic changes in the offspring metabolism. This study evaluated the potential effects of metabolic programming on the impairment of insulin signalling in recently weaned offspring from obese dams. Additionally, we investigated if early exposure to an obesogenic environment could exacerbate the impairment of glucose metabolism in adult life in response to a HFD. Swiss female mice were fed with Standard Chow (SC) or a HFD during gestation and lactation and tissues from male offspring were analysed at d28 and d82. Offspring from obese dams had greater weight gain and higher adiposity and food intake than offspring from control dams. Furthermore, they showed impairment in insulin signalling in central and peripheral tissues, which was associated with the activation of inflammatory pathways. Adipose tissue was ultimately the most affected in adult offspring after HFD rechallenge; this may have contributed to the metabolic deregulation observed. Overall, our results suggest that diet-induced maternal obesity leads to increased susceptibility to obesity and impairment of insulin signalling in offspring in early and late life that cannot be reversed by SC consumption, but can be aggravated by HFD re-exposure.

  16. Diet-Induced Maternal Obesity Alters Insulin Signalling in Male Mice Offspring Rechallenged with a High-Fat Diet in Adulthood

    PubMed Central

    de Fante, Thaís; Simino, Laís Angélica; Reginato, Andressa; Payolla, Tanyara Baliani; Vitoréli, Débora Cristina Gustavo; de Souza, Monique; Torsoni, Márcio Alberto; Milanski, Marciane; Torsoni, Adriana Souza

    2016-01-01

    Modern lifestyle has resulted in an increase in the prevalence of obesity and its comorbidities in pregnant women and the young population. It has been well established that the consumption of a high-fat diet (HFD) has many direct effects on glucose metabolism. However, it is important to assess whether maternal consumption of a HFD during critical periods of development can lead to metabolic changes in the offspring metabolism. This study evaluated the potential effects of metabolic programming on the impairment of insulin signalling in recently weaned offspring from obese dams. Additionally, we investigated if early exposure to an obesogenic environment could exacerbate the impairment of glucose metabolism in adult life in response to a HFD. Swiss female mice were fed with Standard Chow (SC) or a HFD during gestation and lactation and tissues from male offspring were analysed at d28 and d82. Offspring from obese dams had greater weight gain and higher adiposity and food intake than offspring from control dams. Furthermore, they showed impairment in insulin signalling in central and peripheral tissues, which was associated with the activation of inflammatory pathways. Adipose tissue was ultimately the most affected in adult offspring after HFD rechallenge; this may have contributed to the metabolic deregulation observed. Overall, our results suggest that diet-induced maternal obesity leads to increased susceptibility to obesity and impairment of insulin signalling in offspring in early and late life that cannot be reversed by SC consumption, but can be aggravated by HFD re-exposure. PMID:27479001

  17. 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.

  18. 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.

  19. Obesity

    MedlinePlus

    Obesity means having too much body fat. It is different from being overweight, which means weighing too ... what's considered healthy for his or her height. Obesity occurs over time when you eat more calories ...

  20. Interventions to prevent maternal obesity before conception, during pregnancy, and post partum.

    PubMed

    Hanson, Mark; Barker, Mary; Dodd, Jodie M; Kumanyika, Shiriki; Norris, Shane; Steegers, Eric; Stephenson, Judith; Thangaratinam, Shakila; Yang, Huixia

    2017-01-01

    Prevention of obesity in women of reproductive age is widely recognised to be important both for their health and for that of their offspring. Weight-control interventions, including drug treatment, in pregnant women who are obese or overweight have not had sufficient impact on pregnancy and birth outcomes, which suggests that the focus for intervention should include preconception or post-partum periods. Further research is needed into the long-term effects of nutritional and lifestyle interventions before conception. To improve preconception health, an integrated approach, including pregnancy prevention, planning, and preparation is needed, involving more than the primary health-care sector and adopting an ecological approach to risk reduction that addresses personal, societal, and cultural influences. Raising awareness of the importance of good health in the period before pregnancy will require a new social movement: combining bottom-up mobilisation of individuals and communities with a top-down approach from policy initiatives. Interventions to reduce or prevent obesity before conception and during pregnancy could contribute substantially to achievement of the global Sustainable Development Goals, in terms of health, wellbeing, productivity, and equity in current and future generations.

  1. Maternal obesity, length of gestation, risk of postdates pregnancy and spontaneous onset of labour at term.

    PubMed

    Denison, F C; Price, J; Graham, C; Wild, S; Liston, W A

    2008-05-01

    To investigate the effect of maternal body mass index (BMI) on postdates pregnancy, length of gestation and likelihood of spontaneous onset of labour at term. Retrospective cohort study. Swedish Medical Birth Register. A total of 186 087 primiparous women (of whom 143 519 had spontaneous onset of labour at term) who gave birth between 1998 and 2002. Mann-Whitney test, one-way analysis of variance, linear regression and single variable logistic regression. Postdates pregnancy (>/=294 days or 42(+0) weeks), length of gestation and likelihood of spontaneous onset of labour at term. About 6.8% of pregnancies delivered postdates. Higher maternal BMI (kg/m(2)) during the first trimester was associated with longer gestation (P < 0.001) as was a greater change in BMI between the first and third trimesters (BMI measured on admission prior to delivery) with mean (SD) gestation at delivery of 280.7 (8.6) and 283.2 (8.6) days for increases in BMI of <2 and >/=10 kg/m(2), respectively. Higher BMI during the first trimester was associated with a lower chance of spontaneous onset of labour at term. Compared with BMI 20 to <25 kg/m(2), the odds ratios (95% CI) for spontaneous onset of labour at term were 1.21 (1.15-1.27) for BMI of <20 kg/m(2), 0.71 (0.69-0.74) for BMI of 25 to <30 kg/m(2), 0.57 (0.54-0.60) for BMI of 30 to <35 kg/m(2) and 0.43 (0.40-0.47) for BMI of >/=35 kg/m(2). Higher BMI during the first trimester (BMI of >/=35 kg/m(2) compared with BMI of 20 to <25 kg/m(2)) was also associated with an increased risk of complications including stillbirth (OR 3.90, 95% CI 2.44-6.22), gestational diabetes (OR 5.61, 95% CI 4.61-6.83) and caesarean section (OR 2.39; 95% CI 2.20-2.59). Higher maternal BMI in the first trimester and a greater change in BMI during pregnancy were associated with longer gestation and an increased risk of postdates pregnancy. Higher maternal BMI during the first trimester was also associated with decreased likelihood of spontaneous onset of labour at

  2. Proteome analysis of human amniotic mesenchymal stem cells (hA-MSCs) reveals impaired antioxidant ability, cytoskeleton and metabolic functionality in maternal obesity

    PubMed Central

    Capobianco, Valentina; Caterino, Marianna; Iaffaldano, Laura; Nardelli, Carmela; Sirico, Angelo; Del Vecchio, Luigi; Martinelli, Pasquale; Pastore, Lucio; Pucci, Pietro; Sacchetti, Lucia

    2016-01-01

    Maternal obesity increases the risk of obesity and/or obesity-related diseases in the offspring of animal models. The aim of this study was to identify metabolic dysfunctions that could represent an enhanced risk for human obesity or obesity-related diseases in newborn or in adult life, similar to what occurs in animal models. To this aim, we studied the proteome of 12 obese (Ob-) and 6 non-obese (Co-) human amniotic mesenchymal stem cells (hA-MSCs) obtained from women at delivery by cesarean section (pre-pregnancy body mass index [mean ± SD]: 42.7 ± 7.7 and 21.3 ± 3.3 kg/m2, respectively). The proteome, investigated by two-dimensional fluorescence difference gel electrophoresis/mass spectrometry, revealed 62 differently expressed proteins in Ob- vs Co-hA-MSCs (P < 0.05), nine of which were confirmed by western blotting. Bioinformatics analysis showed that these 62 proteins are involved in several statistically significant pathways (P < 0.05), including the stress response, cytoskeleton and metabolic pathways. Oxidative stress was shown to be an early triggering factor of tissue fat accumulation and obesity-related disorders in the offspring of obese animal models. Our finding of a reduced stress response in Ob-hA-MSCs suggests that a similar mechanism could occur also in humans. Long-term follow-up studies of newborns of obese mothers are required to verify this hypothesis. PMID:27125468

  3. Proteome analysis of human amniotic mesenchymal stem cells (hA-MSCs) reveals impaired antioxidant ability, cytoskeleton and metabolic functionality in maternal obesity.

    PubMed

    Capobianco, Valentina; Caterino, Marianna; Iaffaldano, Laura; Nardelli, Carmela; Sirico, Angelo; Del Vecchio, Luigi; Martinelli, Pasquale; Pastore, Lucio; Pucci, Pietro; Sacchetti, Lucia

    2016-04-29

    Maternal obesity increases the risk of obesity and/or obesity-related diseases in the offspring of animal models. The aim of this study was to identify metabolic dysfunctions that could represent an enhanced risk for human obesity or obesity-related diseases in newborn or in adult life, similar to what occurs in animal models. To this aim, we studied the proteome of 12 obese (Ob-) and 6 non-obese (Co-) human amniotic mesenchymal stem cells (hA-MSCs) obtained from women at delivery by cesarean section (pre-pregnancy body mass index [mean ± SD]: 42.7 ± 7.7 and 21.3 ± 3.3 kg/m(2), respectively). The proteome, investigated by two-dimensional fluorescence difference gel electrophoresis/mass spectrometry, revealed 62 differently expressed proteins in Ob- vs Co-hA-MSCs (P < 0.05), nine of which were confirmed by western blotting. Bioinformatics analysis showed that these 62 proteins are involved in several statistically significant pathways (P < 0.05), including the stress response, cytoskeleton and metabolic pathways. Oxidative stress was shown to be an early triggering factor of tissue fat accumulation and obesity-related disorders in the offspring of obese animal models. Our finding of a reduced stress response in Ob-hA-MSCs suggests that a similar mechanism could occur also in humans. Long-term follow-up studies of newborns of obese mothers are required to verify this hypothesis.

  4. The impact of maternal overnutrition and obesity on hypothalamic-pituitary-adrenal axis response of offspring to stress.

    PubMed

    Long, N M; Nathanielsz, P W; Ford, S P

    2012-05-01

    We evaluated the effect of maternal obesity before and throughout gestation on offspring hypothalamic-pituitary-adrenal axis function. Multiparous Rambouillet by Columbia crossbred ewes were fed either 100% of National Research Council (NRC) recommendations (control, C) or 150% of NRC recommendations (obese, OB) from 60 d before mating until lambing. Ten lambs born to OB ewes (five males and five females), and eight lambs born to C ewes (three male and five female) were studied. From delivery to weaning lambs were maintained with their mothers, who were all fed 100% NRC recommendations. After weaning, all lambs were group housed and fed the same diet to meet NRC requirements. At 19 mo of age lambs were placed in individual pens and fed a pelletized diet to meet maintenance requirements. Jugular vein catheters were placed and 2 d later lambs received an intravenous (i.v.) adrenocorticotropic hormone (ACTH) challenge followed by an i.v. corticotropin-releasing hormone (CRH)/arginine vasopressin (AVP) challenge 1 d later. Thirty d later offspring were again catheterized and placed into metabolism crates for 2 d before receiving an isolation stress test. ACTH and cortisol responses to the isolation stress test and CRH/AVP challenge and cortisol responses to ACTH challenge were determined. Cortisol was quantified via radioimmunoassay and ACTH was quantified using an Immulite 1000; both were analyzed using repeated measures using the MIXED procedure of SAS. Offspring from OB ewes had elevated basal plasma ACTH and cortisol compared with C offspring before all three challenges (P < 0.05). Offspring from OB mothers tended (P = 0.06) to have a greater ACTH response after an i.v. CRH/AVP injection than offspring from C mothers (12,340 ± 1,430 vs 8,170 ± 1,570 area under the curve, respectively). Cortisol response to the CRH/AVP and ACTH challenges was not influenced by maternal nutrition (P = 0.46) and averaged 4.77 ± 0.2 μg/dL and 1.94 ± 0.01 μg/dL, respectively. The

  5. Multi-generational Impact of Maternal Overnutrition/Obesity in the Sheep on the Neonatal Leptin Surge in Granddaughters

    PubMed Central

    Shasa, Desiree R.; Odhiambo, John F.; Long, Nathan M.; Tuersunjiang, Nuermaimaiti; Nathanielsz, Peter W.; Ford, Stephen P.

    2014-01-01

    Background/Objectives We have reported that maternal overnutrition/obesity (OB) in sheep resulting from feeding 150% of National Research Council (NRC) requirements throughout gestation, leads to maternal hyperglycemia and hyperinsulinemia. Further, newborn lambs born to OB vs. control-fed (CON, 100% of NRC) ewes exhibited greater adiposity, increased blood cortisol, insulin and glucose and the elimination of the postnatal leptin spike seen in lambs born to CON ewes. This early postnatal leptin peak is necessary for development of hypothalamic circuits which program appetite in later life. This study evaluated the multigenerational impact of OB on insulin:glucose dynamics of mature female F1 offspring fed only to requirements throughout gestation, and on their lambs (F2 generation). Design and Methods Adult F1 female offspring born to OB (n=10) or CON (n=7) ewes were utilized. All F1 ewes were subjected to a glucose tolerance test at midgestation and late gestation. Jugular blood was obtained from F2 lambs at birth (day 1) through postnatal day 11, and plasma glucose, insulin, cortisol and leptin concentrations determined. Dual Energy X-ray Absorptiometry (DEXA) was utilized to determine bone mineral density (BMD), bone mineral content (BMC), lean tissue mass, and fat tissue mass. Results Fasted blood glucose and insulin concentrations were greater (P < 0.05) in OBF1 than CONF1 ewes at mid- and late gestation. Further, after glucose infusion, both glucose and insulin concentrations remained higher in OBF1 ewes (P < 0.05) than CONF1 ewes demonstrating greater insulin resistance. Blood concentrations of glucose, insulin, and cortisol, and adiposity were higher (P < 0.01) in OBF2 lambs than CONF2 lambs at birth. Importantly, OBF2 lambs failed to exhibit the early postnatal leptin peak exhibited by CONF2 lambs. Conclusions These data suggest that these OBF2 lambs are predisposed to exhibit the same metabolic alterations as their mothers, suggesting a multi

  6. Cord blood erythropoietin and cord blood nucleated red blood cells for prediction of adverse neonatal outcome associated with maternal obesity in term pregnancy: prospective cohort study.

    PubMed

    Ibrahim, Mahmoud H; Moustafa, Asmaa N; Saedii, Ahmed A Fadil; Hassan, Ebtesam E

    2017-09-01

    To determine the adverse pregnancy outcomes associated with maternal pre-pregnancy overweight and obesity and we measure cord blood erythropoietin and NRBC count as indices of hypoxia and predictors of neonatal outcome. This prospective cohort study was done in Minia University Hospital, carried out from May 2015 to April 2016. Two hundred and seventy full-term neonates born to mothers of various body mass indices were included. Excluded were neonates with major factors known to be associated with a potential increase in fetal erythropoiesis. Pre-pregnancy maternal BMI was calculated from maternally reported weight and height. Cord blood erythropoietin and nucleated red blood cells were measured. There is a significant increase of various adverse pregnancy outcomes as cesarean section. Postpartum hemorrhage and macrosomia with the increase of maternal pre-pregnancy BMI. Significant positive correlations between cord blood erythropoietin and nucleated red blood cells with maternal BMI. The increase in the maternal pre-pregnancy BMI is associated with poor pregnancy outcomes. Cord blood erythropoietin and nucleated red blood cells can predict the poor neonatal outcome.

  7. IFPA meeting 2015 workshop report IV: placenta and obesity; stem cells of the feto-maternal interface; placental immunobiology and infection.

    PubMed

    Abumaree, M H; Almutairi, A; Cash, S; Boeuf, P; Chamley, L W; Gamage, T; James, J L; Kalionis, B; Khong, T Y; Kolahi, K S; Lim, R; Liong, S; Morgan, T K; Motomura, K; Peiris, H N; Pelekanos, R A; Pelzer, E; Shafiee, A; Lash, G E; Natale, D

    2016-12-01

    Workshops are an important part of the IFPA annual meeting as they allow for discussion of specialised topics. At the 2015 IFPA annual meeting there were 12 themed workshops, three of which are summarized in this report. These workshops related to various aspects of placental biology and collectively covered areas of obesity and the placenta, stem cells of the feto-maternal interface, and placental immunobiology and infection. Copyright © 2016 Elsevier Ltd. All rights reserved.

  8. Maternal perspectives on lifestyle habits that put children of Mexican descent at risk for obesity.

    PubMed

    Gallagher, Martina Raquel

    2010-01-01

    This article presents the views that mothers of Mexican descent have related to lifestyle habits that put children at risk for obesity. A qualitative, naturalistic design using ethnographic interviews was selected for this study. Informational redundancy was reached with 9 mothers of Mexican descent. Spradley's Developmental Research Sequence guided data collection and analysis. Participants held views that were congruent with the American Academy of Pediatrics' recommendations. Findings provide nurses with knowledge on how mothers of Mexican descent view appropriate nutrition, discipline in feeding, and the place of physical activity and television in young preschool children's lives.

  9. Maternal obesity disturbs the postnatal development of gonocytes in the rat without impairment of testis structure at prepubertal age.

    PubMed

    Christante, Caroline Maria; Taboga, Sebastião Roberto; Pinto-Fochi, Maria Etelvina; Góes, Rejane Maira

    2013-12-01

    In this study, we evaluated whether maternal obesity (MO) affects testis development and gonocyte differentiation in the rat from 0.5 to 14.5 postnatal days. Male Wistar rats were used at 0.5, 4.5, 7.5, and 14.5 days post partum (dpp). These rats were born from obese mothers, previously fed with a high-fat diet (20% saturated fat), for 15 weeks, or normal mothers that had received a balanced murine diet (4% lipids). MO did not affect testis weight or histology at birth but changed the migratory behavior of gonocytes. The density of relocated cells was higher in MO pups at 0.5 dpp, decreased at 4.5 dpp, and differed from those of control pups, where density increased exponentially from 0.5 to 7.5 dpp. The numerical density of gonocytes within seminiferous cords did not vary in MO, in relation to control neonates, for any age considered, but the testis weight was 50% lower at 4.5 dpp. A wide variation in plasmatic testosterone and estrogen levels was observed among the groups during the first week of age and MO pups exhibited higher steroid concentrations at 4.5 dpp, in comparison with controls. At this age, higher estrogen levels of MO pups impaired the gonocyte proliferation. At 7.5 dpp, the testicular size and other parameters of gonocyte development are retrieved. In conclusion, MO and saturated lipid diets disturb gonocyte development and sexual steroid levels during the first days of life, with recovery at prepubertal age.

  10. Long-term effect of maternal obesity on pancreatic beta cells of offspring: reduced beta cell adaptation to high glucose and high-fat diet challenges in adult female mouse offspring.

    PubMed

    Han, J; Xu, J; Epstein, P N; Liu, Y Qi

    2005-09-01

    Obesity is a global problem with high risks of cardiovascular diseases, stroke and type 2 diabetes. It is well known that maternal obesity affects offspring by inducing malformation, functional abnormalities in many organs and cells, and by increased risk of obesity and type 2 diabetes. However, little is known about abnormalities induced by maternal obesity in pancreatic beta cells of offspring. We used mouse mothers with the Agouti yellow modification on a C57BL/6 background as a maternal model of normoglycaemic obesity, and produced Agouti-negative offspring. Half of the offspring were fed a high-fat diet. Offspring glucose tolerance was tested at different ages, and animals were killed at 50 weeks of age for islet function analysis. Maternal obesity impaired glucose tolerance in female offspring fed a high-fat diet, and significantly reduced insulin secretion at 50 weeks of age in female offspring that had been fed a normal diet and high-fat diet. Insulin secretion and glucose potentiation from these islets were significantly reduced. Islet protein, DNA and insulin contents were increased while glyceraldehyde-3-phosphate dehydrogenase and transketolase activities were reduced in female offspring. Our results indicate that maternal obesity has a long-term effect on the beta cells of female, but not of male, offspring, and leads to increased risk of gestational diabetes and type 2 diabetes in the offspring's later lives.

  11. The association of maternal obesity with fetal pH and base deficit at cesarean delivery.

    PubMed

    Edwards, Rodney K; Cantu, Jessica; Cliver, Suzanne; Biggio, Joseph R; Owen, John; Tita, Alan T N

    2013-08-01

    To evaluate the association between maternal body mass index (BMI) and umbilical cord acid-base status at the time of cesarean delivery. We conducted a retrospective multicenter cohort study using data from the Cesarean Section Registry of the Eunice Kennedy Shriver National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network. Women were included if they delivered a live, nonanomalous singleton at 37-41 weeks of gestation by prelabor cesarean under spinal anesthesia. We excluded women with diagnoses that might be associated with uteroplacental insufficiency. Body mass index at delivery was examined both as a continuous and categorical exposure, and acid-base status was based on cord arterial pH and base deficit. There were 5,742 mother-neonate pairs who met criteria for analysis. Among possible confounders (including sociodemographic variables, number of previous uterine incisions, diabetes, hematocrit, neonatal gender, and birth weight), African American race, birth weight, parity, and smoking status were significantly associated with both BMI and acid-base parameters. Adjusted for those four factors, with increasing BMI category (less than 25, 25-29.9, 30-34.9, 35-39.9, and 40 or higher), mean pH decreased from 7.25 to 7.22 (P<.001), proportion with pH less than 7.1 increased from 3.5% to 7.7% (P=.011), mean base deficit increased from 4.01 mmol/L to 4.83 mmol/L (P=.030), and proportion with base deficit of 12 mmol/L or more increased from 0.6% to 4.7% (P=.003). When BMI was analyzed continuously and adjusted for these confounders, for every 10-unit increase in BMI, cord arterial pH decreased by 0.01 (P<.001) and base deficit increased by 0.26 mmol/L (P=.005). For women undergoing nonemergent prelabor cesarean delivery under spinal anesthesia, fetal pH declines and base deficit rises as maternal BMI increases. II.

  12. Maternal obesity induced by diet in rats permanently influences central processes regulating food intake in offspring.

    PubMed

    Kirk, Shona L; Samuelsson, Anne-Maj; Argenton, Marco; Dhonye, Hannah; Kalamatianos, Theodosis; Poston, Lucilla; Taylor, Paul D; Coen, Clive W

    2009-06-11

    Hypothalamic systems which regulate appetite may be permanently modified during early development. We have previously reported hyperphagia and increased adiposity in the adult offspring of rodents fed an obesogenic diet prior to and throughout pregnancy and lactation. We now report that offspring of obese (OffOb) rats display an amplified and prolonged neonatal leptin surge, which is accompanied by elevated leptin mRNA expression in their abdominal white adipose tissue. At postnatal Day 30, before the onset of hyperphagia in these animals, serum leptin is normal, but leptin-induced appetite suppression and phosphorylation of STAT3 in the arcuate nucleus (ARC) are attenuated; the level of AgRP-immunoreactivity in the hypothalamic paraventricular nucleus (PVH), which derives from neurones in the ARC and is developmentally dependent on leptin, is also diminished. We hypothesise that prolonged release of abnormally high levels of leptin by neonatal OffOb rats leads to leptin resistance and permanently affects hypothalamic functions involving the ARC and PVH. Such effects may underlie the developmental programming of hyperphagia and obesity in these rats.

  13. Overweight is more prevalent than stunting and is associated with socioeconomic status, maternal obesity, and a snacking dietary pattern in school children from Bogota, Colombia.

    PubMed

    McDonald, Christine M; Baylin, Ana; Arsenault, Joanne E; Mora-Plazas, Mercedes; Villamor, Eduardo

    2009-02-01

    The objectives of this study were to estimate the prevalence of overweight in school-aged children from Bogotá, Colombia and to examine its associations with sociodemographic characteristics, dietary patterns, and indicators of physical activity. We measured height and weight in 3075 children between 5 and 12 y of age who attended public primary schools in 2006 and we obtained information on maternal sociodemographic and anthropometric characteristics. The survey was representative of children from low and middle socioeconomic backgrounds. The prevalences of child overweight (including obesity) and obesity according to the International Obesity Task Force criteria were 11.1 and 1.8%, respectively. The prevalence of stunting was 9.8%. In multivariate analysis, child overweight was positively associated with indicators of higher socioeconomic status (SES), including low maternal parity and ownership of household assets. The prevalence of overweight was 3.6 times greater in children whose mothers were obese compared with children whose mothers had an adequate BMI (adjusted prevalence ratio = 3.61; 95% CI = 2.64, 4.93). Child overweight was positively associated with adherence to a "snacking" dietary pattern (P-trend = 0.06) and to frequent intake of hamburgers or hot dogs (adjusted prevalence ratio for at least once per week vs. never = 1.93; 95% CI = 1.03, 3.62), independent of total energy intake and other potential confounders. Time spent viewing television or playing outside the household were not significantly related to the prevalence of child overweight. In conclusion, child overweight in Bogotá is more common than stunting and is associated with higher SES, maternal obesity, and a snacking dietary pattern.

  14. Prenatal origin of obesity and their complications: Gestational diabetes, maternal overweight and the paradoxical effects of fetal growth restriction and macrosomia.

    PubMed

    Ornoy, Asher

    2011-09-01

    Pregestational (PGDM) and gestational (GDM) diabetes may be associated with a variety of fetal effects including increased rate of spontaneous abortions, intrauterine fetal death, congenital anomalies, neurodevelopmental problems and increased risk of perinatal complications. Additional problems of concern are fetal growth disturbances causing increased or decreased birth weight. Optimal control of maternal blood glucose is known to reduce these changes. Among the long lasting effects of these phenomena are a high rate of overweight and obesity at childhood and a high tendency to develop the "metabolic syndrome" characterized by hypertension, cardio-vascular complications and type 2 diabetes. Similarly, maternal overweight and obesity during pregnancy or excessive weight gain are also associated with increased obesity and complications in the offspring. Although there are different causes for fetal growth restriction (FGR) or for fetal excessive growth (macrosomis), paradoxically both are associated with the "metabolic syndrome" and its long term consequences. The exact mechanism(s) underlying these long term effects on growth are not fully elucidated, but they involve insulin resistance, fetal hyperleptinemia, hypothalamic changes and most probably epigenetic changes. Preventive measures to avoid the metabolic syndrome and its complications seem to be a tight dietary control and physical activity in the children born to obese or diabetic mothers or who had antenatal growth disturbances for other known or unknown reasons.

  15. 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.

  16. NGF up-regulates TRPA1: implications for orofacial pain.

    PubMed

    Diogenes, A; Akopian, A N; Hargreaves, K M

    2007-06-01

    The transient receptor potential ankyrin repeat 1 (TRPA1) channel is believed to be involved in many forms of acute and chronic hyperalgesia. Nerve Growth Factor (NGF) regulates chronic inflammatory hyperalgesia by controlling gene expression in sensory neurons, including genes involved in inflammatory hyperalgesia in the dental pulp. We hypothesized that NGF increases functional activities of the TRPA1 channel in trigeminal ganglion neurons. Here, we show that NGF induced a concentration- and time-dependent up-regulation of TRPA1 mRNA in trigeminal ganglia neurons, as detected by real-time RT-PCR and in situ hybridization. In addition, NGF evoked a time-dependent increase of mustard oil (MO)-evoked TRPA1 activation in trigeminal ganglia neurons. Collectively, these findings demonstrate that NGF participates in the functional up-regulation of TRPA1 in trigeminal ganglia neurons. These enhanced activities of TRPA1 could play an important role in the development of hyperalgesia following nerve injury and inflammation in the orofacial region.

  17. The effect of pre-existing maternal obesity on the placental proteome: two-dimensional difference gel electrophoresis coupled with mass spectrometry.

    PubMed

    Oliva, Karen; Barker, Gillian; Riley, Clyde; Bailey, Mark J; Permezel, Michael; Rice, Gregory E; Lappas, Martha

    2012-04-01

    Our aim was to study the protein expression profiles of placenta obtained from lean and obese pregnant women with normal glucose tolerance at the time of term Caesarean section. We used two-dimensional difference gel electrophoresis (2D-DIGE), utilising narrow-range immobilised pH gradient strips that encompassed the broad pH range of 4-5 and 5-6, followed by MALDI-TOF mass spectrometry of selected protein spots. Western blot and quantitative RT-PCR (qRT-PCR) analyses were performed to validate representative findings from the 2D-DIGE analysis. Eight proteins were altered (six down-regulated and two up-regulated on obese placentas). Annexin A5 (ANXA5), ATP synthase subunit beta, mitochondria (ATPB), brain acid soluble protein 1 (BASP1), ferritin light chain (FTL), heterogeneous nuclear ribonucleoprotein C (HNRPC) and vimentin (VIME) were all lower in obese patients. Alpha-1-antitrypsin (A1AT) and stress-70 protein, mitochondrial (GRP75) were higher in obese patients. Western blot analysis of ANXA5, ATPB, FTL, VIME, A1AT and GRP75 confirmed the findings from the 2D-DIGE analysis. For brain acid soluble protein 1 and HNRPC, qRT-PCR analysis also confirmed the findings from the 2D-DIGE analysis. Immunohistochemical analysis was also used to determine the localisation of the proteins in human placenta. In conclusion, proteomic analysis of placenta reveals differential expression of several proteins in patients with pre-existing obesity. These proteins are implicated in a variety of cellular functions such as regulation of growth, cytoskeletal structure, oxidative stress, inflammation, coagulation and apoptosis. These disturbances may have significant implications for fetal growth and development.

  18. Price and maternal obesity influence purchasing of low- and high-energy-dense foods2

    PubMed Central

    Epstein, Leonard H; Dearing, Kelly K; Paluch, Rocco A; Roemmich, James N; Cho, David

    2007-01-01

    Background Price can influence food purchases, which can influence consumption. Limited laboratory research has assessed the effect of price changes on food purchases, and no research on individual differences that may interact with price to influence purchases exists. Objective We aimed to assess the influence of price changes of low-energy-density (LED) and high-energy-density (HED) foods on mother’s food purchases in a laboratory food-purchasing analogue. Design Mothers were randomly assigned to price conditions in which the price of either LED or HED foods was manipulated from 75% to 125% of the reference purchase price, whereas the price of the alternative foods was kept at the reference value. Mothers completed purchases for 2 income levels ($15 or $30 per family member). Results Purchases were reduced when prices of LED (P < 0.01) and HED (P < 0.001) foods were increased. Maternal BMI interacted with price to influence purchases of HED foods when the price of HED foods increased (P = 0.016) and interacted with price to influence purchases of LED foods when the price of HED foods increased (P = 0.008). Conclusion These results show the relevance of considering price change as a way to influence food purchases of LED compared with HED foods and the possibility that individual differences may influence the own-price elasticity of HED foods and substitution of LED for HED foods. PMID:17921365

  19. 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.

  20. Association between Maternal Fish Consumption and Gestational Weight Gain: Influence of Molecular Genetic Predisposition to Obesity

    PubMed Central

    Larsen, Sofus C.; Ängquist, Lars; Laurin, Charles; Morgen, Camilla S.; Jakobsen, Marianne U.; Paternoster, Lavinia; Smith, George Davey; Olsen, Sjurdur F.; Sørensen, Thorkild I. A.; Nohr, Ellen A.

    2016-01-01

    Background Studies suggest that fish consumption can restrict weight gain. However, little is known about how fish consumption affects gestational weight gain (GWG), and whether this relationship depends on genetic makeup. Objective To examine the association between fish consumption and GWG, and whether this relationship is dependent on molecular genetic predisposition to obesity. Design A nested case-cohort study based on the Danish National Birth Cohort (DNBC) sampling the most obese women (n = 990) and a random sample of the remaining participants (n = 1,128). Replication of statistically significant findings was attempted in the Avon Longitudinal Study of Parents and Children (ALSPAC) (n = 4,841). We included 32 body mass index (BMI) associated single nucleotide polymorphisms (SNPs) and 5 SNPs found associated with GWG. BMI associated SNPs were combined in a genetic risk score (GRS). Associations between consumption of fish, GRS or individual variants and GWG were analysed, and interactions between fish and the GRS or individual variants were examined. Results In the DNBC, each portion/week (150 g) of fatty fish was associated with a higher GWG of 0.58 kg (95% CI: 0.16, 0.99, P<0.01). For total fish and lean fish, similar patterns were observed, but these associations were not statistically significant. We found no association between GRS and GWG, and no interactions between GRS and dietary fish on GWG. However, we found an interaction between the PPARG Pro12Ala variant and dietary fish. Each additional Pro12Ala G-allele was associated with a GWG of -0.83 kg (95% CI: -1.29, -0.37, P<0.01) per portion/week of dietary fish, with the same pattern for both lean and fatty fish. In ALSPAC, we were unable to replicate these findings. Conclusion We found no consistent evidence of association between fish consumption and GWG, and our results indicate that the association between dietary fish and GWG has little or no dependency on GRS or individual SNPs. PMID:26930408

  1. Association between Maternal Fish Consumption and Gestational Weight Gain: Influence of Molecular Genetic Predisposition to Obesity.

    PubMed

    Larsen, Sofus C; Ängquist, Lars; Laurin, Charles; Morgen, Camilla S; Jakobsen, Marianne U; Paternoster, Lavinia; Smith, George Davey; Olsen, Sjurdur F; Sørensen, Thorkild I A; Nohr, Ellen A

    2016-01-01

    Studies suggest that fish consumption can restrict weight gain. However, little is known about how fish consumption affects gestational weight gain (GWG), and whether this relationship depends on genetic makeup. To examine the association between fish consumption and GWG, and whether this relationship is dependent on molecular genetic predisposition to obesity. A nested case-cohort study based on the Danish National Birth Cohort (DNBC) sampling the most obese women (n = 990) and a random sample of the remaining participants (n = 1,128). Replication of statistically significant findings was attempted in the Avon Longitudinal Study of Parents and Children (ALSPAC) (n = 4,841). We included 32 body mass index (BMI) associated single nucleotide polymorphisms (SNPs) and 5 SNPs found associated with GWG. BMI associated SNPs were combined in a genetic risk score (GRS). Associations between consumption of fish, GRS or individual variants and GWG were analysed, and interactions between fish and the GRS or individual variants were examined. In the DNBC, each portion/week (150 g) of fatty fish was associated with a higher GWG of 0.58 kg (95% CI: 0.16, 0.99, P<0.01). For total fish and lean fish, similar patterns were observed, but these associations were not statistically significant. We found no association between GRS and GWG, and no interactions between GRS and dietary fish on GWG. However, we found an interaction between the PPARG Pro12Ala variant and dietary fish. Each additional Pro12Ala G-allele was associated with a GWG of -0.83 kg (95% CI: -1.29, -0.37, P<0.01) per portion/week of dietary fish, with the same pattern for both lean and fatty fish. In ALSPAC, we were unable to replicate these findings. We found no consistent evidence of association between fish consumption and GWG, and our results indicate that the association between dietary fish and GWG has little or no dependency on GRS or individual SNPs.

  2. Fit for Birth - the effect of weight changes in obese pregnant women on maternal and neonatal outcomes: a pilot prospective cohort study.

    PubMed

    Narayanan, R P; Weeks, A D; Quenby, S; Rycroft, D; Hart, A; Longworth, H; Charnley, M; Abayomi, J; Topping, J; Turner, M A; Wilding, J P H

    2016-02-01

    The 'Fit for Birth' study aimed to explore patterns of gestational weight gain and their relationship with pregnancy outcomes. The study had three aims: 1. To explore the feasibility of conducting a large cohort study in this setting. 2. To describe patterns of weight gain through pregnancy in obese women. 3. To explore associations of weight change during pregnancy with outcomes. Pregnant women with a BMI ≥ 30 kg m(-2) at first antenatal clinic visit. This was a single centre pilot observational study based at the Liverpool Women's Hospital, a large UK maternity hospital.Women were recruited into the study at their antenatal booking visit and had weights measured throughout pregnancy. Patterns of weight gain were described and related to maternal and neonatal outcomes. The primary outcome was a composite measure consisting of any of 12 adverse maternal and foetal outcomes. This was compared by categorized pregnancy weight gain (<0 kg, 0-5 kg, 5.1-9 kg and >9 kg). Eight hundred and twenty four women consented to participation between June 2009 and June 2010. Weight data were collected on 756 women. Only 385 women had weights measured in all three study assessment periods (6-20 weeks, 20 + 1 to 32 weeks and >32 weeks gestation) while 427 women had weights measured in period 3. Individual patterns of weight gain varied widely and missing data were common and non-random. There was a significant association between increased weight gain during pregnancy and poor maternal and foetal outcome. Weight gain in obese women during pregnancy can be highly variable. Our study supports an association between increased weight gain in pregnancy and adverse perinatal outcomes. © 2015 World Obesity.

  3. Obesity.

    PubMed

    González-Muniesa, Pedro; Mártinez-González, Miguel-Angel; Hu, Frank B; Després, Jean-Pierre; Matsuzawa, Yuji; Loos, Ruth J F; Moreno, Luis A; Bray, George A; Martinez, J Alfredo

    2017-06-15

    Excessive fat deposition in obesity has a multifactorial aetiology, but is widely considered the result of disequilibrium between energy intake and expenditure. Despite specific public health policies and individual treatment efforts to combat the obesity epidemic, >2 billion people worldwide are overweight or obese. The central nervous system circuitry, fuel turnover and metabolism as well as adipose tissue homeostasis are important to comprehend excessive weight gain and associated comorbidities. Obesity has a profound impact on quality of life, even in seemingly healthy individuals. Diet, physical activity or exercise and lifestyle changes are the cornerstones of obesity treatment, but medical treatment and bariatric surgery are becoming important. Family history, food environment, cultural preferences, adverse reactions to food, perinatal nutrition, previous or current diseases and physical activity patterns are relevant aspects for the health care professional to consider when treating the individual with obesity. Clinicians and other health care professionals are often ill-equipped to address the important environmental and socioeconomic drivers of the current obesity epidemic. Finally, understanding the epigenetic and genetic factors as well as metabolic pathways that take advantage of 'omics' technologies could play a very relevant part in combating obesity within a precision approach.

  4. Effect of Maternal Age at Childbirth on Obesity in Postmenopausal Women: A Nationwide Population-Based Study in Korea.

    PubMed

    We, Ji-Sun; Han, Kyungdo; Kwon, Hyuk-Sang; Kil, Kicheol

    2016-05-01

    The object of this study was to assess the obesity in postmenopausal women, according to age at childbirth.We analyzed the association between age at first childbirth, age at last childbirth, parity, and subject obesity status (general obesity; BMI >25 kg/m, nongeneral obesity; BMI ≤25 kg/m, abdominal obesity; waist circumference >85 cm, nonabdominal obesity; waist circumference ≤85 cm), using data from a nationwide population-based survey, the 2010 to 2012 Korean National Health and Nutrition Examination Survey. Data from a total of 4382 postmenopausal women were analyzed using multivariate regression analysis with complex survey design sampling. And, the subjects were subdivided into groups according to obesity or not. Age, smoking, alcohol consumption, exercise, education, income level, number of pregnancies, oral contraceptive uses, breast feeding experience were adjusted as the confounders.The prevalence of general obesity among Korean postmenopausal women was 37.08%. Women with general obesity and abdominal obesity were significantly younger at first childbirth compared with women with nongeneral obesity and no abdominal obesity (23.89 ± 0.1 vs. 23.22 ± 0.1, P <0.001). Age at first childbirth was inversely associated with obesity, while age at last childbirth was not associated with obesity or abdominal obesity. Women with a higher number of pregnancies were also more likely to have obesity and abdominal obesity. Age at first childbirth remained significantly associated with obesity, after adjusting for confounding factors.Obesity in postmenopausal women is associated with first childbirth at a young age, and higher parity. Further research is needed to clarify the association between obesity and reproductive characteristics.

  5. 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

  6. 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.

  7. Dog Ownership during Pregnancy, Maternal Activity, and Obesity: A Cross-Sectional Study

    PubMed Central

    Westgarth, Carri; Liu, Jihong; Heron, Jon; Ness, Andrew R.; Bundred, Peter; Gaskell, Rosalind M.; German, Alexander J.; McCune, Sandra; Dawson, Susan

    2012-01-01

    The Avon Longitudinal Study of Parents and Children (ALSPAC) is an observational study of 14273 UK pregnant singleton mothers in 1990/1991. We examined outcomes of self report of strenuous activity (hours per week) at 18 and 32 weeks of gestation, hours spent in leisure-time physical activities and types, and pre-pregnancy b