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Sample records for glucose intolerance hypertension

  1. Fatty acid nitroalkenes ameliorate glucose intolerance and pulmonary hypertension in high-fat diet-induced obesity

    PubMed Central

    Kelley, Eric E.; Baust, Jeff; Bonacci, Gustavo; Golin-Bisello, Franca; Devlin, Jason E.; St. Croix, Claudette M.; Watkins, Simon C.; Gor, Sonia; Cantu-Medellin, Nadiezhda; Weidert, Eric R.; Frisbee, Jefferson C.; Gladwin, Mark T.; Champion, Hunter C.; Freeman, Bruce A.; Khoo, Nicholas K.H.

    2014-01-01

    Aims Obesity is a risk factor for diabetes and cardiovascular diseases, with the incidence of these disorders becoming epidemic. Pathogenic responses to obesity have been ascribed to adipose tissue (AT) dysfunction that promotes bioactive mediator secretion from visceral AT and the initiation of pro-inflammatory events that induce oxidative stress and tissue dysfunction. Current understanding supports that suppressing pro-inflammatory and oxidative events promotes improved metabolic and cardiovascular function. In this regard, electrophilic nitro-fatty acids display pleiotropic anti-inflammatory signalling actions. Methods and results It was hypothesized that high-fat diet (HFD)-induced inflammatory and metabolic responses, manifested by loss of glucose tolerance and vascular dysfunction, would be attenuated by systemic administration of nitrooctadecenoic acid (OA-NO2). Male C57BL/6j mice subjected to a HFD for 20 weeks displayed increased adiposity, fasting glucose, and insulin levels, which led to glucose intolerance and pulmonary hypertension, characterized by increased right ventricular (RV) end-systolic pressure (RVESP) and pulmonary vascular resistance (PVR). This was associated with increased lung xanthine oxidoreductase (XO) activity, macrophage infiltration, and enhanced expression of pro-inflammatory cytokines. Left ventricular (LV) end-diastolic pressure remained unaltered, indicating that the HFD produces pulmonary vascular remodelling, rather than LV dysfunction and pulmonary venous hypertension. Administration of OA-NO2 for the final 6.5 weeks of HFD improved glucose tolerance and significantly attenuated HFD-induced RVESP, PVR, RV hypertrophy, lung XO activity, oxidative stress, and pro-inflammatory pulmonary cytokine levels. Conclusions These observations support that the pleiotropic signalling actions of electrophilic fatty acids represent a therapeutic strategy for limiting the complex pathogenic responses instigated by obesity. PMID:24385344

  2. Beneficial Effects of Calcitriol on Hypertension, Glucose Intolerance, Impairment of Endothelium-Dependent Vascular Relaxation, and Visceral Adiposity in Fructose-Fed Hypertensive Rats

    PubMed Central

    Chou, Chu-Lin; Pang, Cheng-Yoong; Lee, Tony J. F.; Fang, Te-Chao

    2015-01-01

    Besides regulating calcium homeostasis, the effects of vitamin D on vascular tone and metabolic disturbances remain scarce in the literature despite an increase intake with high-fructose corn syrup worldwide. We investigated the effects of calcitriol, an active form of vitamin D, on vascular relaxation, glucose tolerance, and visceral fat pads in fructose-fed rats. Male Wistar-Kyoto rats were divided into 4 groups (n = 6 per group). Group Con: standard chow diet for 8 weeks; Group Fru: high-fructose diet (60% fructose) for 8 weeks; Group Fru-HVD: high-fructose diet as Group Fru, high-dose calcitriol treatment (20 ng / 100 g body weight per day) 4 weeks after the beginning of fructose feeding; and Group Fru-LVD: high-fructose diet as Group Fru, low-dose calcitriol treatment (10 ng / 100 g body weight per day) 4 weeks after the beginning of fructose feeding. Systolic blood pressure was measured twice a week by the tail-cuff method. Blood was examined for serum ionized calcium, phosphate, creatinine, glucose, triglycerides, and total cholesterol. Intra-peritoneal glucose intolerance test, aortic vascular reactivity, the weight of visceral fat pads, adipose size, and adipose angiotensin II levels were analyzed at the end of the study. The results showed that the fructose-fed rats significantly developed hypertension, impaired glucose tolerance, heavier weight and larger adipose size of visceral fat pads, and raised adipose angiotensin II expressions compared with the control rats. High- and low-dose calcitriol reduced modestly systolic blood pressure, increased endothelium-dependent aortic relaxation, ameliorated glucose intolerance, reduced the weight and adipose size of visceral fat pads, and lowered adipose angiotensin II expressions in the fructose-fed rats. However, high-dose calcitriol treatment mildly increased serum ionized calcium levels (1.44 ± 0.05 mmol/L). These results suggest a protective role of calcitriol treatment on endothelial function, glucose tolerance, and visceral adiposity in fructose-fed rats. PMID:25774877

  3. Aldosterone aggravates glucose intolerance induced by high fructose

    PubMed Central

    Sherajee, Shamshad J.; Rafiq, Kazi; Nakano, Daisuke; Mori, Hirohito; Kobara, Hideki; Hitomi, Hirofumi; Fujisawa, Yoshihide; Kobori, Hiroyuki; Masaki, Tsutomu; Nishiyama, Akira

    2013-01-01

    We previously reported that aldosterone impaired vascular insulin signaling in vivo and in vitro. Fructose-enriched diet induces metabolic syndrome including hypertension, insulin resistance, hyperlipidemia and diabetes in animal. In the current study, we hypothesized that aldosterone aggravated fructose feeding-induced glucose intolerance in vivo. Rats were divided into five groups for six-week treatment; uninephrectomy (Unx, n=8), Unx+aldosterone (aldo, 0.75 μg/h, s.c., n=8), Unx+fructose (fruc, 10% in drinking water, n=8), Unx+aldo+fruc, (aldo+fruc, n=8), and Unx+aldo+fruc+spironolactone, a mineralocorticoid receptor antagonist (aldo+fruc+spiro, 20 mg/kg/day, p.o., n=8). Aldo+fruc rats manifested the hypertension, and induced glucose intolerance compared to fruc intake rats assessed by oral glucose tolerance test, homeostasis model assessment of insulin resistance and hyperinsulinemic-euglycemic clamp study. Spironolactone, significantly improved the aldosterone-accelerated glucose intolerance. Along with improvement in insulin resistance, spironolactone suppressed upregulated mineralocorticoid receptor (MR) target gene, serum and glucocorticoid-regulated kinases-1 mRNA expression in skeletal muscle in aldo+fruc rats. In conclusion, these data suggested that aldosterone aggravates fructose feeding-induced glucose intolerance through MR activation. PMID:24201309

  4. Blood pressure is reduced and insulin sensitivity increased in glucose-intolerant, hypertensive subjects after 15 days of consuming high-polyphenol dark chocolate.

    PubMed

    Grassi, Davide; Desideri, Giovambattista; Necozione, Stefano; Lippi, Cristina; Casale, Raffaele; Properzi, Giuliana; Blumberg, Jeffrey B; Ferri, Claudio

    2008-09-01

    Flavanols from chocolate appear to increase nitric oxide bioavailability, protect vascular endothelium, and decrease cardiovascular disease (CVD) risk factors. We sought to test the effect of flavanol-rich dark chocolate (FRDC) on endothelial function, insulin sensitivity, beta-cell function, and blood pressure (BP) in hypertensive patients with impaired glucose tolerance (IGT). After a run-in phase, 19 hypertensives with IGT (11 males, 8 females; 44.8 +/- 8.0 y) were randomized to receive isocalorically either FRDC or flavanol-free white chocolate (FFWC) at 100 g/d for 15 d. After a wash-out period, patients were switched to the other treatment. Clinical and 24-h ambulatory BP was determined by sphygmometry and oscillometry, respectively, flow-mediated dilation (FMD), oral glucose tolerance test, serum cholesterol and C-reactive protein, and plasma homocysteine were evaluated after each treatment phase. FRDC but not FFWC ingestion decreased insulin resistance (homeostasis model assessment of insulin resistance; P < 0.0001) and increased insulin sensitivity (quantitative insulin sensitivity check index, insulin sensitivity index (ISI), ISI(0); P < 0.05) and beta-cell function (corrected insulin response CIR(120); P = 0.035). Systolic (S) and diastolic (D) BP decreased (P < 0.0001) after FRDC (SBP, -3.82 +/- 2.40 mm Hg; DBP, -3.92 +/- 1.98 mm Hg; 24-h SBP, -4.52 +/- 3.94 mm Hg; 24-h DBP, -4.17 +/- 3.29 mm Hg) but not after FFWC. Further, FRDC increased FMD (P < 0.0001) and decreased total cholesterol (-6.5%; P < 0.0001), and LDL cholesterol (-7.5%; P < 0.0001). Changes in insulin sensitivity (Delta ISI - Delta FMD: r = 0.510, P = 0.001; Delta QUICKI - Delta FMD: r = 0.502, P = 0.001) and beta-cell function (Delta CIR(120) - Delta FMD: r = 0.400, P = 0.012) were directly correlated with increases in FMD and inversely correlated with decreases in BP (Delta ISI - Delta 24-h SBP: r = -0.368, P = 0.022; Delta ISI - Delta 24-h DBP r = -0.384, P = 0.017). Thus, FRDC ameliorated insulin sensitivity and beta-cell function, decreased BP, and increased FMD in IGT hypertensive patients. These findings suggest flavanol-rich, low-energy cocoa food products may have a positive impact on CVD risk factors. PMID:18716168

  5. Uteroplacental insufficiency leads to hypertension, but not glucose intolerance or impaired skeletal muscle mitochondrial biogenesis, in 12-month-old rats.

    PubMed

    Tran, Melanie; Young, Margaret E; Jefferies, Andrew J; Hryciw, Deanne H; Ward, Michelle M; Fletcher, Erica L; Wlodek, Mary E; Wadley, Glenn D

    2015-09-01

    Growth restriction impacts on offspring development and increases their risk of disease in adulthood which is exacerbated with "second hits." The aim of this study was to investigate if blood pressure, glucose tolerance, and skeletal muscle mitochondrial biogenesis were altered in 12-month-old male and female offspring with prenatal or postnatal growth restriction. Bilateral uterine vessel ligation induced uteroplacental insufficiency and growth restriction in offspring (Restricted). A sham surgery was also performed during pregnancy (Control) and some litters from sham mothers had their litter size reduced (Reduced litter), which restricted postnatal growth. Growth-restricted females only developed hypertension at 12 months, which was not observed in males. In Restricted females only homeostasis model assessment for insulin resistance was decreased, indicating enhanced hepatic insulin sensitivity, which was not observed in males. Plasma leptin was increased only in the Reduced males at 12 months compared to Control and Restricted males, which was not observed in females. Compared to Controls, leptin, ghrelin, and adiponectin were unaltered in the Restricted males and females, suggesting that at 12 months of age the reduction in body weight in the Restricted offspring is not a consequence of circulating adipokines. Skeletal muscle PGC-1α levels were unaltered in 12-month-old male and female rats, which indicate improvements in lean muscle mass by 12 months of age. In summary, sex strongly impacts the cardiometabolic effects of growth restriction in 12-month-old rats and it is females who are at particular risk of developing long-term hypertension following growth restriction. PMID:26416974

  6. Hepatic lipase deficiency produces glucose intolerance, inflammation and hepatic steatosis.

    PubMed

    Andrés-Blasco, Irene; Herrero-Cervera, Andrea; Vinué, Ángela; Martínez-Hervás, Sergio; Piqueras, Laura; Sanz, María Jesús; Burks, Deborah Jane; González-Navarro, Herminia

    2015-12-01

    Metabolic syndrome and type 2 diabetes mellitus constitute a major problem to global health, and their incidence is increasing at an alarming rate. Non-alcoholic fatty liver disease, which affects up to 90% of obese people and nearly 70% of the overweight, is commonly associated with MetS characteristics such as obesity, insulin resistance, hypertension and dyslipidemia. In the present study, we demonstrate that hepatic lipase (HL)-inactivation in mice fed with a high-fat, high-cholesterol diet produced dyslipidemia including hypercholesterolemia, hypertriglyceridemia and increased non-esterified fatty acid levels. These changes were accompanied by glucose intolerance, pancreatic and hepatic inflammation and steatosis. In addition, compared with WT mice, HL(-/-) mice exhibited enhanced circulating MCP1 levels, monocytosis and higher percentage of CD4+Th17+ cells. Consistent with increased inflammation, livers from HL(-/-) mice had augmented activation of the stress SAPK/JNK- and p38-pathways compared with the activation levels of the kinases in livers from WT mice. Analysis of HL(-/-) and WT mice fed regular chow diet showed dyslipidemia and glucose intolerance in HL(-/-) mice without any other changes in inflammation or hepatic steatosis. Altogether, these results indicate that dyslipidemia induced by HL-deficiency in combination with a high-fat, high-cholesterol diet promotes hepatic steatosis and inflammation in mice which are, at least in part, mediated by the activation of the stress SAPK/JNK- and p38-pathways. Future studies are warranted to asses the viability of therapeutic strategies based on the modulation of these kinases to reduce hepatic steatosis associated to lipase dysfunction. PMID:26423094

  7. Thyroid hormone excess and glucose intolerance.

    PubMed

    Dimitriadis, G D; Raptis, S A

    2001-01-01

    The elevated plasma glucose levels in hyperthyroidism may be explained by increased rates of endogenous glucose production, due mainly to increased gluconeogenesis. The rates of insulin-stimulated glucose disposal in peripheral tissues in hyperthyroidism have been found, in general, either normal or increased. Skeletal muscle is the most important tissue for the disposal of glucose in response to insulin. In this tissue, insulin increases glucose disposal by stimulating glucose transport, glucose phosphorylation/glycolysis, glycogen synthesis and glucose oxidation. Studies examining insulin-stimulated glucose metabolism in skeletal muscle have suggested that, in the hyperthyroid state, it may be of primary importance to increase the rates of glycolysis and lactate formation relative to glucose oxidation in this tissue in order to provide substrate for gluconeogenesis (increase Cori cycle activity). This effect will be achieved primarily by a decrease in glycogen synthesis and an increase in glycogenolysis. When hyperthyroidism becomes more severe, an increased rate of glucose uptake into muscle may then be necessary since the increased conversion of glycogen to lactate could not be sustained for prolonged periods and might lead to a depletion in glycogen stores. This mechanism would ensure that the level of glucose in plasma is kept normal or slightly increased. Thus, an increased Cori cycle activity may be a necessary mechanism to provide optimal conditions in hyperthyroidism for the control of glucose utilization without increasing the risk of hypoglycemia. In addition to lactate, increased rates of gluconeogenesis in hyperthyroidism can also be sustained by increased plasma concentrations of amino acids (mostly glutamine and alanine) and glycerol, as well as by increased plasma concentrations of free fatty acids. PMID:11460573

  8. [Essential arterial hypertension, cellular intolerance to sodium].

    PubMed

    Meyer, P; Devynck, M A; Cloix, J F; Deray, G

    1984-04-01

    Much experimental and clinical evidence points to the fact that increased intracellular Na+ concentration could play an important pathogenic role in hypertension, especially where cells of excitable tissues are concerned. Active extrusion of Na+ (from the cells to the extracellular space) depends mainly on the activity of the system of membrane transport known as the Na+ pump. The extrusion of Na+ occurs in exchange for K+ and the activity of the pump depends on the enzyme Na+-K+-ATPase. The Na+ pump is inhibited by cardiotonic glycosides such as digitalis and ouabain . The results obtained in our laboratory suggest that the activity of the Na+ pump is controlled by an endogenic system acting in a similar manner to ouabain and digitalis. Experimental and clinical studies show: -- that the administration of Na+ increases the inhibitor effect both in urine and plasma; -- that the inhibitor is increased in about 50 p. 100 of patients with essential hypertension; -- that this increase seems to depend on familial or genetic factors. The biochemical identification of this endogenic inhibitor is now under way; it has a small molecular weight (less than 3000), is thermostable and anionic. This factor could have both a regulating role on Na+ turnover and a pathological role in hypertension. Its activity comes into competition cations also capable of inhibiting the Na+ pump, including K+. PMID:6329120

  9. Exercise intolerance in pulmonary arterial hypertension.

    PubMed

    Fowler, Robin M; Gain, Kevin R; Gabbay, Eli

    2012-01-01

    Pulmonary arterial hypertension (PAH) is associated with symptoms of dyspnea and fatigue, which contribute to exercise limitation. The origins and significance of dyspnea and fatigue in PAH are not completely understood. This has created uncertainly among healthcare professionals regarding acceptable levels of these symptoms, on exertion, for patients with PAH. Dysfunction of the right ventricle (RV) contributes to functional limitation and mortality in PAH; however, the role of the RV in eliciting dyspnea and fatigue has not been thoroughly examined. This paper explores the contribution of the RV and systemic and peripheral abnormalities to exercise limitation and symptoms in PAH. Further, it explores the relationship between exercise abnormalities and symptoms, the utility of the cardiopulmonary exercise test in identifying RV dysfunction, and offers suggestions for further research. PMID:22737582

  10. Exercise Intolerance in Pulmonary Arterial Hypertension

    PubMed Central

    Fowler, Robin M.; Gain, Kevin R.; Gabbay, Eli

    2012-01-01

    Pulmonary arterial hypertension (PAH) is associated with symptoms of dyspnea and fatigue, which contribute to exercise limitation. The origins and significance of dyspnea and fatigue in PAH are not completely understood. This has created uncertainly among healthcare professionals regarding acceptable levels of these symptoms, on exertion, for patients with PAH. Dysfunction of the right ventricle (RV) contributes to functional limitation and mortality in PAH; however, the role of the RV in eliciting dyspnea and fatigue has not been thoroughly examined. This paper explores the contribution of the RV and systemic and peripheral abnormalities to exercise limitation and symptoms in PAH. Further, it explores the relationship between exercise abnormalities and symptoms, the utility of the cardiopulmonary exercise test in identifying RV dysfunction, and offers suggestions for further research. PMID:22737582

  11. Perceived psychosocial stress and glucose intolerance among pregnant Hispanic women

    PubMed Central

    Silveira, M.L.; Whitcomb, B.W.; Pekow, P.; Braun, B.; Markenson, G.; Dole, N.; Manson, J.E.; Solomon, C.G.; Carbone, E.T.; Chasan-Taber, L.

    2016-01-01

    Aim Prior literature suggests a positive association between psychosocial stress and the risk of diabetes in non-pregnant populations, but studies during pregnancy are sparse. We evaluated the relationship between stress and glucose intolerance among 1115 Hispanic (predominantly Puerto Rican) prenatal care patients in Proyecto Buena Salud, a prospective cohort study in Western Massachusetts (2006–2011). Methods Cohen’s Perceived Stress Scale (PSS-14) was administered in early (mean = 12.3 weeks gestation; range 4.1–18 weeks) and mid-(mean = 21.3 weeks gestation; range 18.1–26 weeks) pregnancy. Participants were classified as having a pregnancy complicated by gestational diabetes mellitus, impaired glucose tolerance, and abnormal glucose tolerance, based on the degree of abnormality on glucose tolerance testing between 24 and 28 weeks of gestation. Results The prevalence of gestational diabetes mellitus, impaired glucose tolerance, and abnormal glucose tolerance was 4.1%, 7.2%, and 14.5%, respectively. Absolute levels of early or mid-pregnancy stress were not significantly associated with glucose intolerance. However, participants with an increase in stress from early to mid-pregnancy had a 2.6-fold increased odds of gestational diabetes mellitus (95% confidence intervals: 1.0–6.9) as compared to those with no change or a decrease in stress after adjusting for age and pre-pregnancy body mass index. In addition, every one-point increase in stress scores was associated with a 5.5 mg/dL increase in screening glucose level (β = 5.5; standard deviation = 2.8; P = 0.05), after adjusting for the same variables. Conclusion In this population of predominantly Puerto Rican women, stress patterns during pregnancy may influence the risk of glucose intolerance. PMID:24948416

  12. Glucose intolerance associated with hypoxia in people living at high altitudes in the Tibetan highland

    PubMed Central

    Okumiya, Kiyohito; Sakamoto, Ryota; Ishimoto, Yasuko; Kimura, Yumi; Fukutomi, Eriko; Ishikawa, Motonao; Suwa, Kuniaki; Imai, Hissei; Chen, Wenling; Kato, Emiko; Nakatsuka, Masahiro; Kasahara, Yoriko; Fujisawa, Michiko; Wada, Taizo; Wang, Hongxin; Dai, Qingxiang; Xu, Huining; Qiao, Haisheng; Ge, Ri-Li; Norboo, Tsering; Tsering, Norboo; Kosaka, Yasuyuki; Nose, Mitsuhiro; Yamaguchi, Takayoshi; Tsukihara, Toshihiro; Ando, Kazuo; Inamura, Tetsuya; Takeda, Shinya; Ishine, Masayuki; Otsuka, Kuniaki; Matsubayashi, Kozo

    2016-01-01

    Objectives To clarify the association between glucose intolerance and high altitudes (2900–4800 m) in a hypoxic environment in Tibetan highlanders and to verify the hypothesis that high altitude dwelling increases vulnerability to diabetes mellitus (DM) accelerated by lifestyle change or ageing. Design Cross-sectional epidemiological study on Tibetan highlanders. Participants We enrolled 1258 participants aged 40–87 years. The rural population comprised farmers in Domkhar (altitude 2900–3800 m) and nomads in Haiyan (3000–3100 m), Ryuho (4400 m) and Changthang (4300–4800 m). Urban area participants were from Leh (3300 m) and Jiegu (3700 m). Main outcome measure Participants were classified into six glucose tolerance-based groups: DM, intermediate hyperglycaemia (IHG), normoglycaemia (NG), fasting DM, fasting IHG and fasting NG. Prevalence of glucose intolerance was compared in farmers, nomads and urban dwellers. Effects of dwelling at high altitude or hypoxia on glucose intolerance were analysed with the confounding factors of age, sex, obesity, lipids, haemoglobin, hypertension and lifestyle, using multiple logistic regression. Results The prevalence of DM (fasting DM)/IHG (fasting IHG) was 8.9% (6.5%)/25.1% (12.7%), respectively, in all participants. This prevalence was higher in urban dwellers (9.5% (7.1%)/28.5% (11.7%)) and in farmers (8.5% (6.1%)/28.5% (18.3%)) compared with nomads (8.2% (5.7%)/15.7% (9.7%)) (p=0.0140/0.0001). Dwelling at high altitude was significantly associated with fasting IHG+fasting DM/fasting DM (ORs for >4500 and 3500–4499 m were 3.59/4.36 and 2.07/1.76 vs <3500 m, respectively). After adjusting for lifestyle change, hypoxaemia and polycythaemia were closely associated with glucose intolerance. Conclusions Socioeconomic factors, hypoxaemia and the effects of altitudes >3500 m play a major role in the high prevalence of glucose intolerance in highlanders. Tibetan highlanders may be vulnerable to glucose intolerance, with polycythaemia as a sign of poor hypoxic adaptation, accelerated by lifestyle change and ageing. PMID:26908520

  13. Healthy diet and lifestyle clustering and glucose intolerance.

    PubMed

    Perry, I J

    2002-11-01

    Glucose intolerance represents a spectrum of abnormalities, including impaired fasting glucose, impaired glucose tolerance and type 2 diabetes. It is a major public health challenge worldwide, with rapidly increasing prevalence rates in both developed and developing countries. This global epidemic of diabetes is largely driven by the globalisation of Western culture and lifestyles. Specifically, there is now evidence from large-scale observational studies, and from intervention studies, of powerful synergistic interactions between diet, obesity, exercise, smoking and alcohol in the development of glucose intolerance. It is estimated that >90% of cases of type 2 diabetes in the population could be prevented with the adoption of a prudent diet (high in cereal fibre and polyunsaturated fatty acids and low in trans-fatty acids and glycaemic load), avoidance of overweight and obesity (BMI<25 kg/m2), engagement in moderate to vigorous physical activity for at least 0.5 h/d, non-smoking and moderate alcohol consumption. These findings are biologically plausible and have major public health implications. They form the basis for a clear, simple and coherent message for health promotion and public policy. However, to make progress on these issues health will need to be placed at the centre of public policy and relevant vested interests tackled, notably in the food, entertainment, tobacco and automobile industries. PMID:12691184

  14. High iron level in early pregnancy increased glucose intolerance.

    PubMed

    Zein, Salam; Rachidi, Samar; Awada, Sanaa; Osman, Mireille; Al-Hajje, Amal; Shami, Nadine; Sharara, Iman; Cheikh-Ali, Khawla; Salameh, Pascale; Hininger-Favier, Isabelle

    2015-04-01

    High iron stores in pregnancy are essential in preventing negative outcomes for both infants and mothers; however the risk of gestational diabetes mellitus (GDM) might also be increased. We intend to study the relationship between increased iron stores in early pregnancy and the risk of glucose intolerance and GDM. This prospective, observational, single-hospital study involved 104 non-anemic pregnant women, divided into 4 groups based on the quartile values for ferritin at the first trimester of pregnancy. All participants were screened for GDM with 75-g oral glucose tolerance test (OGTT) at 24-28 weeks' gestation. We observed that ferritin levels at early pregnancy were significantly correlated to glucose level after OGTT at 1-h and 2-h (rho=0.21, p<0.05; rho=0.43, p<0.001 respectively). Furthermore, in the higher quartile for ferritin (>38.8μg/L) glycemia at 2-h OGTT was significantly higher than in the others quartiles (p=0.002). In multivariate regression analysis, serum ferritin was a significant determinant of glycemia at 2-h OGTT. Although we did not find a significant association in the incidence of GDM in women with higher serum ferritin levels, probably in reason to the limit power of our study, our data demonstrated that the role of iron excess is tightly involved in the pathogenesis of glucose intolerance. We report for the first time that high ferritin values in early pregnancy are predictors of impaired glucose tolerance in non-anemic women. Individual iron supplementation should be evaluated in order to minimize glucose impairment risk in women with high risk of diabetes. PMID:25441227

  15. Glucose Homeostatic Law: Insulin Clearance Predicts the Progression of Glucose Intolerance in Humans

    PubMed Central

    Uda, Shinsuke; Kubota, Hiroyuki; Iwaki, Toshinao; Fukuzawa, Hiroki; Komori, Yasunori; Fujii, Masashi; Toyoshima, Yu; Sakaguchi, Kazuhiko; Ogawa, Wataru; Kuroda, Shinya

    2015-01-01

    Homeostatic control of blood glucose is regulated by a complex feedback loop between glucose and insulin, of which failure leads to diabetes mellitus. However, physiological and pathological nature of the feedback loop is not fully understood. We made a mathematical model of the feedback loop between glucose and insulin using time course of blood glucose and insulin during consecutive hyperglycemic and hyperinsulinemic-euglycemic clamps in 113 subjects with variety of glucose tolerance including normal glucose tolerance (NGT), impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2DM). We analyzed the correlation of the parameters in the model with the progression of glucose intolerance and the conserved relationship between parameters. The model parameters of insulin sensitivity and insulin secretion significantly declined from NGT to IGT, and from IGT to T2DM, respectively, consistent with previous clinical observations. Importantly, insulin clearance, an insulin degradation rate, significantly declined from NGT, IGT to T2DM along the progression of glucose intolerance in the mathematical model. Insulin clearance was positively correlated with a product of insulin sensitivity and secretion assessed by the clamp analysis or determined with the mathematical model. Insulin clearance was correlated negatively with postprandial glucose at 2h after oral glucose tolerance test. We also inferred a square-law between the rate constant of insulin clearance and a product of rate constants of insulin sensitivity and secretion in the model, which is also conserved among NGT, IGT and T2DM subjects. Insulin clearance shows a conserved relationship with the capacity of glucose disposal among the NGT, IGT and T2DM subjects. The decrease of insulin clearance predicts the progression of glucose intolerance. PMID:26623647

  16. Artificial sweeteners induce glucose intolerance by altering the gut microbiota.

    PubMed

    Suez, Jotham; Korem, Tal; Zeevi, David; Zilberman-Schapira, Gili; Thaiss, Christoph A; Maza, Ori; Israeli, David; Zmora, Niv; Gilad, Shlomit; Weinberger, Adina; Kuperman, Yael; Harmelin, Alon; Kolodkin-Gal, Ilana; Shapiro, Hagit; Halpern, Zamir; Segal, Eran; Elinav, Eran

    2014-10-01

    Non-caloric artificial sweeteners (NAS) are among the most widely used food additives worldwide, regularly consumed by lean and obese individuals alike. NAS consumption is considered safe and beneficial owing to their low caloric content, yet supporting scientific data remain sparse and controversial. Here we demonstrate that consumption of commonly used NAS formulations drives the development of glucose intolerance through induction of compositional and functional alterations to the intestinal microbiota. These NAS-mediated deleterious metabolic effects are abrogated by antibiotic treatment, and are fully transferrable to germ-free mice upon faecal transplantation of microbiota configurations from NAS-consuming mice, or of microbiota anaerobically incubated in the presence of NAS. We identify NAS-altered microbial metabolic pathways that are linked to host susceptibility to metabolic disease, and demonstrate similar NAS-induced dysbiosis and glucose intolerance in healthy human subjects. Collectively, our results link NAS consumption, dysbiosis and metabolic abnormalities, thereby calling for a reassessment of massive NAS usage. PMID:25231862

  17. Human Gut Microbiota Changes Reveal the Progression of Glucose Intolerance

    PubMed Central

    Zhang, Xiuying; Shen, Dongqian; Fang, Zhiwei; Jie, Zhuye; Qiu, Xinmin; Zhang, Chunfang; Chen, Yingli; Ji, Linong

    2013-01-01

    To explore the relationship of gut microbiota with the development of type 2 diabetes (T2DM), we analyzed 121 subjects who were divided into 3 groups based on their glucose intolerance status: normal glucose tolerance (NGT; n = 44), prediabetes (Pre-DM; n = 64), or newly diagnosed T2DM (n = 13). Gut microbiota characterizations were determined with 16S rDNA-based high-throughput sequencing. T2DM-related dysbiosis was observed, including the separation of microbial communities and a change of alpha diversity between the different glucose intolerance statuses. To assess the correlation between metabolic parameters and microbiota diversity, clinical characteristics were also measured and a significant association between metabolic parameters (FPG, CRP) and gut microbiota was found. In addition, a total of 28 operational taxonomic units (OTUs) were found to be related to T2DM status by the Kruskal-Wallis H test, most of which were enriched in the T2DM group. Butyrate-producing bacteria (e.g. Akkermansia muciniphila ATCCBAA-835, and Faecalibacterium prausnitzii L2-6) had a higher abundance in the NGT group than in the pre-DM group. At genus level, the abundance of Bacteroides in the T2DM group was only half that of the NGT and Pre-DM groups. Previously reported T2DM-related markers were also compared with the data in this study, and some inconsistencies were noted. We found that Verrucomicrobiae may be a potential marker of T2DM as it had a significantly lower abundance in both the pre-DM and T2DM groups. In conclusion, this research provides further evidence of the structural modulation of gut microbiota in the pathogenesis of diabetes. PMID:24013136

  18. Vitamin E and Vitamin C supplementation does not prevent glucose intolerance in obese-prone rats

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Obesity-induced glucose intolerance affects over 70 million Americans. Elevated oxidative stress is associated with development of glucose intolerance. In this work, we tested the hypothesis that supplementation with the anti-oxidants vitamin E (d-alpha-tocopherol acetate; 0.4 g/kg diet) and vitamin...

  19. Effects of exercise and metformin on the prevention of glucose intolerance: a comparative study.

    PubMed

    Molena-Fernandes, C; Bersani-Amado, C A; Ferraro, Z M; Hintze, L J; Nardo, N; Cuman, R K N

    2015-12-01

    We aimed to evaluate the effects of aerobic exercise training (4 days) and metformin exposure on acute glucose intolerance after dexamethasone treatment in rats. Forty-two adult male Wistar rats (8 weeks old) were divided randomly into four groups: sedentary control (SCT), sedentary dexamethasone-treated (SDX), training dexamethasone-treated (DPE), and dexamethasone and metformin treated group (DMT). Glucose tolerance tests and in situ liver perfusion were undertaken on fasting rats to obtain glucose profiles. The DPE group displayed a significant decrease in glucose values compared with the SDX group. Average glucose levels in the DPE group did not differ from those of the DMT group, so we suggest that exercise training corrects dexamethasone-induced glucose intolerance and improves glucose profiles in a similar manner to that observed with metformin. These data suggest that exercise may prevent the development of glucose intolerance induced by dexamethasone in rats to a similar magnitude to that observed after metformin treatment. PMID:26421869

  20. Effects of exercise and metformin on the prevention of glucose intolerance: a comparative study

    PubMed Central

    Molena-Fernandes, C.; Bersani-Amado, C. A.; Ferraro, Z. M.; Hintze, L. J.; Nardo, N.; Cuman, R. K. N.

    2015-01-01

    We aimed to evaluate the effects of aerobic exercise training (4 days) and metformin exposure on acute glucose intolerance after dexamethasone treatment in rats. Forty-two adult male Wistar rats (8 weeks old) were divided randomly into four groups: sedentary control (SCT), sedentary dexamethasone-treated (SDX), training dexamethasone-treated (DPE), and dexamethasone and metformin treated group (DMT). Glucose tolerance tests and in situ liver perfusion were undertaken on fasting rats to obtain glucose profiles. The DPE group displayed a significant decrease in glucose values compared with the SDX group. Average glucose levels in the DPE group did not differ from those of the DMT group, so we suggest that exercise training corrects dexamethasone-induced glucose intolerance and improves glucose profiles in a similar manner to that observed with metformin. These data suggest that exercise may prevent the development of glucose intolerance induced by dexamethasone in rats to a similar magnitude to that observed after metformin treatment. PMID:26421869

  1. Intermittent hypoxia-induced glucose intolerance is abolished by ?-adrenergic blockade or adrenal medullectomy

    PubMed Central

    Shin, Mi-Kyung; Devera, Ronald; Yao, Qiaoling; Mesarwi, Omar; Bevans-Fonti, Shannon; Polotsky, Vsevolod Y.

    2014-01-01

    Obstructive sleep apnea causes intermittent hypoxia (IH) during sleep and is associated with dysregulation of glucose metabolism. We developed a novel model of clinically realistic IH in mice to test the hypothesis that IH causes hyperglycemia, glucose intolerance, and insulin resistance via activation of the sympathetic nervous system. Mice were exposed to acute hypoxia of graded severity (21, 14, 10, and 7% O2) or to IH of graded frequency [oxygen desaturation index (ODI) of 0, 15, 30, or 60, SpO2 nadir 80%] for 30 min to measure levels of glucose fatty acids, glycerol, insulin, and lactate. Glucose tolerance tests and insulin tolerance tests were then performed under each hypoxia condition. Next, we examined these outcomes in mice that were administered phentolamine (?-adrenergic blockade) or propranolol (?-adrenergic blockade) or that underwent adrenal medullectomy before IH exposure. In all experiments, mice were maintained in a thermoneutral environment. Sustained and IH induced hyperglycemia, glucose intolerance, and insulin resistance in a dose-dependent fashion. Only severe hypoxia (7% O2) increased lactate, and only frequent IH (ODI 60) increased plasma fatty acids. Phentolamine or adrenal medullectomy both prevented IH-induced hyperglycemia and glucose intolerance. IH inhibited glucose-stimulated insulin secretion, and phentolamine prevented the inhibition. Propranolol had no effect on glucose metabolism but abolished IH-induced lipolysis. IH-induced insulin resistance was not affected by any intervention. Acutely hypoxia causes hyperglycemia, glucose intolerance, and insulin resistance in a dose-dependent manner. During IH, circulating catecholamines act upon ?-adrenoreceptors to cause hyperglycemia and glucose intolerance. PMID:25315697

  2. Genetic disruption of SOD1 gene causes glucose intolerance and impairs β-cell function.

    PubMed

    Muscogiuri, Giovanna; Salmon, Adam B; Aguayo-Mazzucato, Cristina; Li, Mengyao; Balas, Bogdan; Guardado-Mendoza, Rodolfo; Giaccari, Andrea; Reddick, Robert L; Reyna, Sara M; Weir, Gordon; Defronzo, Ralph A; Van Remmen, Holly; Musi, Nicolas

    2013-12-01

    Oxidative stress has been associated with insulin resistance and type 2 diabetes. However, it is not clear whether oxidative damage is a cause or a consequence of the metabolic abnormalities present in diabetic subjects. The goal of this study was to determine whether inducing oxidative damage through genetic ablation of superoxide dismutase 1 (SOD1) leads to abnormalities in glucose homeostasis. We studied SOD1-null mice and wild-type (WT) littermates. Glucose tolerance was evaluated with intraperitoneal glucose tolerance tests. Peripheral and hepatic insulin sensitivity was quantitated with the euglycemic-hyperinsulinemic clamp. β-Cell function was determined with the hyperglycemic clamp and morphometric analysis of pancreatic islets. Genetic ablation of SOD1 caused glucose intolerance, which was associated with reduced in vivo β-cell insulin secretion and decreased β-cell volume. Peripheral and hepatic insulin sensitivity were not significantly altered in SOD1-null mice. High-fat diet caused glucose intolerance in WT mice but did not further worsen the glucose intolerance observed in standard chow-fed SOD1-null mice. Our findings suggest that oxidative stress per se does not play a major role in the pathogenesis of insulin resistance and demonstrate that oxidative stress caused by SOD1 ablation leads to glucose intolerance secondary to β-cell dysfunction. PMID:24009256

  3. Cassia cinnamon for the attenuation of glucose intolerance and insulin resistance resulting from sleep loss.

    PubMed

    Jitomir, Jean; Willoughby, Darryn S

    2009-06-01

    Epidemiological investigations reveal a concomitant increase in sleep loss and metabolic diseases, including type 2 diabetes mellitus, over the past several decades. An increasing body of scientific evidence indicates that acute sleep loss induces insulin resistance and glucose intolerance profiles similar to those of type 2 diabetes mellitus patients. Experimentally, cassia cinnamon (Cinnamomum cassia) supplementation facilitates glucose disposal in healthy humans, which may be achieved by enhancing (1) insulin sensitivity via increased phosphorylation of signaling proteins and (2) insulin-sensitive glucose transporter 4-mediated glucose uptake into muscle cells. Because peripheral insulin resistance is primarily a consequence of reduced muscle insulin sensitivity, C. cassia and C. cassia extracts may attenuate insulin resistance and glucose intolerance observed following sleep loss. PMID:19627193

  4. Muscle Histidine-Containing Dipeptides Are Elevated by Glucose Intolerance in Both Rodents and Men

    PubMed Central

    Stegen, Sanne; Everaert, Inge; Deldicque, Louise; Vallova, Silvia; de Courten, Barbora; Ukropcova, Barbara; Ukropec, Jozef; Derave, Wim

    2015-01-01

    Objective Muscle carnosine and its methylated form anserine are histidine-containing dipeptides. Both dipeptides have the ability to quench reactive carbonyl species and previous studies have shown that endogenous tissue levels are decreased in chronic diseases, such as diabetes. Design and Methods Rodent study: Skeletal muscles of rats and mice were collected from 4 different diet-intervention studies, aiming to induce various degrees of glucose intolerance: 45% high-fat feeding (male rats), 60% high-fat feeding (male rats), cafeteria feeding (male rats), 70% high-fat feeding (female mice). Body weight, glucose-tolerance and muscle histidine-containing dipeptides were assessed. Human study: Muscle biopsies were taken from m. vastus lateralis in 35 males (9 lean, 8 obese, 9 prediabetic and 9 newly diagnosed type 2 diabetic patients) and muscle carnosine and gene expression of muscle fiber type markers were measured. Results Diet interventions in rodents (cafeteria and 70% high-fat feeding) induced increases in body weight, glucose intolerance and levels of histidine-containing dipeptides in muscle. In humans, obese, prediabetic and diabetic men had increased muscle carnosine content compared to the lean (+21% (p>0.1), +30% (p<0.05) and +39% (p<0.05), respectively). The gene expression of fast-oxidative type 2A myosin heavy chain was increased in the prediabetic (1.8-fold, p<0.05) and tended to increase in the diabetic men (1.6-fold, p = 0.07), compared to healthy lean subjects. Conclusion Muscle histidine-containing dipeptides increases with progressive glucose intolerance, in male individuals (cross-sectional). In addition, high-fat diet-induced glucose intolerance was associated with increased muscle histidine-containing dipeptides in female mice (interventional). Increased muscle carnosine content might reflect fiber type composition and/or act as a compensatory mechanism aimed at preventing cell damage in states of impaired glucose tolerance. PMID:25803044

  5. Defective insulin secretion by chronic glucagon receptor activation in glucose intolerant mice.

    PubMed

    Ahlkvist, Linda; Omar, Bilal; Valeur, Anders; Fosgerau, Keld; Ahrén, Bo

    2016-03-01

    Stimulation of insulin secretion by short-term glucagon receptor (GCGR) activation is well characterized; however, the effect of long-term GCGR activation on β-cell function is not known, but of interest, since hyperglucagonemia occurs early during development of type 2 diabetes. Therefore, we examined whether chronic GCGR activation affects insulin secretion in glucose intolerant mice. To induce chronic GCGR activation, high-fat diet fed mice were continuously (2 weeks) infused with the stable glucagon analog ZP-GA-1 and challenged with oral glucose and intravenous glucose±glucagon-like peptide 1 (GLP1). Islets were isolated to evaluate the insulin secretory response to glucose±GLP1 and their pancreas were collected for immunohistochemical analysis. Two weeks of ZP-GA-1 infusion reduced insulin secretion both after oral and intravenous glucose challenges in vivo and in isolated islets. These inhibitory effects were corrected for by GLP1. Also, we observed increased β-cell area and islet size. We conclude that induction of chronic ZP-GA-1 levels in glucose intolerant mice markedly reduces insulin secretion, and thus, we suggest that chronic activation of the GCGR may contribute to the failure of β-cell function during development of type 2 diabetes. PMID:26698567

  6. Assessment of the mechanisms exerting glucose-lowering effects of dried peas in glucose-intolerant rats.

    PubMed

    Whitlock, Kevin A; Kozicky, Lisa; Jin, Alena; Yee, Homun; Ha, Christine; Morris, Jill; Field, Catherine J; Bell, Rhonda C; Ozga, Jocelyn A; Chan, Catherine B

    2012-08-01

    The present study compared the effects of feeding uncooked pea fractions (embryo v. seed coat) on glucose homeostasis in glucose-intolerant rats and examined potential mechanisms influencing glucose homeostasis. Rats were made glucose intolerant by high-fat feeding, after which diets containing both high-fat and pea fractions were fed for 4 weeks. Rats fed diets containing uncooked pea seed coats low (non-coloured seed coat; NSC) or high (coloured seed coat; CSC) in proanthocyanidins but not embryos had improved oral glucose tolerance (P < 0·05). NSC also lowered fasting and glucose-stimulated insulin secretion (P < 0·05), decreased β-cell mass by 50 % (P < 0·05) and lowered levels of malondialdehyde, a marker of oxidative stress. Furthermore, NSC decreased the mucosal thickness of the colon by 25 % (P < 0·05), which might affect fibre fermentation and other gut functions. Small but statistically significant (P < 0·05) effects consistent with enhanced glucose transport or metabolism were observed in the skeletal muscle of rats fed NSC or CSC, for example, increased levels of AMP-dependent kinase or akt. We conclude that pea seed coats are the fraction exerting beneficial effects on glucose tolerance. Most of the changes were small in amplitude, suggesting that additive effects on multiple tissues may be important. NSC content appeared to have the most beneficial effects in improving glucose homeostasis but our ability to detect the effect of flavonoids may have been limited by their low concentration in the diet. PMID:22916820

  7. Glucose intolerance induced by blockade of central FGF receptors is linked to an acute stress response

    PubMed Central

    Rojas, Jennifer M.; Matsen, Miles E.; Mundinger, Thomas O.; Morton, Gregory J.; Stefanovski, Darko; Bergman, Richard N.; Kaiyala, Karl J.; Taborsky, Gerald J.; Schwartz, Michael W.

    2015-01-01

    Objective Central administration of ligands for fibroblast growth factor receptors (FGFRs) such as fibroblast growth factor-19 (FGF19) and FGF21 exert glucose-lowering effects in rodent models of obesity and type 2 diabetes (T2D). Conversely, intracerebroventricular (icv) administration of the non-selective FGFR inhibitor (FGFRi) PD173074 causes glucose intolerance, implying a physiological role for neuronal FGFR signaling in glucose homeostasis. The current studies were undertaken to identify neuroendocrine mechanisms underlying the glucose intolerance induced by pharmacological blockade of central FGFRs. Methods Overnight fasted, lean, male, Long-Evans rats received icv injections of either PD173074 or vehicle (Veh) followed 30 min later by performance of a frequently sampled intravenous glucose tolerance test (FSIGT). Minimal model analysis of glucose and insulin data from the FSIGT was performed to estimate insulin-dependent and insulin-independent components of glucose disposal. Plasma levels of lactate, glucagon, corticosterone, non-esterified free fatty acids (NEFA) and catecholamines were measured before and after intravenous (iv) glucose injection. Results Within 20 min of icv PD173074 injection (prior to the FSIGT), plasma levels of lactate, norepinephrine and epinephrine increased markedly, and each returned to baseline rapidly (within 8 min) following the iv glucose bolus. In contrast, plasma glucagon levels were not altered by icv FGFRi at either time point. Consistent with a previous report, glucose tolerance was impaired following icv PD173074 compared to Veh injection and, based on minimal model analysis of FSIGT data, this effect was attributable to reductions of both insulin secretion and the basal insulin effect (BIE), consistent with the inhibitory effect of catecholamines on pancreatic β-cell secretion. By comparison, there were no changes in glucose effectiveness at zero insulin (GEZI) or the insulin sensitivity index (SI). To determine if iv glucose (given during the FSIGT) contributed to the rapid resolution of the sympathoadrenal response induced by icv FGFRi, we performed an additional study comparing groups that received iv saline or iv glucose 30 min after icv FGFRi. Our finding that elevated plasma catecholamine levels returned rapidly to baseline irrespective of whether rats subsequently received an iv bolus of saline or glucose indicates that the rapid reversal of sympathoadrenal activation following icv FGFRi was unrelated to the subsequent glucose bolus. Conclusions The effect of acute inhibition of central FGFR signaling to impair glucose tolerance likely involves a stress response associated with pronounced, but transient, sympathoadrenal activation and an associated reduction of insulin secretion. Whether this effect is a true consequence of FGFR blockade or involves an off-target effect of the FGFR inhibitor requires additional study. PMID:26266088

  8. Arsenic Exposure and Glucose Intolerance/Insulin Resistance in Estrogen-Deficient Female Mice

    PubMed Central

    Huang, Chun-Fa; Yang, Ching-Yao; Chan, Ding-Cheng; Wang, Ching-Chia; Huang, Kuo-How; Wu, Chin-Ching; Tsai, Keh-Sung; Yang, Rong-Sen

    2015-01-01

    Background Epidemiological studies have reported that the prevalence of diabetes in women > 40 years of age, especially those in the postmenopausal phase, was higher than in men in areas with high levels of arsenic in drinking water. The detailed effect of arsenic on glucose metabolism/homeostasis in the postmenopausal condition is still unclear. Objectives We investigated the effects of arsenic at doses relevant to human exposure from drinking water on blood glucose regulation in estrogen-deficient female mice. Methods Adult female mice who underwent ovariectomy or sham surgery were exposed to drinking water contaminated with arsenic trioxide (0.05 or 0.5 ppm) in the presence or absence of 17β-estradiol supplementation for 2–6 weeks. Assays related to glucose metabolism were performed. Results Exposure of sham mice to arsenic significantly increased blood glucose, decreased plasma insulin, and impaired glucose tolerance, but did not induce insulin resistance. Blood glucose and insulin were higher, and glucose intolerance, insulin intolerance, and insulin resistance were increased in arsenic-treated ovariectomized mice compared with arsenic-treated sham mice. Furthermore, liver phosphoenolpyruvate carboxykinase (PEPCK) mRNA expression was increased and liver glycogen content was decreased in arsenic-treated ovariectomized mice compared with arsenic-treated sham mice. Glucose-stimulated insulin secretion in islets isolated from arsenic-treated ovariectomized mice was also significantly decreased. Arsenic treatment significantly decreased plasma adiponectin levels in sham and ovariectomized mice. Altered glucose metabolism/homeostasis in arsenic-treated ovariectomized mice was reversed by 17β-estradiol supplementation. Conclusions Our findings suggest that estrogen deficiency plays an important role in arsenic-altered glucose metabolism/homeostasis in females. Citation Huang CF, Yang CY, Chan DC, Wang CC, Huang KH, Wu CC, Tsai KS, Yang RS, Liu SH. 2015. Arsenic exposure and glucose intolerance/insulin resistance in estrogen-deficient female mice. Environ Health Perspect 123:1138–1144; http://dx.doi.org/10.1289/ehp.1408663 PMID:25859628

  9. Autoantibodies to pancreatic hsp60 precede the development of glucose intolerance in patients with cystic fibrosis.

    PubMed

    Jensen, P; Johansen, H K; Carmi, P; Høiby, N; Cohen, I R

    2001-09-01

    Persons expressing the genetic disease cystic fibrosis (CF) suffer from a high risk of developing impaired glucose tolerance and diabetes. The development of diabetes in CF has been attributed, in the past, to the destruction of pancreatic islets and their resident beta-cells secondary to the destruction of the surrounding tissue by mechanical clogging of the pancreatic exocrine ducts. However, the discovery that autoimmunity to the 60-kDa heat shock protein (hsp60) may cause type I diabetes in NOD mice raises the possibility that hsp60 autoimmunity may be involved in CF diabetes too; could the hyperimmunization to bacterial hsp60 characteristic of CF spread to self-hsp60 and hence to autoimmune diabetes? We now report that rising levels of IgG autoantibodies to hsp60 do indeed precede the appearance of glucose intolerance and diabetes in CF patients. We produced a recombinant human pancreatic hsp60 protein and investigated the IgG antibody response to hsp60 in prediabetic and non-diabetic patients with CF. To detect hsp60 autoantibodies in the presence of high levels of antibodies to bacterial hsp60, we absorbed test sera with the 60-kDa GroEL of Pseudomonas aeruginosa and used an immunostaining technique. Using this technique, 32 prediabetic CF patients were evaluated over a five-year period, three years, on the average, before the onset of glucose intolerance. We found that a significant increase in hsp60 autoantibody preceded impaired glucose tolerance (P=0.042, n=17), diabetes (P=0.011, n=15) and glucose intolerance (P=0.005, n=32). As has been observed in NOD mice and in type I diabetic patients, the hsp60 autoantibodies decline at the outbreak of glucose intolerance in the CF patients. The association of CF diabetes with the rise and fall of hsp60 autoimmunity suggests that the pathogenesis of the diabetes may not be merely mechanical, but arise in the wake of bacterial hyperimmunisation. PMID:11591125

  10. Ozone induces glucose intolerance and systemic metabolic effects in young and aged brown Norway rats

    SciTech Connect

    Bass, V.; Gordon, C.J.; Jarema, K.A.; MacPhail, R.C.; Cascio, W.E.; Phillips, P.M.; Ledbetter, A.D.; Schladweiler, M.C.; Andrews, D.; Miller, D.; Doerfler, D.L.; Kodavanti, U.P.

    2013-12-15

    Air pollutants have been associated with increased diabetes in humans. We hypothesized that ozone would impair glucose homeostasis by altering insulin signaling and/or endoplasmic reticular (ER) stress in young and aged rats. One, 4, 12, and 24 month old Brown Norway (BN) rats were exposed to air or ozone, 0.25 or 1.0 ppm, 6 h/day for 2 days (acute) or 2 d/week for 13 weeks (subchronic). Additionally, 4 month old rats were exposed to air or 1.0 ppm ozone, 6 h/day for 1 or 2 days (time-course). Glucose tolerance tests (GTT) were performed immediately after exposure. Serum and tissue biomarkers were analyzed 18 h after final ozone for acute and subchronic studies, and immediately after each day of exposure in the time-course study. Age-related glucose intolerance and increases in metabolic biomarkers were apparent at baseline. Acute ozone caused hyperglycemia and glucose intolerance in rats of all ages. Ozone-induced glucose intolerance was reduced in rats exposed for 13 weeks. Acute, but not subchronic ozone increased α{sub 2}-macroglobulin, adiponectin and osteopontin. Time-course analysis indicated glucose intolerance at days 1 and 2 (2 > 1), and a recovery 18 h post ozone. Leptin increased day 1 and epinephrine at all times after ozone. Ozone tended to decrease phosphorylated insulin receptor substrate-1 in liver and adipose tissues. ER stress appeared to be the consequence of ozone induced acute metabolic impairment since transcriptional markers of ER stress increased only after 2 days of ozone. In conclusion, acute ozone exposure induces marked systemic metabolic impairments in BN rats of all ages, likely through sympathetic stimulation. - Highlights: • Air pollutants have been associated with increased diabetes in humans. • Acute ozone exposure produces profound metabolic alterations in rats. • Age influences metabolic risk factors in aging BN rats. • Acute metabolic effects are reversible and repeated exposure reduces these effects. • Ozone metabolic effects are only slightly exacerbated in geriatric rats.

  11. Delayed effects of proton irradiation in Macaca mulatta. III. Glucose intolerance. Interim report 1964-1983

    SciTech Connect

    Salmon, Y.L.; Yochmowitz, M.G.; Wood, D.H.

    1984-03-01

    A group of rhesus monkeys is being studied in a lifetime survey of the delayed effects of proton irradiation. The animals were exposed during the period 1964 - 1969 to single total-body doses of protons covering the spectrum of energies and total doses that might be expected to occur in space during a major solar flare event. This report describes the results of intravenous glucose tolerance test and the insulin response to glucose challenge in 106 irradiated animals, their control group of 42, and 10 younger control animals. The results indicate that the clearance rate of blood glucose is influenced by the age of the animal and by the type and energy of the radiation. Animals receiving greater than 360 rads of proton irradiation of energies above 138 MeV had significantly slower glucose clearance than nonirradiated controls. Seventeen-twenty-year-old controls were less glucose tolerant than 9-11-year-old controls. Animals with normal glucose tolerance showed considerable individual variation in insulin response, while in animals with marked glucose intolerance (clearance rate < 1.0 %/min), low insulin response was a consistent finding.

  12. Antidiabetic-drug combination treatment for glucose intolerance in adult female rats treated acutely with olanzapine.

    PubMed

    Boyda, Heidi N; Procyshyn, Ric M; Asiri, Yahya; Wu, Claire; Wang, Cathy K; Lo, Ryan; Pang, Catherine C Y; Honer, William G; Barr, Alasdair M

    2014-01-01

    Second generation antipsychotic drugs are routinely used as treatment for psychotic disorders. Many of these compounds, including olanzapine, cause metabolic side-effects such as impaired glucose tolerance and insulin resistance. Individual antidiabetic drugs can help control elevated glucose levels in patients treated with antipsychotics, but the effects of combining antidiabetics, which routinely occurs with Type 2 diabetes mellitus patients, have never been studied. Presently, we compared the effects of the three different antidiabetics metformin (500mg/kg, p.o.), rosiglitazone (30mg/kg, p.o.) and glyburide (10mg/kg, p.o.) on metabolic dysregulation in adult female rats treated acutely with olanzapine. In addition, dual combinations of each of these antidiabetics were compared head-to-head against each other and the individual drugs. The animals received two daily treatments with antidiabetics and were then treated acutely with olanzapine (10mg/kg, i.p.). Fasting glucose and insulin levels were measured, followed by a 2h glucose tolerance test. Olanzapine caused a large and highly significant glucose intolerance compared to vehicle treated rats. Rosiglitazone decreased glucose levels non-significantly, while both metformin and glyburide significantly decreased glucose levels compared to olanzapine-only treated animals. For antidiabetic dual-drug combinations, the rosiglitazone-metformin group showed an unexpected increase in glucose levels compared to all of the single antidiabetic drugs. However, both the metformin-glyburide and rosiglitazone-glyburide groups showed significantly greater reductions in glucose levels following olanzapine than with single drug treatment alone for metformin or rosiglitazone, bringing glucose levels down to values equivalent to vehicle-only treated animals. These findings indicate that further study of antidiabetic dual-drug combinations in patients treated with antipsychotic drugs is warranted. PMID:24140931

  13. Reduced insulin secretion and glucose intolerance are involved in the fasting susceptibility of common vampire bats.

    PubMed

    Freitas, Mariella B; Queiroz, Joicy F; Dias Gomes, Carolinne I; Collares-Buzato, Carla B; Barbosa, Helena C; Boschero, Antonio C; Gonçalves, Carlos A; Pinheiro, Eliana C

    2013-03-01

    Susceptibility during fasting has been reported for the common vampire bat (Desmodus rotundus), to the point of untimely deaths after only 2-3 nights of fasting. To investigate the underlying physiology of this critical metabolic condition, we analyzed serum insulin levels, pancreatic islets morphometry and immunocytochemistry (ICC), static insulin secretion in pancreas fragments, and insulin signaling mechanism in male vampire bats. A glucose tolerance test (ipGTT) was also performed. Serum insulin was found to be lower in fed vampires compared to other mammals, and was significantly reduced after 24h fasting. Morphometrical analyses revealed small irregular pancreatic islets with reduced percentage of β-cell mass compared to other bats. Static insulin secretion analysis showed that glucose-stimulated insulin secretion was impaired, as insulin levels did not reach significance under high glucose concentrations, whereas the response to the amino acid leucin was preserved. Results from ipGTT showed a failure on glucose clearance, indicating glucose intolerance due to diminished pancreatic insulin secretion and/or decreased β-cell response to glucose. In conclusion, data presented here indicate lower insulinemia and impaired insulin secretion in D. rotundus, which is consistent with the limited ability to store body energy reserves, previously reported in these animals. Whether these metabolic and hormonal features are associated with their blood diet remains to be determined. The peculiar food sharing through blood regurgitation, reported to this species, might be an adaptive mechanism overcoming this metabolic susceptibility. PMID:23262275

  14. Hepatic Glucose Intolerance Precedes Hepatic Steatosis in the Male Aromatase Knockout (ArKO) Mouse

    PubMed Central

    Van Sinderen, Michelle L.; Steinberg, Gregory R.; Jørgensen, Sebastian B.; To, Sarah Q.; Knower, Kevin C.; Clyne, Colin D.; Honeyman, Jane; Chow, Jenny D.; Herridge, Kerrie A.; Jones, Margaret E. E.; Simpson, Evan R.; Boon, Wah Chin

    2014-01-01

    Estrogens are known to play a role in modulating metabolic processes within the body. The Aromatase knockout (ArKO) mice have been shown to harbor factors of Metabolic syndrome with central adiposity, hyperinsulinemia and male-specific hepatic steatosis. To determine the effects of estrogen ablation and subsequent replacement in males on whole body glucose metabolism, three- and six-month-old male ArKO mice were subjected to whole body glucose, insulin and pyruvate tolerance tests and analyzed for ensuing metabolic changes in liver, adipose tissue, and skeletal muscle. Estrogen-deficient male ArKO mice showed increased gonadal adiposity which was significantly reduced upon 17β-estradiol (E2) treatment. Concurrently, elevated ArKO serum leptin levels were significantly reduced upon E2 treatment and lowered serum adiponectin levels were restored to wild type levels. Three-month-old male ArKO mice were hyperglycemic, and both glucose and pyruvate intolerant. These phenotypes continued through to 6 months of age, highlighting a loss of glycemic control. ArKO livers displayed changes in gluconeogenic enzyme expression, and in insulin signaling pathways upon E2 treatment. Liver triglycerides were increased in the ArKO males only after 6 months of age, which could be reversed by E2 treatment. No differences were observed in insulin-stimulated ex vivo muscle glucose uptake nor changes in ArKO adipose tissue and muscle insulin signaling pathways. Therefore, we conclude that male ArKO mice develop hepatic glucose intolerance by the age of 3 months which precedes the sex-specific development of hepatic steatosis. This can be reversed upon the administration of exogenous E2. PMID:24520329

  15. Arsenate-induced maternal glucose intolerance and neural tube defects in a mouse model

    SciTech Connect

    Hill, Denise S.; Wlodarczyk, Bogdan J.; Mitchell, Laura E.; Finnell, Richard H.

    2009-08-15

    Background: Epidemiological studies have linked environmental arsenic (As) exposure to increased type 2 diabetes risk. Periconceptional hyperglycemia is a significant risk factor for neural tube defects (NTDs), the second most common structural birth defect. A suspected teratogen, arsenic (As) induces NTDs in laboratory animals. Objectives: We investigated whether maternal glucose homeostasis disruption was responsible for arsenate-induced NTDs in a well-established dosing regimen used in studies of arsenic's teratogenicity in early neurodevelopment. Methods: We evaluated maternal intraperitoneal (IP) exposure to As 9.6 mg/kg (as sodium arsenate) in LM/Bc/Fnn mice for teratogenicity and disruption of maternal plasma glucose and insulin levels. Selected compounds (insulin pellet, sodium selenate (SS), N-acetyl cysteine (NAC), L-methionine (L-Met), N-tert-Butyl-{alpha}-phenylnitrone (PBN)) were investigated for their potential to mitigate arsenate's effects. Results: Arsenate caused significant glucose elevation during an IP glucose tolerance test (IPGTT). Insulin levels were not different between arsenate and control dams before (arsenate, 0.55 ng/dl; control, 0.48 ng/dl) or after glucose challenge (arsenate, 1.09 ng/dl; control, 0.81 ng/dl). HOMA-IR index was higher for arsenate (3.9) vs control (2.5) dams (p = 0.0260). Arsenate caused NTDs (100%, p < 0.0001). Insulin pellet and NAC were the most successful rescue agents, reducing NTD rates to 45% and 35%. Conclusions: IPGTT, insulin assay, and HOMA-IR results suggest a modest failure of glucose stimulated insulin secretion and insulin resistance characteristic of glucose intolerance. Insulin's success in preventing arsenate-induced NTDs provides evidence that these arsenate-induced NTDs are secondary to elevated maternal glucose. The NAC rescue, which did not restore maternal glucose or insulin levels, suggests oxidative disruption plays a role.

  16. ARSENATE-INDUCED MATERNAL GLUCOSE INTOLERANCE AND NEURAL TUBE DEFECTS IN A MOUSE MODEL

    PubMed Central

    Hill, Denise S.; Wlodarczyk, Bogdan J.; Mitchell, Laura E.; Finnell, Richard H.

    2009-01-01

    Background Epidemiological studies have linked environmental arsenic (As) exposure to increased type 2 diabetes risk. Periconceptional hyperglycemia is a significant risk factor for neural tube defects (NTDs), the second most common structural birth defect. A suspected teratogen, arsenic (As) induces NTDs in laboratory animals. Objectives We investigated whether maternal glucose homeostasis disruption was responsible for arsenate-induced NTDs in a well-established dosing regimen used in studies of arsenic’s teratogenicity in early neurodevelopment. Methods We evaluated maternal intraperitoneal (I.P.) exposure to As 9.6 mg/kg (as sodium arsenate) in LM/Bc/Fnn mice for teratogenicity and disruption of maternal plasma glucose and insulin levels. Selected compounds (insulin pellet, sodium selenate (SS), N-acetyl cysteine (NAC), L-methionine (L-Met), N-tert-Butyl-α-phenylnitrone (PBN)) were investigated for their potential to mitigate arsenate’s effects. Results Arsenate caused significant glucose elevation during an I.P. glucose tolerance test (IPGTT). Insulin levels were not different between arsenate and control dams before (arsenate, 0.55 ng/dl; control, 0.48 ng/dl) or after glucose challenge (arsenate, 1.09 ng/dl; control, 0.81 ng/dl). HOMA-IR index was higher for arsenate (3.9) vs control (2.5) dams (p=0.0260). Arsenate caused NTDs (100%, p<0.0001). Insulin pellet and NAC were the most successful rescue agents, reducing NTD rates to 45% and 35%. Conclusions IPGTT, insulin assay, and HOMA-IR results suggest a modest failure of glucose stimulated insulin secretion and insulin resistance characteristic of glucose intolerance. Insulin’s success in preventing arsenate-induced NTDs provides evidence that these arsenate-induced NTDs are secondary to elevated maternal glucose. The NAC rescue, which did not restore maternal glucose or insulin levels, suggests oxidative disruption plays a role. PMID:19446573

  17. Beneficial effect of dietary Ephedra sinica on obesity and glucose intolerance in high-fat diet-fed mice

    PubMed Central

    SONG, MOON-KOO; UM, JAE-YOUNG; JANG, HYEUNG-JIN; LEE, BYUNG-CHEOL

    2012-01-01

    Obesity is a major contributor to both glucose intolerance and metabolic syndrome. In this study, we investigated the anti-obesity and anti-hyperglycemic effects of Ephedra sinica on high-fat diet-fed mice. Male ICR mice were divided into four groups; the normal group, the obese and diabetic control group treated with a high-fat diet, the positive control group treated with a high-fat diet containing acarbose, and the experimental group treated with a high-fat diet containing Ephedra sinica. The effects of Ephedra sinica on obesity and glucose intolerance were measured by an oral glucose tolerance test (OGTT), plasma biochemistry, body and epididymal fat weight; the expression of adiponectin, peroxisome-proliferator-activated receptor ? (PPAR-?), tumor necrosis factor ? (TNF-?) and leptin was also determined. Ephedra sinica reduced weight gain and epididymal fat accumulation, improved glucose intolerance on the OGTT, decreased triglycerides and increased high-density lipoprotein cholesterol compared to the controls. Moreover, it reduced weight gain and fasting glucose levels and improved HDL-cholesterol levels more than acarbose. Gene expression analysis revealed that Ephedra sinica upregulated the expression of adiponectin and PPAR-?, and downregulated the expression of TNF-?. From these results, we suggest that Ephedra sinica may reduce obesity and hyperglycemia by increasing PPAR-? and adiponectin and reducing TNF-?, and that it may have the potential to be used clinically as an ingredient in food or drugs effective in obesity-related glucose intolerance treatments. PMID:22969956

  18. An asymptomatic, normotensive sipple syndrome patient with glucose intolerance and hypercholesterolemia, and her kindred.

    PubMed

    Wakasugi, T; Aoyama, T; Hirai, J; Saga, T

    1991-01-01

    The proband, a 42-year-old woman without any symptoms or hypertension, was admitted for examination of accidentally discovered bilateral adrenal masses. Physical examination disclosed bilateral nodular goiter and mild sinus tachycardia. Pheochromocytomas and medullary thyroid carcinomas were revealed by biochemical and histopathological examinations. Hypercholesterolemia and abnormal glucose metabolism returned to normal after bilateral total adrenalectomy and thyroidectomy. Screening examination showed four affected family members. Three of them were also asymptomatic and normotensive. In pheochromocytoma patients, normotension, hypercholesterolemia, and impaired glucose metabolism might be signs of excess secretion of epinephrine rather than norepinephrine. PMID:1678022

  19. Liraglutide counteracts obesity and glucose intolerance in a mouse model of glucocorticoid-induced metabolic syndrome

    PubMed Central

    2014-01-01

    Background Glucocorticoid excess is commonly associated with diabetogenic effects, including insulin resistance and glucose intolerance. The effects of the long-term glucagon-like peptide 1 receptor agonist treatment on the metabolic syndrome-like conditions are not yet fully elucidated. Thus, we aimed to test whether long-term liraglutide treatment could be effective as a therapy to counteract the metabolic dysfunctions induced by chronic glucocorticoid exposure. Methods Mice were given corticosterone or vehicle via their drinking water for five consecutive weeks. In addition, mice were treated with once-daily injections of either PBS or liraglutide. Results Liraglutide treatment slowed progression towards obesity and ectopic fat deposition in liver that otherwise occurred in corticosterone-treated mice. The drug reduced the increment in serum insulin caused by corticosterone, but did not affect the reduction of insulin sensitivity. Furthermore, liraglutide improved glucose control in mice exposed to corticosterone as evident by a delay in the progression towards post-prandial hyperglycemia and enhanced glucose clearance during a glucose tolerance test. Glucose-stimulated C-peptide levels were higher in those mice that had received liraglutide and corticosterone compared to mice that had been treated with corticosterone alone, indicating a positive role of liraglutide for beta-cell function. Morphometric analysis revealed increased beta- and alpha-cell masses that were associated with more Ki67-positive islet cells in corticosterone-treated mice irrespective of whether they were co-treated with liraglutide or not. Liraglutide had no discernible effect on alpha-cell mass. Conclusion Liraglutide can be beneficial for subjects at risk of developing metabolic complications as a result of glucocorticoid excess. PMID:24423471

  20. The effect of combined treatment with canagliflozin and teneligliptin on glucose intolerance in Zucker diabetic fatty rats.

    PubMed

    Oguma, Takahiro; Kuriyama, Chiaki; Nakayama, Keiko; Matsushita, Yasuaki; Yoshida, Kumiko; Kiuchi, Satoko; Ikenaga, Yuka; Nakamaru, Yoshinobu; Hikida, Kumiko; Saito, Akira; Arakawa, Kenji; Oka, Kozo; Ueta, Kiichiro; Shiotani, Masaharu

    2015-04-01

    To assess the impact of concomitant inhibition of sodium-glucose cotransporter (SGLT) 2 and dipeptidyl peptidase IV (DPP4) for the treatment of type 2 diabetes mellitus (T2DM), the effect of combined treatment with canagliflozin, a novel SGLT2 inhibitor, and teneligliptin, a DPP4 inhibitor, on glucose intolerance was investigated in Zucker diabetic fatty (ZDF) rats. Canagliflozin potently inhibited human and rat SGLT2 and moderately inhibited human and rat SGLT1 activities but did not affect DPP4 activity. In contrast, teneligliptin inhibited human and rat DPP4 activities but not SGLT activities. A single oral treatment of canagliflozin and teneligliptin suppressed plasma glucose elevation in an oral glucose tolerance test in 13 week-old ZDF rats. This combination of agents elevated plasma active GLP-1 levels in a synergistic manner, probably mediated by intestinal SGLT1 inhibition, and further improved glucose intolerance. In the combination-treated animals, there was no pharmacokinetic interaction of the drugs and no further inhibition of plasma DPP4 activity compared with that in the teneligliptin-treated animals. These results suggest that the inhibition of SGLT2 and DPP4 improves glucose intolerance and that combined treatment with canagliflozin and teneligliptin is a novel therapeutic option for glycemic control in T2DM. PMID:25892328

  1. Glucose intolerance and pancreatic β-cell dysfunction in the anorectic anx/anx mouse.

    PubMed

    Lindfors, Charlotte; Katz, Abram; Selander, Lars; Johansen, Jeanette E; Marconi, Giulia; Schalling, Martin; Hökfelt, Tomas; Berggren, Per-Olof; Zaitsev, Sergei; Nilsson, Ida A K

    2015-08-15

    Inflammation and impaired mitochondrial oxidative phosphorylation are considered key players in the development of several metabolic disorders, including diabetes. We have previously shown inflammation and mitochondrial dysfunction in the hypothalamus of an animal model for anorexia, the anx/anx mouse. Moreover, increased incidence of eating disorders, e.g., anorexia nervosa, has been observed in diabetic individuals. In the present investigation we evaluated whether impaired mitochondrial phosphorylation and inflammation also occur in endocrine pancreas of anorectic mice, and if glucose homeostasis is disturbed. We show that anx/anx mice exhibit marked glucose intolerance associated with reduced insulin release following an intraperitoneal injection of glucose. In contrast, insulin release from isolated anx/anx islets is increased after stimulation with glucose or KCl. In isolated anx/anx islets there is a strong downregulation of the mitochondrial complex I (CI) assembly factor, NADH dehydrogenase (ubiquinone) 1α subcomplex, assembly factor 1 (Ndufaf1), and a reduced CI activity. In addition, we show elevated concentrations of free fatty acids (FFAs) in anx/anx serum and increased macrophage infiltration (indicative of inflammation) in anx/anx islets. However, isolated islets from anx/anx mice cultured in the absence of FFAs do not exhibit increased inflammation. We conclude that the phenotype of the endocrine pancreas of the anx/anx mouse is characterized by increased levels of circulating FFAs, as well as inflammation, which can inhibit insulin secretion in vivo. The anx/anx mouse may represent a useful tool for studying molecular mechanisms underlying the association between diabetes and eating disorders. PMID:26126683

  2. Changes in hippocampal synaptic functions and protein expression in monosodium glutamate-treated obese mice during development of glucose intolerance.

    PubMed

    Sasaki-Hamada, Sachie; Hojo, Yuki; Koyama, Hajime; Otsuka, Hayuma; Oka, Jun-Ichiro

    2015-05-01

    Glucose is the sole neural fuel for the brain and is essential for cognitive function. Abnormalities in glucose tolerance may be associated with impairments in cognitive function. Experimental obese model mice can be generated by an intraperitoneal injection of monosodium glutamate (MSG; 2 mg/g) once a day for 5 days from 1 day after birth. MSG-treated mice have been shown to develop glucose intolerance and exhibit chronic neuroendocrine dysfunction associated with marked cognitive malfunctions at 28-29  weeks old. Although hippocampal synaptic plasticity is impaired in MSG-treated mice, changes in synaptic transmission remain unknown. Here, we investigated whether glucose intolerance influenced cognitive function, synaptic properties and protein expression in the hippocampus. We demonstrated that MSG-treated mice developed glucose intolerance due to an impairment in the effectiveness of insulin actions, and showed cognitive impairments in the Y-maze test. Moreover, long-term potentiation (LTP) at Schaffer collateral-CA1 pyramidal synapses in hippocampal slices was impaired, and the relationship between the slope of extracellular field excitatory postsynaptic potential and stimulus intensity of synaptic transmission was weaker in MSG-treated mice. The protein levels of vesicular glutamate transporter 1 and GluA1 glutamate receptor subunits decreased in the CA1 region of MSG-treated mice. These results suggest that deficits in glutamatergic presynapses as well as postsynapses lead to impaired synaptic plasticity in MSG-treated mice during the development of glucose intolerance, though it remains unknown whether impaired LTP is due to altered inhibitory transmission. It may be important to examine changes in glucose tolerance in order to prevent cognitive malfunctions associated with diabetes. PMID:25851080

  3. Glucose Intolerance and Lipid Metabolic Adaptations in Response to Intrauterine and Postnatal Calorie Restriction in Male Adult Rats

    PubMed Central

    Thamotharan, Manikkavasagar; Dai, Yun; Lagishetty, Venu; Matveyenko, Aleksey V.; Lee, W. N. Paul

    2013-01-01

    Enhanced de novo lipogenesis (DNL), an adult hepatic adaption, is seen with high carbohydrate or low-fat diets. We hypothesized that ad libitum intake after prenatal calorie restriction will result in adult-onset glucose intolerance and enhanced DNL with modified lipid metabolic gene expression profile. Stable isotopes were used in 15-month-old adult male rat offspring exposed to prenatal (IUGR), pre- and postnatal (IPGR), or postnatal (PNGR) caloric restriction vs. controls (CON). IUGR vs. CON were heavier with hepatomegaly but unchanged visceral white adipose tissue (WAT), glucose intolerant with reduced glucose-stimulated insulin secretion (GSIS), pancreatic ?-cell mass, and total glucose clearance rate but unsuppressed hepatic glucose production. Liver glucose transporter (Glut) 1 and DNL increased with decreased hepatic acetyl-CoA carboxylase (ACC) and fatty acid synthase but increased WAT fatty acid transport protein-1 and peroxisomal proliferator-activated receptor-?, resistin, and visfatin gene expression. In contrast, PNGR and IPGR were lighter, had reduced visceral WAT, and were glucose tolerant with unchanged hepatic glucose production but with increased GSIS, ?-cell mass, glucose clearance rate, and WAT insulin receptor. Hepatic Glut1 and DNL were also increased in lean IPGR and PNGR with increased hepatic ACC, phosphorylated ACC, and pAMPK and reduced WAT fatty acid transport protein-1, peroxisomal proliferator-activated receptor-?, and ACC?. We conclude the following: 1) the heavy, glucose-intolerant and insulin-resistant IUGR adult phenotype is ameliorated by postnatal caloric restriction; 2) increased DNL paralleling hepatic Glut1 is a biomarker of exposure to early caloric restriction rather than the adult metabolic status; 3) hepatic lipid enzyme expression reflects GSIS rather than DNL; and 4) WAT gene expression reflects an obesogenic vs. lean phenotype. PMID:23183174

  4. Relationship of serum adiponectin and resistin to glucose intolerance and fat topography in south-Asians

    PubMed Central

    Wasim, Hanif; Al-Daghri, Nasser M; Chetty, Raja; McTernan, Phillip G; Barnett, A H; Kumar, Sudhesh

    2006-01-01

    Objectives South-Asians have lower adiponectin levels compared to Caucasians. It was not clear however, if this intrinsic feature is related to aspects of glucose metabolism. This study aims to determine the relationship between body fat distribution and adipocytokine in South-Asian subjects by measuring serum adipocytokines, adiposity, insulinemia, and glucose tolerance levels. Methods In this cross-sectional study, 150 South-Asians (80 males, 70 females) were included, 60 had NGT (Control group, Age 51.33 ± 11.5, BMI 27 ± 2.3), 60 had IGT (Age 57.7 ± 12.5, BMI 27.2 ± 2.7), 30 had type 2 DM (Age 49.5 ± 10.9, BMI 28 ± 1.7). Measures of adiposity, adipocytokines and other metabolic parameters were determined. Parameters were measured using the following: a) Plasma glucose by glucose oxidase method b) CRP by immunoturbidimetric method (Roche/Hitachi analyser) c) insulin by Medgenix INS-ELISA immunoenzymetric assay by Biosource (Belgium) d) Leptin, Adiponectin by radioimmunoassay kits by Linco Research (St. Charles MO) e) Resistin by immunoassay kits by Phoenix Pharmaceuticals INC (530 Harbor Boulevard, Belmont CA 94002, USA). Results Adiponectin concentrations were highest in NGT, decreased in IGT and lowest in DMT2, (both p < 0.01). Leptin was significantly higher in DMT2 than IGT and NGT p = 0.02 and 0.04 respectively. There was a significant positive relationships between log adiponectin and 2-hr insulin values, p = 0.028 and history of hypertensions and a ischemic heart disease p = 0.008 with R = 0.65. There was a significant inverse correlation between log adiponectin and resistin, p < 0.01. Conclusion Resistin levels had an inverse correlation with adiponectin levels, indicating an inverse relationship between pro-inflammatory cytokines and adiponectin. Adiponectin levels were related to glucose tolerance. PMID:16669997

  5. Postprandial Hypertriglyceridemia Predicts Development of Insulin Resistance Glucose Intolerance and Type 2 Diabetes

    PubMed Central

    Aslam, Mohammad; Aggarwal, Sarla; Sharma, Krishna Kumar; Galav, Vikas; Madhu, Sri Venkata

    2016-01-01

    Insulin resistance (IR) and type 2 diabetes mellitus (T2DM) have been found to be associated with postprandial hypertriglyceridemia (PPHTg). However, whether PPHTg can cause IR and diabetes is not clear. We therefore investigated the role of PPHTg in development of T2DM in rat model of T2DM. 96 male Wistar rats were randomized into four groups (24 rats each). Control Group A, high sucrose diet (HSD) Group B, HSD+Pioglitazone (10mg/kg/day) Group C and HSD+Atorvastatin (20mg/kg/day) Group D. Fat and glucose tolerance tests were done at regular intervals in all groups besides insulin and body weight measurement. At 26 weeks, low dose streptozotocin (15mg/kg,i.p.) was given to half of the rats. All rats were followed up till 48 weeks. PPHTg developed as early as week 2 in Group B and stabilized by week 14. Group B displayed highest PPHTg compared to other groups. Atorvastatin treatment (Group D) abolished PPHTg which became comparable to controls, pioglitazone treatment partially blunted PPHTg resulting in intermediate PPHTg. Group B with highest PPHTg showed highest subsequent IR, glucose intolerance (GI) and highest incidence of prediabetes at week 26 and diabetes at week 34 and 46 compared to other groups. Group D rats displayed lower IR, GI, low incidence of prediabetes and diabetes at these time points compared to Groups B and C. ROC analysis showed that triglyceride area under the curve of each time point significantly predicts the risk of diabetes. Present study provides the evidence that PPHTg predicts the development of IR, GI and T2DM in rat model of diet induced T2DM. PMID:26808523

  6. MyD88 regulates physical inactivity-induced skeletal muscle inflammation, ceramide biosynthesis signaling, and glucose intolerance.

    PubMed

    Kwon, Oh Sung; Tanner, Ruth E; Barrows, Katherine M; Runtsch, Marah; Symons, J David; Jalili, Thunder; Bikman, Benjamin T; McClain, Donald A; O'Connell, Ryan M; Drummond, Micah J

    2015-07-01

    Physical inactivity in older adults is a risk factor for developing glucose intolerance and impaired skeletal muscle function. Elevated inflammation and ceramide biosynthesis have been implicated in metabolic disruption and are linked to Toll-like receptor (TLR)/myeloid differentiation primary response 88 (MyD88) signaling. We hypothesize that a physical inactivity stimulus, capable of inducing glucose intolerance, would increase skeletal muscle inflammation and ceramide biosynthesis signaling and that this response would be regulated by the TLR/MyD88 pathway. Therefore, we subjected wild-type (WT) and MyD88(-/-) mice to hindlimb unloading (HU) for 14 days or an ambulatory control period. We observed impaired glucose uptake, muscle insulin signaling (p-Akt), and increased markers of NF-?B signaling (p-I?B?), inflammation (p-JNK, IL-6), TLR4, and the rate-limiting enzyme of ceramide biosynthesis, SPT2, with HU WT (P < 0.05), but not in HU MyD88(-/-) mice. Concurrently, we found that 5 days of bed rest in older adults resulted in whole body glucose dysregulation, impaired skeletal muscle insulin signaling, and upregulation of muscle IL-6 and SPT2 (P < 0.05). Post-bed rest TLR4 abundance was tightly correlated with impaired postprandial insulin and glucose levels. In conclusion, MyD88 signaling is necessary for the increased inflammation, ceramide biosynthesis signaling, and compromised metabolic function that accompanies physical inactivity. PMID:25968578

  7. Ferritin as a Risk Factor for Glucose Intolerance amongst Men and Women Originating from the Indian Subcontinent

    PubMed Central

    Hughes, Elizabeth A.; Patel, Jeetesh V.; Bredow, Zosia; Gill, Paramjit S.; Chackathayil, Julia; Agaoglu, Elif S.; Flinders, Paul; Mirrielees, Rebecca

    2015-01-01

    Background. Serum ferritin predicts the onset of diabetes; however, this relationship is not clear amongst South Asians, a population susceptible to glucose intolerance and anaemia. Objective. This study tests whether ferritin levels reflect glucose tolerance in South Asians, independent of lifestyle exposures associated with Indian or British residence. Methods. We randomly sampled 227 Gujaratis in Britain (49.8 (14.4) years, 50% men) and 277 contemporaries living in Gujarati villages (47.6 (11.8) years, 41% men). Both groups underwent a 75 g oral-glucose-tolerance test. We evaluated lifestyle parameters with standardised questionnaires and conducted comprehensive clinical and lab measurements. Results. Across sites, the age-adjusted prevalence of diabetes was 9.8%. Serum ferritin was higher amongst diabetics (P = 0.005), irrespective of site, gender, and central obesity (P ≤ 0.02), and was associated with fasting and postchallenge glucose, anthropometry, blood pressure, triglycerides, and nonesterified fatty acids (P < 0.001). Diabetes was less in those with low ferritin (<20 mg/mL), P < 0.008, and risk estimate = 0.35 (95% CI 0.15–0.81), as were blood pressure and metabolic risk factors. On multivariate analysis, diabetes was independently associated with ferritin (P = 0.001) and age (P < 0.001). Conclusion. Ferritin levels are positively associated with glucose intolerance in our test groups, independent of gender and Indian or UK lifestyle factors. PMID:26347777

  8. Periodontal Bacteria and Prediabetes Prevalence in ORIGINS: The Oral Infections, Glucose Intolerance, and Insulin Resistance Study.

    PubMed

    Demmer, R T; Jacobs, D R; Singh, R; Zuk, A; Rosenbaum, M; Papapanou, P N; Desvarieux, M

    2015-09-01

    Periodontitis and type 2 diabetes mellitus are known to be associated. The relationship between periodontal microbiota and early diabetes risk has not been studied. We investigated the association between periodontal bacteria and prediabetes prevalence among diabetes-free adults. ORIGINS (the Oral Infections, Glucose Intolerance and Insulin Resistance Study) cross sectionally enrolled 300 diabetes-free adults aged 20 to 55 y (mean SD, 34 10 y; 77% female). Prediabetes was defined as follows: 1) hemoglobin A1c values ranging from 5.7% to 6.4% or 2) fasting plasma glucose ranging from 100 to 125 mg/dL. In 1,188 subgingival plaque samples, 11 bacterial species were assessed at baseline, including Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, and Actinomyces naeslundii. Full-mouth clinical periodontal examinations were performed, and participants were defined as having no/mild periodontitis vs. moderate/severe periodontitis per the definition of the Centers for Disease Control and Prevention / American Academy of Periodontology. Modified Poisson regression evaluated prediabetes prevalence across bacterial tertiles. Prevalence ratios and 95% confidence intervals for third vs. first tertiles are presented. All analyses were adjusted for cardiometabolic risk factors. All results presented currently arise from the baseline cross section. Prediabetes prevalence was 18%, and 58% of participants had moderate/severe periodontitis. Prevalence ratios (95% confidence intervals) summarizing associations between bacterial levels and prediabetes were as follows: A. actinomycetemcomitans, 2.48 (1.34, 4.58), P = 0.004; P. gingivalis, 3.41 (1.78, 6.58), P = 0.0003; T. denticola, 1.99 (0.992, 4.00), P = 0.052; T. forsythia, 1.95 (1.0, 3.84), P = 0.05; A. naeslundii, 0.46 (0.25, 0.85), P = 0.01. The prevalence ratio for prediabetes among participants with moderate/severe vs. no/mild periodontitis was 1.47 (0.78, 2.74), P = 0.23. Higher colonization levels of specific periodontal microbiota are associated with higher prediabetes prevalence among diabetes-free adults. PMID:26082387

  9. NF-κB–inducing kinase (NIK) promotes hyperglycemia and glucose intolerance in obesity by augmenting glucagon action.

    PubMed

    Sheng, Liang; Zhou, Yingjiang; Chen, Zheng; Ren, Decheng; Cho, Kae Won; Jiang, Lin; Shen, Hong; Sasaki, Yoshiteru; Rui, Liangyou

    2012-06-01

    The canonical inhibitor of nuclear factor κB kinase subunit β (IKK-β)–nuclear factor of κ light polypeptide gene enhancer in B cells 1 (NF-κB1) pathway has been well documented to promote insulin resistance; however, the noncanonical NF-κB–inducing kinase (NIK)–NF-κB2 pathway is not well understood in obesity. Additionally, the contribution of counter-regulatory hormones, particularly glucagon, to hyperglycemia in obesity is unclear. Here we show that NIK promotes glucagon responses in obesity. Hepatic NIK was abnormally activated in mice with dietary or genetic obesity. Systemic deletion of Map3k14, encoding NIK, resulted in reduced glucagon responses and hepatic glucose production (HGP). Obesity is associated with high glucagon responses, and liver-specific inhibition of NIK led to lower glucagon responses and HGP and protected against hyperglycemia and glucose intolerance in obese mice. Conversely, hepatocyte-specific overexpression of NIK resulted in higher glucagon responses and HGP. In isolated mouse livers and primary hepatocytes, NIK also promoted glucagon action and glucose production, at least in part by increasing cAMP response element-binding (CREB) stability. Therefore, overactivation of liver NIK in obesity promotes hyperglycemia and glucose intolerance by increasing the hyperglycemic response to glucagon and other factors that activate CREB. PMID:22581287

  10. Hypertension, Insulin, and Proinsulin in Participants With Impaired Glucose Tolerance

    PubMed Central

    2008-01-01

    The association of insulin resistance and hyperinsulinemia to blood pressure has remained controversial. We examined the association of insulinemia to hypertension and blood pressure using baseline measurements for participants of the Diabetes Prevention Program (DPP). The DPP is a multicenter randomized controlled trial of 3819 participants with impaired glucose tolerance, and is designed to evaluate interventions for the delay or prevention of type 2 diabetes. The relationship between hypertension and insulinemia is described overall and by ethnicity. The effects of demographics (age and gender), adiposity, and glucose on the relationship are also presented. Asian Americans and African Americans had a similarly high prevalence of hypertension as did whites; American Indians had a lower prevalence of hypertension. Among participants not on antihypertensive medications, systolic blood pressure was significantly (but weakly) correlated with fasting insulin (r=0.12), homeostasis model assessment of insulin resistance (HOMA IR; r=0.13), and fasting proinsulin (r=0.10) when adjusted for age and gender (all, P<0.001). Systolic blood pressure showed similar correlations to fasting insulin in each ethnic group. After further adjustment for body mass index, the association of fasting insulin to systolic and diastolic blood pressures weakened considerably but remained significant (systolic: r=0.06, P=0.002; DBP: r=0.06, P<0.001). We conclude that a weak but significant association between insulin, (and proinsulin and HOMA IR) and blood pressure exists but is largely explained by overall adiposity. This association is similar among ethnicities, with the possible exception of Hispanics. The relation between insulin concentrations and blood pressure explains relatively little of the ethnic differences in hypertensive prevalence. PMID:12411462

  11. Aerobic Exercise Improves Cognition for Older Adults with Glucose Intolerance, A Risk Factor for Alzheimer’s Disease

    PubMed Central

    Baker, Laura D.; Frank, Laura L.; Foster-Schubert, Karen; Green, Pattie S; Wilkinson, Charles W.; McTiernan, Anne; Cholerton, Brenna A.; Plymate, Stephen R.; Fishel, Mark A.; Watson, G. Stennis; Duncan, Glen E.; Mehta, Pankaj D.; Craft, Suzanne

    2011-01-01

    Impaired glucose regulation is a defining characteristic of type 2 diabetes mellitus (T2DM) pathology and has been linked to increased risk of cognitive impairment and dementia. Although the benefits of aerobic exercise for physical health are well-documented, exercise effects on cognition have not been examined for older adults with poor glucose regulation associated with prediabetes and early T2DM. Using a randomized controlled design, twenty-eight adults (57–83 y old) meeting 2-h tolerance test criteria for glucose intolerance completed 6 months of aerobic exercise or stretching, which served as the control. The primary cognitive outcomes included measures of executive function (Trails B, Task Switching, Stroop, Self-ordered Pointing Test, and Verbal Fluency). Other outcomes included memory performance (Story Recall, List Learning), measures of cardiorespiratory fitness obtained via maximal-graded exercise treadmill test, glucose disposal during hyperinsulinemic-euglycemic clamp, body fat, and fasting plasma levels of insulin, cortisol, brain-derived neurotrophic factor, insulin-like growth factor-1, amyloid-β (Aβ40 and Aβ42). Six months of aerobic exercise improved executive function (MANCOVA, p = 0.04), cardiorespiratory fitness (MANOVA, p = 0.03), and insulin sensitivity (p = 0.05). Across all subjects, 6-month changes in cardiorespiratory fitness and insulin sensitivity were positively correlated (p = 0.01). For Aβ42, plasma levels tended to decrease for the aerobic group relative to controls (p = 0.07). The results of our study using rigorous controlled methodology suggest a cognition-enhancing effect of aerobic exercise for older glucose intolerant adults. Although replication in a larger sample is needed, our findings potentially have important therapeutic implications for a growing number of adults at increased risk of cognitive decline. PMID:20847403

  12. Supplementation of SK1 from Platycodi radix ameliorates obesity and glucose intolerance in mice fed a high-fat diet.

    PubMed

    Kim, Jae-Yong; Moon, Kwang-Deog; Seo, Kwon-Il; Park, Kyung-Wuk; Choi, Myung-Sook; Do, Gyeong-Min; Jeong, Yong-Kee; Cho, Young-Su; Lee, Mi-Kyung

    2009-06-01

    This study investigated the beneficial effects of SK1 on obesity and insulin resistance in C57BL/6 mice, which were fed a high-fat diet (37% calories from fat). SK1 is an edible saponin-rich compound from Platycodi radix. The mice were supplemented with two doses of SK1 (0.5% and 1.0%, wt/wt) for 9 weeks. The body weight, visceral fat mass, and adipocyte area were significantly decreased in the SK1 supplemented-groups in a dose-dependent manner compared to the high-fat group. The SK1 supplement significantly lowered plasma triglycerides, total cholesterol, and free fatty acid levels, whereas it significantly elevated the fecal excretion of lipids in the diet-induced obese mice. Supplementation of SK1 decreased the triglyceride and cholesterol levels and the accumulation of lipid droplets in the liver compared to the high-fat control group. High-fat diet induced glucose intolerance and insulin resistance with the elevation of blood glucose levels compared to the normal group; however, the SK1 supplement significantly improved postprandial glucose levels and insulin resistance index. After 9 weeks of being fed a high-fat diet, the mice presented with significantly increased activities of hepatic fatty acid synthase, fatty acid beta-oxidation, and glucokinase; however, both 0.5% and 1.0% SK1 supplementation normalized these activities. Notably, SK1 supplementation effectively diminished the ratio of fatty acid biosynthesis to fatty acid oxidation compared to the high-fat group. These results indicate that SK1 exhibits a potential anti-obesity effect and may prevent glucose intolerance by reducing body weight and fat accumulation, increasing fecal lipid excretions, and regulating hepatic lipid and glucose metabolism in high-fat fed mice. PMID:19627213

  13. Overexpression of Rad in muscle worsens diet-induced insulin resistance and glucose intolerance and lowers plasma triglyceride level

    NASA Astrophysics Data System (ADS)

    Ilany, Jacob; Bilan, Philip J.; Kapur, Sonia; Caldwell, James S.; Patti, Mary-Elizabeth; Marette, Andre; Kahn, C. Ronald

    2006-03-01

    Rad is a low molecular weight GTPase that is overexpressed in skeletal muscle of some patients with type 2 diabetes mellitus and/or obesity. Overexpression of Rad in adipocytes and muscle cells in culture results in diminished insulin-stimulated glucose uptake. To further elucidate the potential role of Rad in vivo, we have generated transgenic (tg) mice that overexpress Rad in muscle using the muscle creatine kinase (MCK) promoter-enhancer. Rad tg mice have a 6- to 12-fold increase in Rad expression in muscle as compared to wild-type littermates. Rad tg mice grow normally and have normal glucose tolerance and insulin sensitivity, but have reduced plasma triglyceride levels. On a high-fat diet, Rad tg mice develop more severe glucose intolerance than the wild-type mice; this is due to increased insulin resistance in muscle, as exemplified by a rightward shift in the dose-response curve for insulin stimulated 2-deoxyglucose uptake. There is also a unexpected further reduction of the plasma triglyceride levels that is associated with increased levels of lipoprotein lipase in the Rad tg mice. These results demonstrate a potential synergistic interaction between increased expression of Rad and high-fat diet in creation of insulin resistance and altered lipid metabolism present in type 2 diabetes. diabetes mellitus | glucose transport | RGK GTPase | transgenic mouse

  14. Transgenerational Glucose Intolerance of Tumor Necrosis Factor with Epigenetic Alteration in Rat Perirenal Adipose Tissue Induced by Intrauterine Hyperglycemia

    PubMed Central

    Su, Rina; Yan, Jie; Yang, Huixia

    2016-01-01

    Changes in DNA methylation may play a role in the genetic mechanism underlying glucose intolerance in the offspring of mothers with diabetes. Here, we established a rat model of moderate intrauterine hyperglycemia induced by streptozotocin to detect glucose and lipid metabolism of first-generation (F1) and second-generation (F2) offspring. Moderate intrauterine hyperglycemia induced high body weight in F1 and F2 offspring of diabetic mothers. F1 offspring had impaired glucose tolerance and abnormal insulin level. Additionally, F1 and F2 offspring that were exposed to intrauterine hyperglycemia had impaired insulin secretion from the islets. The tumor necrosis factor (Tnf) gene was upregulated in perirenal adipose tissue from F1 offspring and relatively increased in F2 offspring. Both F1 and F2 offspring showed similar hypomethylation level at the −1952 site of Tnf. We confirmed that DNA methylation occurs in offspring exposed to intrauterine hyperglycemia and that the DNA methylation is intergenerational and inherited. PMID:26881249

  15. Chronic erythropoietin treatment improves diet-induced glucose intolerance in rats.

    PubMed

    Caillaud, Corinne; Mechta, Mie; Ainge, Heidi; Madsen, Andreas N; Ruell, Patricia; Mas, Emilie; Bisbal, Catherine; Mercier, Jacques; Twigg, Stephen; Mori, Trevor A; Simar, David; Barrès, Romain

    2015-05-01

    Erythropoietin (EPO) ameliorates glucose metabolism through mechanisms not fully understood. In this study, we investigated the effect of EPO on glucose metabolism and insulin signaling in skeletal muscle. A 2-week EPO treatment of rats fed with a high-fat diet (HFD) improved fasting glucose levels and glucose tolerance, without altering total body weight or retroperitoneal fat mass. Concomitantly, EPO partially rescued insulin-stimulated AKT activation, reduced markers of oxidative stress, and restored heat-shock protein 72 expression in soleus muscles from HFD-fed rats. Incubation of skeletal muscle cell cultures with EPO failed to induce AKT phosphorylation and had no effect on glucose uptake or glycogen synthesis. We found that the EPO receptor gene was expressed in myotubes, but was undetectable in soleus. Together, our results indicate that EPO treatment improves glucose tolerance but does not directly activate the phosphorylation of AKT in muscle cells. We propose that the reduced systemic inflammation or oxidative stress that we observed after treatment with EPO could contribute to the improvement of whole-body glucose metabolism. PMID:25767056

  16. A Transient Metabolic Recovery from Early Life Glucose Intolerance in Cystic Fibrosis Ferrets Occurs During Pancreatic Remodeling.

    PubMed

    Yi, Yaling; Sun, Xingshen; Gibson-Corley, Katherine; Xie, Weiliang; Liang, Bo; He, Nan; Tyler, Scott R; Uc, Aliye; Philipson, Louis H; Wang, Kai; Hara, Manami; Ode, Katie Larson; Norris, Andrew W; Engelhardt, John F

    2016-05-01

    Cystic fibrosis (CF)-related diabetes in humans is intimately related to exocrine pancreatic insufficiency, yet little is known about how these 2 disease processes simultaneously evolve in CF. In this context, we examined CF ferrets during the evolution of exocrine pancreatic disease. At 1 month of age, CF ferrets experienced a glycemic crisis with spontaneous diabetic-level hyperglycemia. This occurred during a spike in pancreatic inflammation that was preceded by pancreatic fibrosis and loss of β-cell mass. Surprisingly, there was spontaneous normalization of glucose levels at 2-3 months, with intermediate hyperglycemia thereafter. Mixed meal tolerance was impaired at all ages, but glucose intolerance was not detected until 4 months. Insulin secretion in response to hyperglycemic clamp and to arginine was impaired. Insulin sensitivity, measured by euglycemic hyperinsulinemic clamp, was normal. Pancreatic inflammation rapidly diminished after 2 months of age during a period where β-cell mass rose and gene expression of islet hormones, peroxisome proliferator-activated receptor-γ, and adiponectin increased. We conclude that active CF exocrine pancreatic inflammation adversely affects β-cells but is followed by islet resurgence. We predict that very young humans with CF may experience a transient glycemic crisis and postulate that pancreatic inflammatory to adipogenic remodeling may facilitate islet adaptation in CF. PMID:26862997

  17. Deletion of nicotinamide nucleotide transhydrogenase: a new quantitive trait locus accounting for glucose intolerance in C57BL/6J mice.

    PubMed

    Freeman, Helen C; Hugill, Alison; Dear, Neil T; Ashcroft, Frances M; Cox, Roger D

    2006-07-01

    The C57BL/6J mouse displays glucose intolerance and reduced insulin secretion. The genetic locus underlying this phenotype was mapped to nicotinamide nucleotide transhydrogenase (Nnt) on mouse chromosome 13, a nuclear-encoded mitochondrial protein involved in beta-cell mitochondrial metabolism. C57BL/6J mice have a naturally occurring in-frame five-exon deletion in Nnt that removes exons 7-11. This results in a complete absence of Nnt protein in these mice. We show that transgenic expression of the entire Nnt gene in C57BL/6J mice rescues their impaired insulin secretion and glucose-intolerant phenotype. This study provides direct evidence that Nnt deficiency results in defective insulin secretion and inappropriate glucose homeostasis in male C57BL/6J mice. PMID:16804088

  18. Hepatic Branch Vagus Nerve Plays a Critical Role in the Recovery of Post-Ischemic Glucose Intolerance and Mediates a Neuroprotective Effect by Hypothalamic Orexin-A

    PubMed Central

    Harada, Shinichi; Yamazaki, Yui; Koda, Shuichi; Tokuyama, Shogo

    2014-01-01

    Orexin-A (a neuropeptide in the hypothalamus) plays an important role in many physiological functions, including the regulation of glucose metabolism. We have previously found that the development of post-ischemic glucose intolerance is one of the triggers of ischemic neuronal damage, which is suppressed by hypothalamic orexin-A. Other reports have shown that the communication system between brain and peripheral tissues through the autonomic nervous system (sympathetic, parasympathetic and vagus nerve) is important for maintaining glucose and energy metabolism. The aim of this study was to determine the involvement of the hepatic vagus nerve on hypothalamic orexin-A-mediated suppression of post-ischemic glucose intolerance development and ischemic neuronal damage. Male ddY mice were subjected to middle cerebral artery occlusion (MCAO) for 2 h. Intrahypothalamic orexin-A (5 pmol/mouse) administration significantly suppressed the development of post-ischemic glucose intolerance and neuronal damage on day 1 and 3, respectively after MCAO. MCAO-induced decrease of hepatic insulin receptors and increase of hepatic gluconeogenic enzymes on day 1 after was reversed to control levels by orexin-A. This effect was reversed by intramedullary administration of the orexin-1 receptor antagonist, SB334867, or hepatic vagotomy. In the medulla oblongata, orexin-A induced the co-localization of cholin acetyltransferase (cholinergic neuronal marker used for the vagus nerve) with orexin-1 receptor and c-Fos (activated neural cells marker). These results suggest that the hepatic branch vagus nerve projecting from the medulla oblongata plays an important role in the recovery of post-ischemic glucose intolerance and mediates a neuroprotective effect by hypothalamic orexin-A. PMID:24759941

  19. Hepatic branch vagus nerve plays a critical role in the recovery of post-ischemic glucose intolerance and mediates a neuroprotective effect by hypothalamic orexin-A.

    PubMed

    Harada, Shinichi; Yamazaki, Yui; Koda, Shuichi; Tokuyama, Shogo

    2014-01-01

    Orexin-A (a neuropeptide in the hypothalamus) plays an important role in many physiological functions, including the regulation of glucose metabolism. We have previously found that the development of post-ischemic glucose intolerance is one of the triggers of ischemic neuronal damage, which is suppressed by hypothalamic orexin-A. Other reports have shown that the communication system between brain and peripheral tissues through the autonomic nervous system (sympathetic, parasympathetic and vagus nerve) is important for maintaining glucose and energy metabolism. The aim of this study was to determine the involvement of the hepatic vagus nerve on hypothalamic orexin-A-mediated suppression of post-ischemic glucose intolerance development and ischemic neuronal damage. Male ddY mice were subjected to middle cerebral artery occlusion (MCAO) for 2 h. Intrahypothalamic orexin-A (5 pmol/mouse) administration significantly suppressed the development of post-ischemic glucose intolerance and neuronal damage on day 1 and 3, respectively after MCAO. MCAO-induced decrease of hepatic insulin receptors and increase of hepatic gluconeogenic enzymes on day 1 after was reversed to control levels by orexin-A. This effect was reversed by intramedullary administration of the orexin-1 receptor antagonist, SB334867, or hepatic vagotomy. In the medulla oblongata, orexin-A induced the co-localization of cholin acetyltransferase (cholinergic neuronal marker used for the vagus nerve) with orexin-1 receptor and c-Fos (activated neural cells marker). These results suggest that the hepatic branch vagus nerve projecting from the medulla oblongata plays an important role in the recovery of post-ischemic glucose intolerance and mediates a neuroprotective effect by hypothalamic orexin-A. PMID:24759941

  20. Loss of Pgc-1α expression in aging mouse muscle potentiates glucose intolerance and systemic inflammation

    PubMed Central

    Sczelecki, Sarah; Besse-Patin, Aurèle; Abboud, Alexandra; Kleiner, Sandra; Laznik-Bogoslavski, Dina; Wrann, Christiane D.; Ruas, Jorge L.; Haibe-Kains, Benjamin

    2013-01-01

    Diabetes risk increases significantly with age and correlates with lower oxidative capacity in muscle. Decreased expression of peroxisome proliferator-activated receptor-γ coactivator-1α (Pgc-1α) and target gene pathways involved in mitochondrial oxidative phosphorylation are associated with muscle insulin resistance, but a causative role has not been established. We sought to determine whether a decline in Pgc-1α and oxidative gene expression occurs during aging and potentiates the development of age-associated insulin resistance. Muscle-specific Pgc-1α knockout (MKO) mice and wild-type littermate controls were aged for 2 yr. Genetic signatures of skeletal muscle (microarray and mRNA expression) and metabolic profiles (glucose homeostasis, mitochondrial metabolism, body composition, lipids, and indirect calorimetry) of mice were compared at 3, 12, and 24 mo of age. Microarray and gene set enrichment analysis highlighted decreased function of the electron transport chain as characteristic of both aging muscle and loss of Pgc-1α expression. Despite significant reductions in oxidative gene expression and succinate dehydrogenase activity, young mice lacking Pgc-1α in muscle had lower fasting glucose and insulin. Consistent with loss of oxidative capacity during aging, Pgc-1α and Pgc-1β expression were reduced in aged wild-type mouse muscle. Interestingly, the combination of age and loss of muscle Pgc-1α expression impaired glucose tolerance and led to increased fat mass, insulin resistance, and inflammatory markers in white adipose and liver tissues. Therefore, loss of Pgc-1α expression and decreased mitochondrial oxidative capacity contribute to worsening glucose tolerance and chronic systemic inflammation associated with aging. PMID:24280126

  1. Tissue Inhibitor Of Matrix Metalloproteinase-1 Is Required for High-Fat Diet-Induced Glucose Intolerance and Hepatic Steatosis in Mice

    PubMed Central

    Myrmel, Lene Secher; Petersen, Rasmus Koefoed; Hansen, Jakob Bondo; Tastesen, Hanne Sørup; Mandrup-Poulsen, Thomas; Brünner, Nils; Kristiansen, Karsten

    2015-01-01

    Background Plasma levels of tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) are elevated in obesity and obesity-related disorders, such as steatosis, but the metabolic role of TIMP-1 is unclear. Here we investigated how the presence or absence of TIMP-1 affected the development of diet-induced glucose intolerance and hepatic steatosis using the Timp1 null mice. Methods Timp1 knockout (TKO) and wild type (TWT) mice were fed chow, high-fat diet (HFD) or intermediate fat and sucrose diet (IFSD). We determined body weight, body composition, lipid content of the liver, energy intake, energy expenditure, oral glucose tolerance, as well as insulin tolerance. In addition, the histology of liver and adipose tissues was examined and expression of selected genes involved in lipid metabolism and inflammation in liver and adipose tissues was determined by RT-qPCR. Results TKO mice gained less weight and had lower energy efficiency than TWT mice when fed HFD, but not when fed chow or IFSD. Importantly, TKO mice were protected from development of HFD- as well as IFSD-induced glucose intolerance, hepatic steatosis, and altered expression of genes involved in hepatic lipid metabolism and inflammation. Conclusion Collectively, our results indicate that TIMP-1 contributes to the development of diet-induced hepatic steatosis and glucose intolerance and may be a potential therapeutic target. PMID:26168159

  2. Prenatal Testosterone Exposure Leads to Gonadal Hormone-Dependent Hyperinsulinemia and Gonadal Hormone-Independent Glucose Intolerance in Adult Male Rat Offspring.

    PubMed

    More, Amar S; Mishra, Jay S; Gopalakrishnan, Kathirvel; Blesson, Chellakkan S; Hankins, Gary D; Sathishkumar, Kunju

    2016-01-01

    Elevated testosterone levels during prenatal life lead to hyperandrogenism and insulin resistance in adult females. This study evaluated whether prenatal testosterone exposure leads to the development of insulin resistance in adult male rats in order to assess the influence of gonadal hormones on glucose homeostasis in these animals. Male offspring of pregnant rats treated with testosterone propionate or its vehicle (control) were examined. A subset of male offspring was orchiectomized at 7 wk of age and reared to adulthood. At 24 wk of age, fat weights, plasma testosterone, glucose homeostasis, pancreas morphology, and gastrocnemius insulin receptor (IR) beta levels were examined. The pups born to testosterone-treated mothers were smaller at birth and remained smaller through adult life, with levels of fat deposition relatively similar to those in controls. Testosterone exposure during prenatal life induced hyperinsulinemia paralleled by an increased HOMA-IR index in a fasting state and glucose intolerance and exaggerated insulin responses following a glucose tolerance test. Prenatal androgen-exposed males had more circulating testosterone during adult life. Gonadectomy prevented hyperandrogenism, reversed hyperinsulinemia, and attenuated glucose-induced insulin responses but did not alter glucose intolerance in these rats. Prenatal androgen-exposed males had decreased pancreatic islet numbers, size, and beta-cell area along with decreased expression of IR in gastrocnemius muscles. Gonadectomy restored pancreatic islet numbers, size, and beta-cell area but did not normalize IRbeta expression. This study shows that prenatal testosterone exposure leads to a defective pancreas and skeletal muscle function in male offspring. Hyperinsulinemia during adult life is gonad-dependent, but glucose intolerance appears to be independent of postnatal testosterone levels. PMID:26586841

  3. Weight loss results in a small decrease in follicle stimulating hormone in overweight glucose-intolerant postmenopausal women

    PubMed Central

    Kim, Catherine; Randolph, John F.; Golden, Sherita H.; Labrie, Fernand; Kong, Shengchun; Nan, Bin; Barrett-Connor, Elizabeth

    2014-01-01

    Structured Abstract Objective To examine the impact of a weight loss intervention upon follicle stimulating hormone (FSH) levels in postmenopause. Design and Methods Participants were postmenopausal, overweight, glucose-intolerant women not using exogenous estrogen (n=382) in the Diabetes Prevention Program. Women were randomized to intensive lifestyle change (ILS) with the goals of weight reduction of at least 7% of initial weight and 150 minutes per week of moderate intensity exercise, metformin 850 mg, or placebo administered twice a day. Results Randomization to ILS led to small increases in FSH between baseline and 1-year follow-up vs. placebo (2.3 IU/l vs. -0.81 IU/l, p<0.01). Increases in FSH were correlated with decreases in weight (r=-0.165, p<0.01) and E2 (r=-0.464, p<0.0001) after adjustment for age, race/ethnicity, and randomization arm. Changes in FSH were still significantly associated with changes in weight even after adjustment for E2 levels. Metformin users had reductions in weight but non-significant changes in FSH and E2 levels vs. placebo. Conclusions Weight loss leads to small increases in FSH among overweight, postmenopausal women, potentially through pathways mediated by endogenous estrogen as well as other pathways. PMID:25294746

  4. Alteration of NCoR Corepressor Splicing in Mice Causes Increased Body Weight and Hepatosteatosis without Glucose Intolerance

    PubMed Central

    Goodson, Michael L.; Young, Briana M.; Snyder, Chelsea A.; Schroeder, Amy C.

    2014-01-01

    Alternative mRNA splicing is an important means of diversifying function in higher eukaryotes. Notably, both NCoR and SMRT corepressors are subject to alternative mRNA splicing, yielding a series of distinct corepressor variants with highly divergent functions. Normal adipogenesis is associated with a switch in corepressor splicing from NCoRω to NCoRδ, which appears to help regulate this differentiation process. We report here that mimicking this development switch in mice by a splice-specific whole-animal ablation of NCoRω is very different from a whole-animal or tissue-specific total NCoR knockout and produces significantly enhanced weight gain on a high-fat diet. Surprisingly, NCoRω−/− mice are protected against diet-induced glucose intolerance despite enhanced adiposity and the presence of multiple additional, prodiabetic phenotypic changes. Our results indicate that the change in NCoR splicing during normal development both helps drive normal adipocyte differentiation and plays a key role in determining a metabolically appropriate storage of excess calories. We also conclude that whole-gene “knockouts” fail to reveal how important gene products are customized, tailored, and adapted through alternative mRNA splicing and thus do not reveal all the functions of the protein products of that gene. PMID:25182530

  5. Lactose intolerance

    MedlinePlus

    Lactase deficiency; Milk intolerance; Disaccharidase deficiency; Dairy product intolerance ... make the lactase enzyme so they can digest milk, including breast milk. Babies born too early (premature) ...

  6. Increased Myocardial Uptake of Dietary Fatty Acids Linked to Cardiac Dysfunction in Glucose-Intolerant Humans

    PubMed Central

    Labb, Sbastien M.; Grenier-Larouche, Thomas; Noll, Christophe; Phoenix, Serge; Gurin, Brigitte; Turcotte, Eric E.; Carpentier, Andr C.

    2012-01-01

    Impaired cardiac systolic and diastolic function has been observed in preclinical models and in subjects with type 2 diabetes. Using a recently validated positron emission tomography (PET) imaging method with 14(R,S)-[18F]-fluoro-6-thia-heptadecanoic acid to quantify organ-specific dietary fatty acid partitioning, we demonstrate in this study that overweight and obese subjects with impaired glucose tolerance (IGT+) display significant increase in fractional myocardial dietary fatty acid uptake over the first 6 h postprandial compared with control individuals (IGT?). Measured by [11C]acetate with PET, IGT+ subjects have a significant increase in myocardial oxidative index. IGT+ subjects have significantly reduced left ventricular stroke volume and ejection fraction (LVEF) and tend to display impaired diastolic function, as assessed by PET ventriculography. We demonstrate an inverse relationship between increased myocardial dietary fatty acid partitioning and LVEF. Fractional dietary fatty acid uptake is reduced in subcutaneous abdominal and visceral adipose tissues in IGT+ directly associated with central obesity. Fractional dietary fatty acid uptake in skeletal muscles or liver is, however, similar in IGT+ versus IGT?. The current study demonstrates, for the first time, that excessive myocardial partitioning of dietary fatty acids occurs in prediabetic individuals and is associated with early impairment of left ventricular function and increased myocardial oxidative metabolism. PMID:23093657

  7. Indomethacin Treatment Prevents High Fat Diet-induced Obesity and Insulin Resistance but Not Glucose Intolerance in C57BL/6J Mice*

    PubMed Central

    Fjære, Even; Aune, Ulrike L.; Røen, Kristin; Keenan, Alison H.; Ma, Tao; Borkowski, Kamil; Kristensen, David M.; Novotny, Guy W.; Mandrup-Poulsen, Thomas; Hudson, Brian D.; Milligan, Graeme; Xi, Yannan; Newman, John W.; Haj, Fawaz G.; Liaset, Bjørn; Kristiansen, Karsten; Madsen, Lise

    2014-01-01

    Chronic low grade inflammation is closely linked to obesity-associated insulin resistance. To examine how administration of the anti-inflammatory compound indomethacin, a general cyclooxygenase inhibitor, affected obesity development and insulin sensitivity, we fed obesity-prone male C57BL/6J mice a high fat/high sucrose (HF/HS) diet or a regular diet supplemented or not with indomethacin (±INDO) for 7 weeks. Development of obesity, insulin resistance, and glucose intolerance was monitored, and the effect of indomethacin on glucose-stimulated insulin secretion (GSIS) was measured in vivo and in vitro using MIN6 β-cells. We found that supplementation with indomethacin prevented HF/HS-induced obesity and diet-induced changes in systemic insulin sensitivity. Thus, HF/HS+INDO-fed mice remained insulin-sensitive. However, mice fed HF/HS+INDO exhibited pronounced glucose intolerance. Hepatic glucose output was significantly increased. Indomethacin had no effect on adipose tissue mass, glucose tolerance, or GSIS when included in a regular diet. Indomethacin administration to obese mice did not reduce adipose tissue mass, and the compensatory increase in GSIS observed in obese mice was not affected by treatment with indomethacin. We demonstrate that indomethacin did not inhibit GSIS per se, but activation of GPR40 in the presence of indomethacin inhibited glucose-dependent insulin secretion in MIN6 cells. We conclude that constitutive high hepatic glucose output combined with impaired GSIS in response to activation of GPR40-dependent signaling in the HF/HS+INDO-fed mice contributed to the impaired glucose clearance during a glucose challenge and that the resulting lower levels of plasma insulin prevented the obesogenic action of the HF/HS diet. PMID:24742673

  8. The Association of Elective Hormone Therapy with Changes in Lipids Among Glucose Intolerant Postmenopausal Women in the Diabetes Prevention Program

    PubMed Central

    Golden, Sherita H.; Kim, Catherine; Barrett-Connor, Elizabeth; Nan, Bin; Kong, Shengchun; Goldberg, Ronald

    2013-01-01

    Objective It is unclear how lipids change in response to lifestyle modification or metformin among postmenopausal glucose intolerant women using and not using hormone therapy (HT). We examined the one-year changes in lipids among postmenopausal, prediabetic women in the Diabetes Prevention Program (DPP), and whether changes were mediated by sex hormones. Materials/Methods We performed a secondary analysis of a randomized controlled trial of 342 women who used HT at baseline and year 1 and 382 women who did not use HT at either time point. Interventions included intensive lifestyle (ILS) with goals of weight reduction of at least 7% of initial weight and 150 minutes per week of moderate intensity exercise, or metformin or placebo administered 850 mg up to twice a day. Women were not randomized to HT. Main outcome measures were changes between baseline and study year 1 in low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides. Results Compared to placebo, both ILS and metformin significantly reduced LDL-C and raised HDL-C among HT users, changes partially explained by change in estradiol and testosterone but independent of changes in waist circumference and 1/fasting insulin. In contrast, DPP interventions had no effect on LDL-C and HDL-C among non-HT users. ILS significantly lowered triglycerides among non-users but did not significantly change triglycerides among HT users. Metformin did not significantly change triglycerides among non-users but increased triglycerides among HT users. Conclusions The beneficial effects of ILS and metformin on lowering LDL-C and raising HDL-C differ depending upon concurrent HT use. PMID:23660512

  9. The renin-angiotensin system: a target of and contributor to dyslipidemias, altered glucose homeostasis, and hypertension of the metabolic syndrome

    PubMed Central

    Putnam, Kelly; Shoemaker, Robin; Yiannikouris, Frederique

    2012-01-01

    The renin-angiotensin system (RAS) is an important therapeutic target in the treatment of hypertension. Obesity has emerged as a primary contributor to essential hypertension in the United States and clusters with other metabolic disorders (hyperglycemia, hypertension, high triglycerides, low HDL cholesterol) defined within the metabolic syndrome. In addition to hypertension, RAS blockade may also serve as an effective treatment strategy to control impaired glucose and insulin tolerance and dyslipidemias in patients with the metabolic syndrome. Hyperglycemia, insulin resistance, and/or specific cholesterol metabolites have been demonstrated to activate components required for the synthesis [angiotensinogen, renin, angiotensin-converting enzyme (ACE)], degradation (ACE2), or responsiveness (angiotensin II type 1 receptors, Mas receptors) to angiotensin peptides in cell types (e.g., pancreatic islet cells, adipocytes, macrophages) that mediate specific disorders of the metabolic syndrome. An activated local RAS in these cell types may contribute to dysregulated function by promoting oxidative stress, apoptosis, and inflammation. This review will discuss data demonstrating the regulation of components of the RAS by cholesterol and its metabolites, glucose, and/or insulin in cell types implicated in disorders of the metabolic syndrome. In addition, we discuss data supporting a role for an activated local RAS in dyslipidemias and glucose intolerance/insulin resistance and the development of hypertension in the metabolic syndrome. Identification of an activated RAS as a common thread contributing to several disorders of the metabolic syndrome makes the use of angiotensin receptor blockers and ACE inhibitors an intriguing and novel option for multisymptom treatment. PMID:22227126

  10. TLR4 Expression by Liver Resident Cells Mediates the Development of Glucose Intolerance and Insulin Resistance in Experimental Periodontitis

    PubMed Central

    Ilievski, Vladimir; Cho, Yale; Katwala, Priya; Rodriguez, Heriberto; Tulowiecka, Margaret; Kurian, David; Leoni, Lara; Christman, John W.; Unterman, Terry G.; Watanabe, Keiko

    2015-01-01

    Background Results from epidemiological studies indicate a close association between periodontitis and type 2 diabetes mellitus. However, the mechanism linking periodontitis to glucose intolerance (GI) and insulin resistance (IR) is unknown. We therefore tested the hypothesis that periodontitis induces the development of GI/IR through a liver Toll-like receptor 4 (TLR4) dependent mechanism. Methods TLR4 chimeric mice were developed by bone marrow transplantation using green fluorescent protein expressing TLR4WT mouse (GFPWT) as donor and TLR4 WT or TLR4-/- as recipient mice (GFPWT:WT and GFPWT:KO chimeras respectively). These chimeras were subjected to experimental chronic periodontitis induced by repeated applications of LPS to the gingival sulci for 18 weeks. The levels of GI/IR were monitored and plasma cytokines and LPS were determined at 18 weeks when differences in glucose tolerance were most apparent. Cytokine gene expression was measured in liver tissue by qPCR. Results Alveolar bone loss was significantly greater in GFPWT:WT chimeras treated with LPS compared with chimeras treated with PBS or GFPWT:KO chimeras. However, the degree of gingival inflammation was similar between GFPWT:WT and GFPWT:KO mice with LPS application. Severe GI/IR occurred in GFPWT:WT chimeras but not in the GFPWT:KO chimeras that were subjected to 18 weeks of LPS. Serum LPS was detected only in animals to which LPS was applied and the level was similar in GFPWT:WT and GFPWT:KO mice at the 18 week time point. Surprisingly, there was no significant difference in the plasma levels of IL1β, IL6 and TNFα at 18 weeks in spite of the severe GI/IR in the GFPWT:WT chimeras with LPS application. Also, no difference in the expression of TNFα or IL6 mRNA was detected in the liver of GFPWT:WT vs GFPWT:KO mice. In contrast, liver IL1β expression was significantly greater in GFPWT:WT chimeras compared to GFPWT:KO chimeras treated with LPS. Conclusion We observed that GFPWT:WT, but not GFPWT:KO chimeras, treated with LPS developed GI/IR despite similar degrees of gingival inflammation, circulating cytokine levels, and LPS concentrations. We conclude that LPS from periodontitis sites has a pivotal role in triggering the development of GI/IR through a mechanism that involves TLR4 expression by resident macrophages/Kupffer cells in the liver. PMID:26317345

  11. Reversal of glucose intolerance in rat offspring exposed to ethanol before birth through reduction of nuclear skeletal muscle HDAC expression by the bile acid TUDCA

    PubMed Central

    Yao, Xing‐Hai; Nguyen, Khanh H.; Nyomba, B. L. Grégoire

    2014-01-01

    Abstract Prenatal ethanol exposure causes cellular stress, insulin resistance, and glucose intolerance in adult offspring, with increased gluconeogenesis and reduced muscle glucose transporter‐4 (glut4) expression. Impaired insulin activation of Akt and nuclear translocation of histone deacetylases (HDACs) in the liver partly explain increased gluconeogenesis. The mechanism for the reduced glut4 is unknown. Pregnant rats were gavaged with ethanol over the last week of gestation and adult female offspring were studied. Some ethanol exposed offspring was treated with tauroursodeoxycholic acid (TUDCA) for 3 weeks. All these rats underwent intraperitoneal glucose tolerance and insulin tolerance tests. The expression of glut4, HDACs, and markers of endoplasmic reticulum (ER) unfolded protein response (XBP1, CHOP, ATF6) was examined in the gastrocnemius muscle fractions, and in C2C12 muscle cells cultured with ethanol, TUDCA, and HDAC inhibitors. Non‐TUDCA‐treated rats exposed to prenatal ethanol were insulin resistant and glucose intolerant with reduced muscle glut4 expression, increased ER marker expression, and increased nuclear HDACs, whereas TUDCA‐treated rats had normal insulin sensitivity and glucose tolerance with normal glut4 expression, ER marker expression, and HDAC levels. In C2C12 cells, ethanol reduced glut4 expression, but increased ER makers. While TUDCA restored glut4 and ER markers to control levels and HDAC inhibition rescued glut4 expression, HDAC inhibition had no effect on ER markers. The increase in nuclear HDAC levels consequent to prenatal ethanol exposure reduces glut4 expression in adult rat offspring, and this HDAC effect is independent of ER unfolded protein response. HDAC inhibition by TUDCA restores glut4 expression, with improvement in insulin sensitivity and glucose tolerance. PMID:25538147

  12. Maternal High Folic Acid Supplement Promotes Glucose Intolerance and Insulin Resistance in Male Mouse Offspring Fed a High-Fat Diet

    PubMed Central

    Huang, Yifan; He, Yonghan; Sun, Xiaowei; He, Yujie; Li, Ying; Sun, Changhao

    2014-01-01

    Maternal nutrition may influence metabolic profiles in offspring. We aimed to investigate the effect of maternal folic acid supplement on glucose metabolism in mouse offspring fed a high-fat diet (HFD). Sixty C57BL/6 female mice were randomly assigned into three dietary groups and fed the AIN-93G diet containing 2 (control), 5 (recommended folic acid supplement, RFolS) or 40 (high folic acid supplement, HFolS) mg folic acid/kg of diet. All male offspring were fed HFD for eight weeks. Physiological, biochemical and genetic variables were measured. Before HFD feeding, developmental variables and metabolic profiles were comparable among each offspring group. However, after eight weeks of HFD feeding, the offspring of HFolS dams (Off-HFolS) were more vulnerable to suffer from obesity (p = 0.009), glucose intolerance (p < 0.001) and insulin resistance (p < 0.001), compared with the controls. Off-HFolS had reduced serum adiponectin concentration, accompanied with decreased adiponectin mRNA level but increased global DNA methylation level in white adipose tissue. In conclusion, our results suggest maternal HFolS exacerbates the detrimental effect of HFD on glucose intolerance and insulin resistance in male offspring, implying that HFolS during pregnancy should be adopted cautiously in the general population of pregnant women to avoid potential deleterious effect on the metabolic diseases in their offspring. PMID:24736781

  13. Carbenoxolone Treatment Ameliorated Metabolic Syndrome in WNIN/Ob Obese Rats, but Induced Severe Fat Loss and Glucose Intolerance in Lean Rats

    PubMed Central

    Prasad Sakamuri, Siva Sankara Vara; Sukapaka, Mahesh; Prathipati, Vijay Kumar; Nemani, Harishankar; Putcha, Uday Kumar; Pothana, Shailaja; Koppala, Swarupa Rani; Ponday, Lakshmi Raj Kumar; Acharya, Vani; Veetill, Giridharan Nappan; Ayyalasomayajula, Vajreswari

    2012-01-01

    Background 11beta-hydroxysteroid dehydrogenase type 1 (11β-HSD1) regulates local glucocorticoid action in tissues by catalysing conversion of inactive glucocorticoids to active glucocorticoids. 11β-HSD1 inhibition ameliorates obesity and associated co-morbidities. Here, we tested the effect of 11β-HSD inhibitor, carbenoxolone (CBX) on obesity and associated comorbidities in obese rats of WNIN/Ob strain, a new animal model for genetic obesity. Methodology/Principal Findings Subcutaneous injection of CBX (50 mg/kg body weight) or volume-matched vehicle was given once daily for four weeks to three month-old WNIN/Ob lean and obese rats (n = 6 for each phenotype and for each treatment). Body composition, plasma lipids and hormones were assayed. Hepatic steatosis, adipose tissue morphology, inflammation and fibrosis were also studied. Insulin resistance and glucose intolerance were determined along with tissue glycogen content. Gene expressions were determined in liver and adipose tissue. CBX significantly inhibited 11β-HSD1 activity in liver and adipose tissue of WNIN/Ob lean and obese rats. CBX significantly decreased body fat percentage, hypertriglyceridemia, hypercholesterolemia, insulin resistance in obese rats. CBX ameliorated hepatic steatosis, adipocyte hypertrophy, adipose tissue inflammation and fibrosis in obese rats. Tissue glycogen content was significantly decreased by CBX in liver and adipose tissue of obese rats. Severe fat loss and glucose- intolerance were observed in lean rats after CBX treatment. Conclusions/Significance We conclude that 11β-HSD1 inhibition by CBX decreases obesity and associated co-morbidities in WNIN/Ob obese rats. Our study supports the hypothesis that inhibition of 11β-HSD1 is a key strategy to treat metabolic syndrome. Severe fat loss and glucose -intolerance by CBX treatment in lean rats suggest that chronic 11β-HSD1 inhibition may lead to insulin resistance in normal conditions. PMID:23284633

  14. Lactose intolerance among Mexican Americans.

    PubMed

    Sowers, M F; Winterfeldt, E

    1975-07-01

    Thirty-three Mexican Americans between the ages of 9 and 60 were interviewed and tested for lactose intolerance. The participants of the study included 16 children and 17 persons not related by birth, including the parents of the children. Determination of lactose intolerance was based on a rise of less than 25mg/100 ml of blood glucose as measured by an Ames Dextrostix/Reflectance Meter following consumption of a lactose load. Forty-seven percent of the 17 nonrelated Mexican Americans were lactose intolerant. There was a marked relationship between low rise in blood glucose and symptoms of diarrhea, flatulence, and distention. Sixteen children from four families had an incidence of 50 per cent intolerance. The findings of intolerance in two successive generations of three families and in both sexes of the families adds support to the contention that lactose intolerance has a genetic basis, without sex predilection. PMID:1146721

  15. Adult-onset deficiency of acyl CoA:monoacylglycerol acyltransferase 2 protects mice from diet-induced obesity and glucose intolerance[S

    PubMed Central

    Banh, Taylor; Nelson, David W.; Gao, Yu; Huang, Ting-Ni; Yen, Mei-I; Yen, Chi-Liang E.

    2015-01-01

    Acyl-CoA:monoacylglycerol acyltransferase (MGAT) 2 catalyzes triacylglycerol (TAG) synthesis, required in intestinal fat absorption. We previously demonstrated that mice without a functional MGAT2-coding gene (Mogat2−/−) exhibit increased energy expenditure and resistance to obesity induced by excess calories. One critical question raised is whether lacking MGAT2 during early development is required for the metabolic phenotypes in adult mice. In this study, we found that Mogat2−/− pups grew slower than wild-type littermates during the suckling period. To determine whether inactivating MGAT2 in adult mice is sufficient to confer resistance to diet-induced obesity, we generated mice with an inducible Mogat2-inactivating mutation. Mice with adult-onset MGAT2 deficiency (Mogat2AKO) exhibited a transient decrease in food intake like Mogat2−/− mice when fed a high-fat diet and a moderate increase in energy expenditure after acclimatization. They gained less weight than littermate controls, but the difference was smaller than that between wild-type and Mogat2−/− mice. The moderate reduction in weight gain was associated with reduced hepatic TAG and improved glucose tolerance. Similar protective effects were also observed in mice that had gained weight on a high-fat diet before inactivating MGAT2. These findings suggest that adult-onset MGAT2 deficiency mitigates metabolic disorders induced by high-fat feeding and that MGAT2 modulates early postnatal nutrition and may program metabolism later in life. PMID:25535286

  16. Muscle-specific Pikfyve gene disruption causes glucose intolerance, insulin resistance, adiposity, and hyperinsulinemia but not muscle fiber-type switching

    PubMed Central

    Ikonomov, Ognian C.; Sbrissa, Diego; Delvecchio, Khortnal; Feng, Han-Zhong; Cartee, Gregory D.; Jin, Jian-Ping

    2013-01-01

    The evolutionarily conserved kinase PIKfyve that synthesizes PtdIns5P and PtdIns(3,5)P2 has been implicated in insulin-regulated GLUT4 translocation/glucose entry in 3T3-L1 adipocytes. To decipher PIKfyve's role in muscle and systemic glucose metabolism, here we have developed a novel mouse model with Pikfyve gene disruption in striated muscle (MPIfKO). These mice exhibited systemic glucose intolerance and insulin resistance at an early age but had unaltered muscle mass or proportion of slow/fast-twitch muscle fibers. Insulin stimulation of in vivo or ex vivo glucose uptake and GLUT4 surface translocation was severely blunted in skeletal muscle. These changes were associated with premature attenuation of Akt phosphorylation in response to in vivo insulin, as tested in young mice. Starting at 1011 wk of age, MPIfKO mice progressively accumulated greater body weight and fat mass. Despite increased adiposity, serum free fatty acid and triglyceride levels were normal until adulthood. Together with the undetectable lipid accumulation in liver, these data suggest that lipotoxicity and muscle fiber switching do not contribute to muscle insulin resistance in MPIfKO mice. Furthermore, the 80% increase in total fat mass resulted from increased fat cell size rather than altered fat cell number. The observed profound hyperinsulinemia combined with the documented increases in constitutive Akt activation, in vivo glucose uptake, and gene expression of key enzymes for fatty acid biosynthesis in MPIfKO fat tissue suggest that the latter is being sensitized for de novo lipid anabolism. Our data provide the first in vivo evidence that PIKfyve is essential for systemic glucose homeostasis and insulin-regulated glucose uptake/GLUT4 translocation in skeletal muscle. PMID:23673157

  17. Boehmeria nivea Stimulates Glucose Uptake by Activating Peroxisome Proliferator-Activated Receptor Gamma in C2C12 Cells and Improves Glucose Intolerance in Mice Fed a High-Fat Diet

    PubMed Central

    Kim, Sung Hee; Sung, Mi Jeong; Park, Jae Ho; Yang, Hye Jeong; Hwang, Jin-Taek

    2013-01-01

    We examined the antidiabetic property of Boehmeria nivea (L.) Gaud. Ethanolic extract of Boehmeria nivea (L.) Gaud. (EBN) increased the uptake of 2-[N-(nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxy-d-glucose in C2C12 myotubes. To examine the mechanisms underlying EBN-mediated increase in glucose uptake, we examined the transcriptional activity and expression of peroxisome proliferator-activated receptor gamma (PPAR-γ), a pivotal target for glucose metabolism in C2C12 myotubes. We found that the EBN increased both the transcriptional activity and mRNA expression levels of PPAR-γ. In addition, we measured phosphorylation and expression levels of other targets of glucose metabolism, such as AMP-activated protein kinase (AMPK) and protein kinase B (Akt/PKB). We found that EBN did not alter the phosphorylation or expression levels of these proteins in a time- or dose-dependent manner, which suggested that EBN stimulates glucose uptake through a PPAR-γ-dependent mechanism. Further, we investigated the antidiabetic property of EBN using mice fed a high-fat diet (HFD). Administration of 0.5% EBN reduced the HFD-induced increase in body weight, total cholesterol level, and fatty liver and improved the impaired fasting glucose level, blood insulin content, and glucose intolerance. These results suggest that EBN had an antidiabetic effect in cell culture and animal systems and may be useful for preventing diabetes. PMID:23690860

  18. Management of Hypertensive Patients With Multiple Drug Intolerances: A Single-Center Experience of a Novel Treatment Algorithm.

    PubMed

    Antoniou, Sotiris; Saxena, Manish; Hamedi, Nadya; de Cates, Catherine; Moghul, Sakib; Lidder, Satnam; Kapil, Vikas; Lobo, Melvin D

    2016-02-01

    Multiple drug intolerance to antihypertensive medications (MDI-HTN) is an overlooked cause of nonadherence. In this study, 55 patients with MDI-HTN were managed with a novel treatment algorithm utilizing sequentially initiated monotherapies or combinations of maximally tolerated doses of fractional tablet doses, liquid formulations, transdermal preparations, and off-label tablet medications. A total of 10% of referred patients had MDI-HTN, resulting in insufficient pharmacotherapy and baseline office blood pressure (OBP) of 178±24/94±15 mm Hg. At baseline, patients were intolerant to 7.6±3.6 antihypertensives; they were receiving 1.4±1.1 medications. After 6 months on the novel MDI-HTN treatment algorithm, both OBP and home blood pressure (HBP) were significantly reduced, with patients receiving 2.0±1.2 medications. At 12 months, OBP was reduced from baseline by 17±5/9±3 mm Hg (P<.01, P<.05) and HBP was reduced by 11±5/12±3 mm Hg (P<.01 for both) while patients were receiving 1.9±1.1 medications. Application of a stratified medicine approach allowed patients to tolerate increased numbers of medications and achieved significant long-term lowering of blood pressure. PMID:26306794

  19. Long-term exposure to a high-fat diet results in the development of glucose intolerance and insulin resistance in interleukin-1 receptor I-deficient mice

    PubMed Central

    McGillicuddy, Fiona C.; Reynolds, Clare M.; Finucane, Orla; Coleman, Eilish; Harford, Karen A.; Grant, Christine; Sergi, Domenico; Williams, Lynda M.; Mills, Kingston H. G.

    2013-01-01

    Emerging evidence has demonstrated that saturated fatty acids prime pro-IL-1β production and inflammasome-mediated IL-1β activation is critical in obesity-associated insulin resistance (IR). Nonetheless, IL-1 receptor I-deficient (IL-1RI−/−) mice develop mature-onset obesity despite consuming a low-fat diet (LFD). With this apparent contradiction, the present study evaluated whether IL-1RI−/− mice were protected against long-term (6 mo) high-fat diet (HFD)-induced IR. Male wild-type and IL-1RI−/− mice were fed LFD or HFD for 3 or 6 mo, and glucose and insulin tolerance tests were performed. Adipose insulin sensitivity, cytokine profiles, and adipocyte morphology were assessed. The adipogenic potential of stromal vascular fraction was determined. Hepatic lipid accumulation and insulin sensitivity were characterized. IL-1RI−/− mice developed glucose intolerance and IR after 6 mo HFD compared with 3 mo HFD, coincident with enhanced weight gain, hyperinsulinemia, and hyperleptinemia. The aggravated IR phenotype was associated with loss of adipose functionality, switch from adipocyte hyperplasia to hypertrophy and hepatosteatosis. Induction of adipogenic genes was reduced in IL-1RI−/− preadipocytes after 6 mo HFD compared with 3 mo HFD. Obese LFD-IL-1RI−/− mice exhibited preserved metabolic health. IL-1RI−/− mice develop glucose intolerance and IR after 6 mo HFD intervention. While mature-onset obesity is evident in LFD-IL-1RI−/− mice, the additional metabolic insult of HFD was required to drive adipose inflammation and systemic IR. These findings indicate an important interaction between dietary fat and IL-1, relevant to optimal metabolic health. PMID:23921145

  20. [Food intolerance].

    PubMed

    Zugasti Murillo, Ana

    2009-05-01

    Adverse food reactions are common in the general population. Nevertheless, our knowledge of the structure of food allergens and of the mechanisms involved is poor. In 1995 the European Academy of Allergology and Clinical Immunology suggested a classification based on the causative pathogenic mechanism. According to this classification, non-toxic reactions can be divided into food allergies when they recognize immunological mechanisms and food intolerance when there are no immunological implications. The treatment of food intolerance is avoidance of the particular food. There are specific treatments for some food intolerance (beta-galactosidases for the management of lactose intolerance). PMID:19627745

  1. Maternal BMI, glucose tolerance, and adverse pregnancy outcomes

    PubMed Central

    STUEBE, Alison M.; LANDON, Mark B.; LAI, Yinglei; SPONG, Catherine Y.; CARPENTER, Marshall W.; RAMIN, Susan M.; CASEY, Brian; WAPNER, Ronald J.; VARNER, Michael W.; ROUSE, Dwight J.; SCISCIONE, Anthony; CATALANO, Patrick; HARPER, Margaret; SAADE, George; SOROKIN, Yoram; PEACEMAN, Alan M.; TOLOSA, Jorge E.

    2012-01-01

    Objectives To estimate the association of pregravid body mass index (BMI), independent of 3-hour oral glucose tolerance test (OGTT) results, with pregnancy outcome. Study Design In this secondary analysis of a cohort of women with untreated mild gestational glucose intolerance, defined as 50g glucose loading test between 135 and 199 mg/dL and fasting glucose <95 mg/dL, we modeled the association between pregravid BMI, OGTT results, and both pregnancy complications and neonatal adiposity. Results Among 1250 participants, both pregravid BMI and glucose at hour 3 of the OGTT were associated with increased risk of gestational hypertension. Maternal pregravid BMI was also positively associated with LGA, and both maternal BMI and fasting glucose were associated with birth-weight z-score and neonatal fat mass. Conclusions Among women with untreated mild gestational glucose intolerance, pregravid BMI is associated with increased gestational hypertension, birth weight and neonatal fat mass, independent of OGTT values. PMID:22609018

  2. Parathyroidectomy Ameliorates Glucose and Blood Pressure Control in a Patient with Primary Hyperparathyroidism, Type 2 Diabetes, and Hypertension

    PubMed Central

    Kumar, Alok; Singh, Sunita

    2015-01-01

    Effect of parathyroidectomy on glucose control and hypertension is controversial. Here, we report a case of a patient with primary hyperparathyroidism, type 2 diabetes mellitus, and hypertension in whom parathyroidectomy ameliorated both glucose control and blood pressure. Once high serum calcium levels were noticed, ultrasonography of neck confirmed a well-defined oval hypoechoic mass posterior to the right lobe of the thyroid, confirmed by scintiscan. Parathyroidectomy resulted in improvement of blood pressure and blood glucose. We could stop insulin and antihypertensive medications. We conclude that in patients with type 2 diabetes with vague complaints like fatigue, body ache, and refractory hypertension, as a part of the diagnostic workup, clinicians should also check serum calcium levels and parathyroid hormone to rule out hyperparathyroidism. Correction of hyperparathyroidism may result in improvement of hypertension and glucose control. PMID:26380561

  3. LA and ALA prevent glucose intolerance in obese male rats without reducing reactive lipid content, but cause tissue-specific changes in fatty acid composition.

    PubMed

    Matravadia, Sarthak; Zabielski, Piotr; Chabowski, Adrian; Mutch, David M; Holloway, Graham P

    2016-04-01

    While the cause of Type 2 diabetes remains poorly defined, the accumulation of reactive lipids within white adipose tissue, skeletal muscle, and liver have been repeatedly implicated as underlying mechanisms. The ability of polyunsaturated fatty acids (PUFAs) to prevent the development of insulin resistance has gained considerable interest in recent years; however, the mechanisms-of-action remain poorly described. Therefore, we determined the efficacy of diets supplemented with either linoleic acid (LA) or α-linolenic acid (ALA) in preventing insulin resistance and reactive lipid accumulation in key metabolic tissues of the obese Zucker rat. Obese Zucker rats displayed impaired glucose homeostasis and reduced n-3 and n-6 PUFA content in the liver and epididymal white adipose tissue (EWAT). After the 12-wk feeding intervention, both LA- and ALA-supplemented diets prevented whole body glucose and insulin intolerance; however, ALA had a more pronounced effect. These changes occurred in association with n-3 and n-6 accumulation in all tissues studied, albeit to different extents (EWAT > liver > muscle). Triacylglycerol (TAG), diacylglycerol (DAG), ceramide, and sphingolipid accumulation were not attenuated in obese animals supplemented with either LA or ALA, suggesting that preservation of glucose homeostasis occurred independent of changes in reactive lipid content. However, PUFA-supplemented diets differentially altered the fatty acid composition of TAGs, DAGs, and PLs in a tissue-specific manner, suggesting essential fatty acid metabolism differs between tissues. Together, our results indicate that remodeling of the fatty acid composition of various lipid fractions may contribute to the improved glucose tolerance observed in obese rats fed PUFA-supplemented diets. PMID:26764053

  4. Maternal protein restriction induces early-onset glucose intolerance and alters hepatic genes expression in the peroxisome proliferator-activated receptor pathway in offspring

    PubMed Central

    Zheng, Jia; Xiao, Xinhua; Zhang, Qian; Yu, Miao; Xu, Jianping; Wang, Zhixin

    2015-01-01

    Aims/Introduction Maternal undernutrition during pregnancy and/or lactation can alter the offspring's response to environmental challenges, and thus increases the risk of the development of metabolic diseases at a later age. However, whether maternal protein restriction can modulate glucose metabolism in the early life of offspring is less understood. Furthermore, we explored the potential underlying mechanisms that illustrate this phenotype. Materials and Methods To test this hypothesis, we examined the offspring of C57BL/6J mice at weaning to determine the effects of feeding their mothers a low-protein diet or normal chow diet throughout pregnancy and lactation. Gene array experiments and quantitative real-time polymerase chain reaction were utilized to explore the altered hepatic genes expression. Results The offspring of dams fed a low-protein diet had a lower birthweight and bodyweight, impaired glucose tolerance, decreased insulin sensitivity, and decreased serum cholesterol at weaning. Using gene array experiments, 253 differentially expressed genes were identified in the liver tissues of the offspring between the two groups. Bioinformatic analyses showed that all differentially expressed genes were mapped to 11 pathways. We focused on the ‘peroxisome proliferator-activated receptor signaling pathway,’ because peroxisome proliferator-activated receptors have emerged as central regulators of glucose and lipid homeostasis. Quantitative real-time polymerase chain reaction was utilized for the validation of genes in the pathway. Conclusions A maternal low-protein diet during pregnancy and lactation promotes early-onset glucose intolerance in the offspring mice, and the altered hepatic genes expression in peroxisome proliferator-activated receptor signaling pathway could play role in regulating this phenomenon. PMID:25969711

  5. Mice Deficient in Proglucagon-Derived Peptides Exhibit Glucose Intolerance on a High-Fat Diet but Are Resistant to Obesity

    PubMed Central

    Ozaki, Nobuaki; Seino, Yusuke; Murata, Yoshiharu; Oshida, Yoshiharu; Hayashi, Yoshitaka

    2015-01-01

    Homozygous glucagon-GFP knock-in mice (Gcggfp/gfp) lack proglucagon derived-peptides including glucagon and GLP-1, and are normoglycemic. We have previously shown that Gcggfp/gfp show improved glucose tolerance with enhanced insulin secretion. Here, we studied glucose and energy metabolism in Gcggfp/gfp mice fed a high-fat diet (HFD). Male Gcggfp/gfp and Gcggfp/+ mice were fed either a normal chow diet (NCD) or an HFD for 15–20 weeks. Regardless of the genotype, mice on an HFD showed glucose intolerance, and Gcggfp/gfp mice on HFD exhibited impaired insulin secretion whereas Gcggfp/+ mice on HFD exhibited increased insulin secretion. A compensatory increase in β-cell mass was observed in Gcggfp/+mice on HFD, but not in Gcggfp/gfp mice on the same diet. Weight gain was significantly lower in Gcggfp/gfp mice than in Gcggfp/+mice. Oxygen consumption was enhanced in Gcggfp/gfp mice compared to Gcggfp/+ mice on an HFD. HFD feeding significantly increased uncoupling protein 1 mRNA expression in brown adipose and inguinal white adipose tissues of Gcggfp/gfp mice, but not of Gcggfp/+mice. Treatment with the glucagon-like peptide-1 receptor agonist liraglutide (200 mg/kg) improved glucose tolerance in Gcggfp/gfp mice and insulin content in Gcggfp/gfp and Gcggfp/+ mice was similar after liraglutide treatment. Our findings demonstrate that Gcggfp/gfp mice develop diabetes upon HFD-feeding in the absence of proglucagon-derived peptides, although they are resistant to diet-induced obesity. PMID:26378455

  6. Vitamin D and 1-hour post-load plasma glucose in hypertensive patients

    PubMed Central

    2014-01-01

    Background A plasma glucose value ≥155 mg/dl for 1-hour post-load plasma glucose during an oral glucose tolerance test (OGTT) is able to identify subjects with normal glucose tolerance (NGT) at high-risk for type-2 diabetes and with subclinical organ damage. We designed this study to address if 25-hydroxyvitamin D [25(OH)D] circulating levels are associated with glucose tolerance status, and in particular with 1-hour post-load plasma glucose levels. Methods We enrolled 300 consecutive Caucasian hypertensive never-treated outpatients (160 men and 140 women, aged 52.9 ± 9.2 years). Subjects underwent OGTT and measurements of 25(OH)D and standard laboratory tests. Estimated glomerular filtration rate (e-GFR) was calculated by CKD-EPI formula and insulin sensitivity was assessed by Matsuda-index. Results Among participants, 230 were NGT, 44 had impaired glucose tolerance (IGT) and 26 had type-2 diabetes. According to 1-h post-load plasma glucose cut-off point of 155 mg/dL, we divided NGT subjects into: NGT < 155 (n = 156) and NGT > 155 mg/dL (n = 74). NGT ≥ 155 had higher significant fasting and post-load glucose and insulin, parathyroid hormone and hs-CRP levels than NGT < 155. On the contrary, Matsuda-index, e-GFR, and 25(OH)D were significantly lower in NGT ≥ 155 than NGT < 155 subjects. In the multiple regression analysis, 25(OH)D levels resulted the major determinant of 1-h post-load plasma glucose in all population and in the four groups of glucose tolerance status. In the whole population, Matsuda-index, hs-CRP and e-GFR explained another 12.2%, 6.7% and 1.7% of its variation. Conclusions Our data demonstrate a significant and inverse relationship between 25(OH)D levels and glucose tolerance status, particularly with 1-h post-load glucose. PMID:24555478

  7. Hydrolysis enhances bioavailability of proanthocyanidin-derived metabolites and improves β-cell function in glucose intolerant rats.

    PubMed

    Yang, Kaiyuan; Hashemi, Zohre; Han, Wei; Jin, Alena; Yang, Han; Ozga, Jocelyn; Li, Liang; Chan, Catherine B

    2015-08-01

    Proanthocyanidins (PAC) are a highly consumed class of flavonoids and their consumption has been linked to beneficial effects in type 2 diabetes. However, limited gastrointestinal absorption occurs due to the polymeric structure of PAC. We hypothesized that hydrolysis of the PAC polymer would increase bioavailability, thus leading to enhanced beneficial effects on glucose homeostasis and pancreatic β-cell function. PAC-rich pea seed coats (PSC) were supplemented to a high-fat diet (HFD) either in native (PAC) or hydrolyzed (HPAC) form fed to rats for 4 weeks. HFD or low-fat diet groups were controls. PAC-derived compounds were characterized in both PSC and serum. Glucose and insulin tolerance tests were conducted. Pancreatic α-cell and β-cell areas and glucose-stimulated insulin secretion (GSIS) from isolated islets were measured. Increased PAC-derived metabolites were detected in the serum of HPAC-fed rats compared to PAC-fed rats, suggesting hydrolysis of PSC-enhanced PAC bioavailability. This was associated with ~18% less (P<.05) weight gain compared to HFD without affecting food intake, as well as improvement in glucose disposal in vivo. There was a 2-fold decrease of α/β-cell area ratio and a 2.5-fold increase in GSIS from isolated islets of HPAC-fed rats. These results demonstrate that hydrolysis of PSC-derived PAC increased the bioavailability of PAC-derived products, which is critical for enhancing beneficial effects on glucose homeostasis and pancreatic β-cell function. PMID:25987165

  8. Glucose tolerance in hypertensive patients during treatment with the calcium antagonist, felodipine.

    PubMed Central

    Hedner, T; Elmfeldt, D; Von Schenck, H; Sjögren, E; Smith, U

    1987-01-01

    1 Twelve non-diabetic hypertensive male patients insufficiently controlled by a diuretic were included in a double-blind, randomised study. In addition placebo or felodipine was given for 4 weeks followed by a 2 week wash-out period, after which the alternative treatment was given for another 4 weeks. At the end of each treatment period an oral glucose tolerance test (OGTT) was performed and blood pressure, plasma noradrenaline and felodipine levels were measured. 2 There was no change in either glucose, insulin or glucagon levels during the OGTT after felodipine compared with placebo. Blood pressure was significantly reduced during the dosage interval of felodipine (12 h). Plasma noradrenaline increased significantly after felodipine. Side effects were few. 3 In a separate open study 58 hypertensive patients were treated with felodipine in addition to a diuretic and a beta-adrenoceptor blocker for up to 1 year. There were no significant changes in fasting blood glucose levels during the study. PMID:3304386

  9. Catalytic site inhibition of insulin-degrading enzyme by a small molecule induces glucose intolerance in mice

    SciTech Connect

    Deprez-Poulain, Rebecca; Hennuyer, Nathalie; Bosc, Damien; Liang, Wenguang G.; Enée, Emmanuelle; Marechal, Xavier; Charton, Julie; Totobenazara, Jane; Berte, Gonzague; Jahklal, Jouda; Verdelet, Tristan; Dumont, Julie; Dassonneville, Sandrine; Woitrain, Eloise; Gauriot, Marion; Paquet, Charlotte; Duplan, Isabelle; Hermant, Paul; Cantrelle, François- Xavier; Sevin, Emmanuel; Culot, Maxime; Landry, Valerie; Herledan, Adrien; Piveteau, Catherine; Lippens, Guy; Leroux, Florence; Tang, Wei-Jen; van Endert, Peter; Staels, Bart; Deprez, Benoit

    2015-09-23

    Insulin-degrading enzyme (IDE) is a protease that cleaves insulin and other bioactive peptides such as amyloid-β. Knockout and genetic studies have linked IDE to Alzheimer’s disease and type-2 diabetes. As the major insulin-degrading protease, IDE is a candidate drug target in diabetes. Here we have used kinetic target-guided synthesis to design the first catalytic site inhibitor of IDE suitable for in vivo studies (BDM44768). Crystallographic and small angle X-ray scattering analyses show that it locks IDE in a closed conformation. Among a panel of metalloproteases, BDM44768 selectively inhibits IDE. Acute treatment of mice with BDM44768 increases insulin signalling and surprisingly impairs glucose tolerance in an IDE-dependent manner. These results confirm that IDE is involved in pathways that modulate short-term glucose homeostasis, but casts doubt on the general usefulness of the inhibition of IDE catalytic activity to treat diabetes.

  10. Catalytic site inhibition of insulin-degrading enzyme by a small molecule induces glucose intolerance in mice.

    PubMed

    Deprez-Poulain, Rebecca; Hennuyer, Nathalie; Bosc, Damien; Liang, Wenguang G; Enée, Emmanuelle; Marechal, Xavier; Charton, Julie; Totobenazara, Jane; Berte, Gonzague; Jahklal, Jouda; Verdelet, Tristan; Dumont, Julie; Dassonneville, Sandrine; Woitrain, Eloise; Gauriot, Marion; Paquet, Charlotte; Duplan, Isabelle; Hermant, Paul; Cantrelle, François-Xavier; Sevin, Emmanuel; Culot, Maxime; Landry, Valerie; Herledan, Adrien; Piveteau, Catherine; Lippens, Guy; Leroux, Florence; Tang, Wei-Jen; van Endert, Peter; Staels, Bart; Deprez, Benoit

    2015-01-01

    Insulin-degrading enzyme (IDE) is a protease that cleaves insulin and other bioactive peptides such as amyloid-β. Knockout and genetic studies have linked IDE to Alzheimer's disease and type-2 diabetes. As the major insulin-degrading protease, IDE is a candidate drug target in diabetes. Here we have used kinetic target-guided synthesis to design the first catalytic site inhibitor of IDE suitable for in vivo studies (BDM44768). Crystallographic and small angle X-ray scattering analyses show that it locks IDE in a closed conformation. Among a panel of metalloproteases, BDM44768 selectively inhibits IDE. Acute treatment of mice with BDM44768 increases insulin signalling and surprisingly impairs glucose tolerance in an IDE-dependent manner. These results confirm that IDE is involved in pathways that modulate short-term glucose homeostasis, but casts doubt on the general usefulness of the inhibition of IDE catalytic activity to treat diabetes. PMID:26394692

  11. Catalytic site inhibition of insulin-degrading enzyme by a small molecule induces glucose intolerance in mice

    PubMed Central

    Deprez-Poulain, Rebecca; Hennuyer, Nathalie; Bosc, Damien; Liang, Wenguang G.; Enée, Emmanuelle; Marechal, Xavier; Charton, Julie; Totobenazara, Jane; Berte, Gonzague; Jahklal, Jouda; Verdelet, Tristan; Dumont, Julie; Dassonneville, Sandrine; Woitrain, Eloise; Gauriot, Marion; Paquet, Charlotte; Duplan, Isabelle; Hermant, Paul; Cantrelle, François- Xavier; Sevin, Emmanuel; Culot, Maxime; Landry, Valerie; Herledan, Adrien; Piveteau, Catherine; Lippens, Guy; Leroux, Florence; Tang, Wei-Jen; van Endert, Peter; Staels, Bart; Deprez, Benoit

    2015-01-01

    Insulin-degrading enzyme (IDE) is a protease that cleaves insulin and other bioactive peptides such as amyloid-β. Knockout and genetic studies have linked IDE to Alzheimer's disease and type-2 diabetes. As the major insulin-degrading protease, IDE is a candidate drug target in diabetes. Here we have used kinetic target-guided synthesis to design the first catalytic site inhibitor of IDE suitable for in vivo studies (BDM44768). Crystallographic and small angle X-ray scattering analyses show that it locks IDE in a closed conformation. Among a panel of metalloproteases, BDM44768 selectively inhibits IDE. Acute treatment of mice with BDM44768 increases insulin signalling and surprisingly impairs glucose tolerance in an IDE-dependent manner. These results confirm that IDE is involved in pathways that modulate short-term glucose homeostasis, but casts doubt on the general usefulness of the inhibition of IDE catalytic activity to treat diabetes. PMID:26394692

  12. Central inhibition of IKKβ/NF-κB signaling attenuates high-fat diet-induced obesity and glucose intolerance.

    PubMed

    Benzler, Jonas; Ganjam, Goutham K; Pretz, Dominik; Oelkrug, Rebecca; Koch, Christiane E; Legler, Karen; Stöhr, Sigrid; Culmsee, Carsten; Williams, Lynda M; Tups, Alexander

    2015-06-01

    Metabolic inflammation in the central nervous system might be causative for the development of overnutrition-induced metabolic syndrome and related disorders, such as obesity, leptin and insulin resistance, and type 2 diabetes. Here we investigated whether nutritive and genetic inhibition of the central IκB kinase β (IKKβ)/nuclear factor-κB (NF-κB) pathway in diet-induced obese (DIO) and leptin-deficient mice improves these metabolic impairments. A known prominent inhibitor of IKKβ/NF-κB signaling is the dietary flavonoid butein. We initially determined that oral, intraperitoneal, and intracerebroventricular administration of this flavonoid improved glucose tolerance and hypothalamic insulin signaling. The dose-dependent glucose-lowering capacity was profound regardless of whether obesity was caused by leptin deficiency or high-fat diet (HFD). To confirm the apparent central role of IKKβ/NF-κB signaling in the control of glucose and energy homeostasis, we genetically inhibited this pathway in neurons of the arcuate nucleus, one key center for control of energy homeostasis, via specific adeno-associated virus serotype 2-mediated overexpression of IκBα, which inhibits NF-κB nuclear translocation. This treatment attenuated HFD-induced body weight gain, body fat mass accumulation, increased energy expenditure, and reduced arcuate suppressor of cytokine signaling 3 expression, indicative for enhanced leptin signaling. These results reinforce a specific role of central proinflammatory IKKβ/NF-κB signaling in the development and potential treatment of DIO-induced comorbidities. PMID:25626735

  13. Cosmetic intolerance.

    PubMed

    Broeckx, W; Blondeel, A; Dooms-Goossens, A; Achten, G

    1987-04-01

    A study of cosmetic intolerance has been undertaken in 5202 patients tested for possible contact dermatitis. Each patient has been evaluated by medical history and patch testing. Intolerance to cosmetics involved only 5.9% of the total population tested. If other possible sources of allergens (medication, occupation, hobbies etc) are associated, this figure rises to 11.7%. The origin of the cosmetic intolerance is more often an allergy than irritation. Soaps and shampoos are the most important types of cosmetics responsible for adverse reactions. The principal allergens are the fragrances, preservatives, hair dyes and the patients' own products. In this last category, the specific allergen has not always been detected. PMID:3595117

  14. Self-perceived lactose intolerance results in lower intakes of calcium and dairy foods and is associated with hypertension and diabetes in adults

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Self-perceived lactose intolerance may result in adverse dietary modifications; thus, more studies are needed to understand the prevalence of self-perceived lactose intolerance and how it relates to calcium intake and selected health conditions. The objective was to examine the effects of self-perce...

  15. Catalytic site inhibition of insulin-degrading enzyme by a small molecule induces glucose intolerance in mice

    DOE PAGESBeta

    Deprez-Poulain, Rebecca; Hennuyer, Nathalie; Bosc, Damien; Liang, Wenguang G.; Enée, Emmanuelle; Marechal, Xavier; Charton, Julie; Totobenazara, Jane; Berte, Gonzague; Jahklal, Jouda; et al

    2015-09-23

    Insulin-degrading enzyme (IDE) is a protease that cleaves insulin and other bioactive peptides such as amyloid-β. Knockout and genetic studies have linked IDE to Alzheimer’s disease and type-2 diabetes. As the major insulin-degrading protease, IDE is a candidate drug target in diabetes. Here we have used kinetic target-guided synthesis to design the first catalytic site inhibitor of IDE suitable for in vivo studies (BDM44768). Crystallographic and small angle X-ray scattering analyses show that it locks IDE in a closed conformation. Among a panel of metalloproteases, BDM44768 selectively inhibits IDE. Acute treatment of mice with BDM44768 increases insulin signalling and surprisinglymore » impairs glucose tolerance in an IDE-dependent manner. These results confirm that IDE is involved in pathways that modulate short-term glucose homeostasis, but casts doubt on the general usefulness of the inhibition of IDE catalytic activity to treat diabetes.« less

  16. Leptin Production by Encapsulated Adipocytes Increases Brown Fat, Decreases Resistin, and Improves Glucose Intolerance in Obese Mice.

    PubMed

    DiSilvestro, David J; Melgar-Bermudez, Emiliano; Yasmeen, Rumana; Fadda, Paolo; Lee, L James; Kalyanasundaram, Anuradha; Gilor, Chen L; Ziouzenkova, Ouliana

    2016-01-01

    The neuroendocrine effects of leptin on metabolism hold promise to be translated into a complementary therapy to traditional insulin therapy for diabetes and obesity. However, injections of leptin can provoke inflammation. We tested the effects of leptin, produced in the physiological adipocyte location, on metabolism in mouse models of genetic and dietary obesity. We generated 3T3-L1 adipocytes constitutively secreting leptin and encapsulated them in a poly-L-lysine membrane, which protects the cells from immune rejection. Ob/ob mice (OB) were injected with capsules containing no cells (empty, OB[Emp]), adipocytes (OB[3T3]), or adipocytes overexpressing leptin (OB[Lep]) into both visceral fat depots. Leptin was found in the plasma of OB[Lep], but not OB[Emp] and OB[3T3] mice at the end of treatment (72 days). The OB[Lep] and OB[3T3] mice have transiently suppressed appetite and weight loss compared to OB[Emp]. Only OB[Lep] mice have greater brown fat mass, metabolic rate, and reduced resistin plasma levels compared to OB[Emp]. Glucose tolerance was markedly better in OB[Lep] vs. OB[Emp] and OB[3T3] mice as well as in wild type mice with high-fat diet-induced obesity and insulin resistance treated with encapsulated leptin-producing adipocytes. Our proof-of-principle study provides evidence of long-term improvement of glucose tolerance with encapsulated adipocytes producing leptin. PMID:27055280

  17. Leptin Production by Encapsulated Adipocytes Increases Brown Fat, Decreases Resistin, and Improves Glucose Intolerance in Obese Mice

    PubMed Central

    DiSilvestro, David J.; Melgar-Bermudez, Emiliano; Yasmeen, Rumana; Fadda, Paolo; Lee, L. James; Kalyanasundaram, Anuradha; Gilor, Chen L.; Ziouzenkova, Ouliana

    2016-01-01

    The neuroendocrine effects of leptin on metabolism hold promise to be translated into a complementary therapy to traditional insulin therapy for diabetes and obesity. However, injections of leptin can provoke inflammation. We tested the effects of leptin, produced in the physiological adipocyte location, on metabolism in mouse models of genetic and dietary obesity. We generated 3T3-L1 adipocytes constitutively secreting leptin and encapsulated them in a poly-L-lysine membrane, which protects the cells from immune rejection. Ob/ob mice (OB) were injected with capsules containing no cells (empty, OB[Emp]), adipocytes (OB[3T3]), or adipocytes overexpressing leptin (OB[Lep]) into both visceral fat depots. Leptin was found in the plasma of OB[Lep], but not OB[Emp] and OB[3T3] mice at the end of treatment (72 days). The OB[Lep] and OB[3T3] mice have transiently suppressed appetite and weight loss compared to OB[Emp]. Only OB[Lep] mice have greater brown fat mass, metabolic rate, and reduced resistin plasma levels compared to OB[Emp]. Glucose tolerance was markedly better in OB[Lep] vs. OB[Emp] and OB[3T3] mice as well as in wild type mice with high-fat diet-induced obesity and insulin resistance treated with encapsulated leptin-producing adipocytes. Our proof-of-principle study provides evidence of long-term improvement of glucose tolerance with encapsulated adipocytes producing leptin. PMID:27055280

  18. The effective fraction isolated from Radix Astragali alleviates glucose intolerance, insulin resistance and hypertriglyceridemia in db/db diabetic mice through its anti-inflammatory activity

    PubMed Central

    2010-01-01

    Background Macrophage infiltration in adipose tissue together with the aberrant production of pro-inflammatory cytokines has been identified as the key link between obesity and its related metabolic disorders. This study aims to isolate bioactive ingredients from the traditional Chinese herb Radix Astragali (Huangqi) that alleviate obesity-induced metabolic damage through inhibiting inflammation. Methods Active fraction (Rx) that inhibits pro-inflammatory cytokine production was identified from Radix Astragali by repeated bioactivity-guided high-throughput screening. Major constituents in Rx were identified by column chromatography followed by high-performance liquid chromatography (HPLC) and mass-spectrometry. Anti-diabetic activity of Rx was evaluated in db/db mice. Results Treatment with Rx, which included calycosin-7-β-D-glucoside (0.9%), ononin (1.2%), calycosin (4.53%) and formononetin (1.1%), significantly reduced the secretion of pro-inflammatory cytokines (TNF-α, IL-6 and MCP-1) in human THP-1 macrophages and lipopolysaccharide (LPS)-induced activation of NF-κB in mouse RAW-Blue macrophages in a dose-dependent manner. Chronic administration of Rx in db/db obese mice markedly decreased the levels of both fed and fasting glucose, reduced serum triglyceride, and also alleviated insulin resistance and glucose intolerance when compared to vehicle-treated controls. The mRNA expression levels of inflammatory cell markers CD68 and F4/80, and cytokines MCP-1, TNF-α and IL-6 were significantly reduced in epididymal adipose tissue while the alternatively activated macrophage marker arginase I was markedly increased in the Rx-treated mice. Conclusion These findings suggest that suppression of the inflammation pathways in macrophages represents a valid strategy for high-throughput screening of lead compounds with anti-diabetic and insulin sensitizing properties, and further support the etiological role of inflammation in the pathogenesis of obesity-related metabolic disorders. PMID:20735814

  19. Lactose Intolerance (For Kids)

    MedlinePlus

    ... Sledding, Skiing, Snowboarding, Skating Crushes What's a Booger? Lactose Intolerance KidsHealth > For Kids > Lactose Intolerance Print A ... LAK-tose in-TAHL-er-ents). What Is Lactose Intolerance? People who have lactose intolerance have trouble ...

  20. Lactose Intolerance (For Teens)

    MedlinePlus

    ... How Can I Help a Friend Who Cuts? Lactose Intolerance KidsHealth > For Teens > Lactose Intolerance Print A ... dairy than her body can handle. What Is Lactose Intolerance? Lactose intolerance is the inability to digest ...

  1. Naringenin prevents obesity, hepatic steatosis, and glucose intolerance in male mice independent of fibroblast growth factor 21.

    PubMed

    Assini, Julia M; Mulvihill, Erin E; Burke, Amy C; Sutherland, Brian G; Telford, Dawn E; Chhoker, Sanjiv S; Sawyez, Cynthia G; Drangova, Maria; Adams, Andrew C; Kharitonenkov, Alexei; Pin, Christopher L; Huff, Murray W

    2015-06-01

    The molecular mechanisms and metabolic pathways whereby the citrus flavonoid, naringenin, reduces dyslipidemia and improves glucose tolerance were investigated in C57BL6/J wild-type mice and fibroblast growth factor 21 (FGF21) null (Fgf21(-/-)) mice. FGF21 regulates energy homeostasis and the metabolic adaptation to fasting. One avenue of this regulation is through induction of peroxisome proliferator-activated receptor-γ coactivator-1α (Pgc1a), a regulator of hepatic fatty acid oxidation and ketogenesis. Because naringenin is a potent activator of hepatic FA oxidation, we hypothesized that induction of FGF21 might be an integral part of naringenin's mechanism of action. Furthermore, we predicted that FGF21 deficiency would potentiate high-fat diet (HFD)-induced metabolic dysregulation and compromise metabolic protection by naringenin. The absence of FGF21 exacerbated the response to a HFD. Interestingly, naringenin supplementation to the HFD robustly prevented obesity in both genotypes. Gene expression analysis suggested that naringenin was not primarily targeting fatty acid metabolism in white adipose tissue. Naringenin corrected hepatic triglyceride concentrations and normalized hepatic expression of Pgc1a, Cpt1a, and Srebf1c in both wild-type and Fgf21(-/-) mice. HFD-fed Fgf21(-/-) mice displayed greater muscle triglyceride deposition, hyperinsulinemia, and impaired glucose tolerance as compared with wild-type mice, confirming the role of FGF21 in insulin sensitivity; however, naringenin supplementation improved these metabolic parameters in both genotypes. We conclude that FGF21 deficiency exacerbates HFD-induced obesity, hepatic steatosis, and insulin resistance. Furthermore, FGF21 is not required for naringenin to protect mice from HFD-induced metabolic dysregulation. Collectively these studies support the concept that naringenin has potent lipid-lowering effects and may act as an insulin sensitizer in vivo. PMID:25774553

  2. Two-hour glucose predicts the development of hypertension over 5 years: the AusDiab study.

    PubMed

    Boyko, E J; Barr, E L M; Zimmet, P Z; Shaw, J E

    2008-03-01

    Elevated 2-h plasma glucose concentration (2hPG) from an oral glucose tolerance (OGTT) test more strongly predicts risk of subsequent cardiovascular disease than fasting plasma glucose (FPG), but the association between these glucose measurements and hypertension risk is less clear. We examined the association between 2hPG, FPG and risk of hypertension. We conducted a prospective observational study (The Australian Diabetes, Obesity and Lifestyle Study-AusDiab) among 4413 Australian residents who attended a baseline (1999-2000) and follow-up (2004-2005) examinations. Measurements included blood pressure (mean of two readings), 75 g OGTT, fasting insulin, anthropometrics, dietary and alcohol intake, medical history and physical activity. Hypertension was defined as a systolic blood pressure (SBP)> or =140 or a diastolic blood pressure (DBP)> or =90 mm Hg or treatment with medication for hypertension. HOMA-S was calculated as a measure of insulin sensitivity using the HOMA2 calculator. Hypertension developed in 14% of the 4306 subjects available for this analysis. Higher 2hPG was significantly related to greater risk of hypertension after adjustment for age, gender, FPG, BMI (baseline and difference), waist circumference (baseline and difference), education, exercise, alcohol intake, baseline SBP and smoking (OR (95% CI) 1.12 (1.01 to 1.23)), but no significant association was seen between FPG and hypertension in this model (1.02 (0.88-1.19)). Further adjustment for HOMA-S did not change these findings. Higher baseline 2hPG was more strongly associated with an increase in SBP than in DBP over 5 years. We conclude that higher 2hPG predicted future hypertension occurrence in this population. PMID:18046430

  3. Carotid Intima Media Thickness in Nondiabetic Hypertensive Nigerians: Role of Fasting and Postprandial Blood Glucose

    PubMed Central

    Okeahialam, B. N.; Muoneme, S. A.; Kolade-Yunusa, H. O.

    2016-01-01

    Background/Aims. Carotid intima media thickness (CIMT) tracks atherosclerotic vascular disease. Hypertension and diabetes chiefly contribute to atherosclerosis with 75% of symptomatic cardiovascular disease cases having dysglycaemia even in normal cases. Hypothesising that postprandial hyperglycaemia contributes to cardiovascular morbidity, we sought to determine if any relationship existed between glycaemic profile in nondiabetic hypertensives and atherosclerosis. Methods. In a study of CIMT in nondiabetic, statin-naïve hypertensives, we evaluated fasting blood glucose (FBG) and 2-hour postprandial sugar (2hPPBG) in the patients and compared them with the CIMT. CIMT was measured on both sides, 1 cm proximal to the carotid bulb using a 7.5 mHz transducer of ALOKA SSD-3500 ultrasound machine. Results. The subjects with complete data were 86 (63 F). The mean (SD) of CIMT was 0.89 (0.15) mm, FBG 4.8 (0.097) mmol/L, and 2hPPBG 6.5 (1.81) mmol/L. There was no significant correlation between FBG and 2hPPBG with CIMT. Blood pressure had no bearing on this. When blood glucose data were divided into quartiles and post hoc multiple comparison was done, there was significant difference in CIMT for the different ranges. This was not so for 2hPPBG. Conclusion. Though expected from other studies, we did not show any significant correlation between FBG and 2hPPBG status and CIMT. This may be our pattern as the degree of excursion of 2hPPBG was low. There may be a threshold level above which PPBG starts to impact CIMT. PMID:27144025

  4. Transgenerational glucose intolerance with Igf2/H19 epigenetic alterations in mouse islet induced by intrauterine hyperglycemia.

    PubMed

    Ding, Guo-Lian; Wang, Fang-Fang; Shu, Jing; Tian, Shen; Jiang, Ying; Zhang, Dan; Wang, Ning; Luo, Qiong; Zhang, Yu; Jin, Fan; Leung, Peter C K; Sheng, Jian-Zhong; Huang, He-Feng

    2012-05-01

    Gestational diabetes mellitus (GDM) has been shown to be associated with high risk of diabetes in offspring. However, the mechanisms involved and the possibilities of transgenerational transmission are still unclear. We intercrossed male and female adult control and first-generation offspring of GDM (F1-GDM) mice to obtain the second-generation (F2) offspring in four groups: C♂-C♀, C♂-GDM♀, GDM♂-C♀, and GDM♂-GDM♀. We found that birth weight significantly increased in F2 offspring through the paternal line with impaired glucose tolerance (IGT). Regardless of birth from F1-GDM with or without IGT, high risk of IGT appeared as early as 3 weeks in F2 offspring and progressed through both parental lineages, especial the paternal line. IGT in male offspring was more obvious than that in females, with parental characteristics and sex-specific transmission. In both F1 and F2 offspring of GDM, the expression of imprinted genes Igf2 and H19 was downregulated in pancreatic islets, caused by abnormal methylation status of the differentially methylated region, which may be one of the mechanisms for impaired islet ultrastructure and function. Furthermore, altered Igf2 and H19 gene expression was found in sperm of adult F1-GDM, regardless of the presence of IGT, indicating that changes of epigenetics in germ cells contributed to transgenerational transmission. PMID:22447856

  5. Monoclonal Antibody Targeting of Fibroblast Growth Factor Receptor 1c Ameliorates Obesity and Glucose Intolerance via Central Mechanisms

    PubMed Central

    Lelliott, Christopher J.; Ahnmark, Andrea; Admyre, Therese; Ahlstedt, Ingela; Irving, Lorraine; Keyes, Feenagh; Patterson, Laurel; Mumphrey, Michael B.; Bjursell, Mikael; Gorman, Tracy; Bohlooly-Y, Mohammad; Buchanan, Andrew; Harrison, Paula; Vaughan, Tristan; Berthoud, Hans-Rudolf; Lindén, Daniel

    2014-01-01

    We have generated a novel monoclonal antibody targeting human FGFR1c (R1c mAb) that caused profound body weight and body fat loss in diet-induced obese mice due to decreased food intake (with energy expenditure unaltered), in turn improving glucose control. R1c mAb also caused weight loss in leptin-deficient ob/ob mice, leptin receptor-mutant db/db mice, and in mice lacking either the melanocortin 4 receptor or the melanin-concentrating hormone receptor 1. In addition, R1c mAb did not change hypothalamic mRNA expression levels of Agrp, Cart, Pomc, Npy, Crh, Mch, or Orexin, suggesting that R1c mAb could cause food intake inhibition and body weight loss via other mechanisms in the brain. Interestingly, peripherally administered R1c mAb accumulated in the median eminence, adjacent arcuate nucleus and in the circumventricular organs where it activated the early response gene c-Fos. As a plausible mechanism and coinciding with the initiation of food intake suppression, R1c mAb induced hypothalamic expression levels of the cytokines Monocyte chemoattractant protein 1 and 3 and ERK1/2 and p70 S6 kinase 1 activation. PMID:25427253

  6. Monoclonal antibody targeting of fibroblast growth factor receptor 1c ameliorates obesity and glucose intolerance via central mechanisms.

    PubMed

    Lelliott, Christopher J; Ahnmark, Andrea; Admyre, Therese; Ahlstedt, Ingela; Irving, Lorraine; Keyes, Feenagh; Patterson, Laurel; Mumphrey, Michael B; Bjursell, Mikael; Gorman, Tracy; Bohlooly-Y, Mohammad; Buchanan, Andrew; Harrison, Paula; Vaughan, Tristan; Berthoud, Hans-Rudolf; Lindén, Daniel

    2014-01-01

    We have generated a novel monoclonal antibody targeting human FGFR1c (R1c mAb) that caused profound body weight and body fat loss in diet-induced obese mice due to decreased food intake (with energy expenditure unaltered), in turn improving glucose control. R1c mAb also caused weight loss in leptin-deficient ob/ob mice, leptin receptor-mutant db/db mice, and in mice lacking either the melanocortin 4 receptor or the melanin-concentrating hormone receptor 1. In addition, R1c mAb did not change hypothalamic mRNA expression levels of Agrp, Cart, Pomc, Npy, Crh, Mch, or Orexin, suggesting that R1c mAb could cause food intake inhibition and body weight loss via other mechanisms in the brain. Interestingly, peripherally administered R1c mAb accumulated in the median eminence, adjacent arcuate nucleus and in the circumventricular organs where it activated the early response gene c-Fos. As a plausible mechanism and coinciding with the initiation of food intake suppression, R1c mAb induced hypothalamic expression levels of the cytokines Monocyte chemoattractant protein 1 and 3 and ERK1/2 and p70 S6 kinase 1 activation. PMID:25427253

  7. Secreted factors from dental pulp stem cells improve glucose intolerance in streptozotocin-induced diabetic mice by increasing pancreatic β-cell function

    PubMed Central

    Izumoto-Akita, Takako; Tsunekawa, Shin; Yamamoto, Akihito; Uenishi, Eita; Ishikawa, Kota; Ogata, Hidetada; Iida, Atsushi; Ikeniwa, Makoto; Hosokawa, Kaori; Niwa, Yasuhiro; Maekawa, Ryuya; Yamauchi, Yuichiro; Seino, Yusuke; Hamada, Yoji; Hibi, Hideharu; Arima, Hiroshi; Ueda, Minoru; Oiso, Yutaka

    2015-01-01

    Objective Many studies have reported that stem cell transplantation promotes propagation and protection of pancreatic β-cells in streptozotocin (STZ)-induced diabetic mice without the differentiation of transplanted cells into pancreatic β-cells, suggesting that the improvement is due to a paracrine effect of the transplanted cells. We investigated the effects of factors secreted by dental pulp stem cells from human exfoliated deciduous teeth (SHED) on β-cell function and survival. Research design and methods Conditioned medium from SHED (SHED-CM) was collected 48 h after culturing in serum-free Dulbecco's modified Eagle's medium (DMEM). The insulin levels in SHED-CM and serum-free conditioned media from human bone marrow-derived mesenchymal stem cells (BM-CM) were undetectable. STZ-induced diabetic male C57B/6J mice were injected with DMEM as a control, SHED-CM, exendin-4 (Ex-4), or BM-CM for 14 days. Mouse pancreatic β-cell line MIN6 cells were incubated with different concentrations of STZ with SHED-CM, DMEM, Ex-4, or BM-CM for 6 h. Results Administration of 1 mL of SHED-CM twice a day improved glucose intolerance in STZ-induced diabetic mice and the effect continued for 20 days after the end of treatment. SHED-CM treatment increased pancreatic insulin content and β-cell mass through proliferation and an intraperitoneal glucose tolerance test revealed enhanced insulin secretion. Incubation of MIN6 cells (a mouse pancreatic β-cell line) with SHED-CM enhanced insulin secretion in a glucose concentration-dependent manner and reduced STZ-induced cell death, indicating that the amelioration of hyperglycemia was caused by the direct effects of SHED-CM on β-cell function and survival. These effects were more pronounced than with the use of Ex-4, a conventional incretin-based drug, and BM-CM, which is a medium derived from other stem cells. Conclusions These findings suggest that SHED-CM provides direct protection and encourages the propagation of β-cells, and has potential as a novel strategy for treatment of diabetes. PMID:26504525

  8. Statin intolerance.

    PubMed

    Ahmad, Zahid

    2014-05-15

    The term statin intolerance refers to an inability to use statins because of muscle symptoms or elevated creatine kinase, and the major diagnostic challenge is to unambiguously link these to statin use. Roughly 5% to 10% of statin users develop statin intolerance, and because statin use is expected to increase--especially after recent updated guidelines have expanded the statin benefit groups--adverse effects from statins will become a growing issue. Unfortunately, the pathophysiology--and even the terminology--of statin-related muscle injury lacks clarity. Several risk factors have been identified, including advanced age, family history of myopathy and statin dose; many cases manifest only after patients are administered an interacting medication (e.g., azole antifungals, cimetidine, clarithromycin, erythromycin and cyclosporine). The diagnosis of myopathy remains challenging, especially because some patients can have normal serum creatine kinase levels despite demonstrable weakness and muscle biopsy-proven statin-induced myopathy. A statin withdrawal and rechallenge helps patients distinguish whether their myalgia symptoms are because of statins, but, in at least 1 clinical trial, even 5% of placebo-treated patients developed myalgias during a controlled withdrawal and rechallenge. No consensus exists for management of patients with statin intolerance. Many patients can eventually tolerate a statin but often at suboptimal doses. A subset of patients do well with nondaily regimens such as every other day or once weekly dosing. Some patients cannot tolerate statins at all, requiring nonstatin lipid-lowering medications--the benefit of which remains unclear with regard to preventing atherosclerotic events. Ultimately, statin intolerance undermines the drug adherence that is critical for achieving the benefits of lifelong lipid-lowering therapy. In conclusion, statin myopathy is a common challenge in lipid management, and further work is needed to establish a standard diagnostic criterion as well as treatment algorithms. PMID:24792743

  9. Reduced cortical BACE1 content with one bout of exercise is accompanied by declines in AMPK, Akt, and MAPK signaling in obese, glucose-intolerant mice.

    PubMed

    MacPherson, R E K; Baumeister, P; Peppler, W T; Wright, D C; Little, J P

    2015-11-15

    Obesity and type 2 diabetes are significant risk factors in the development of neurodegenerative diseases, such as Alzheimer's disease. A variety of cellular mechanisms, such as altered Akt and AMPK and increased inflammatory signaling, contribute to neurodegeneration. Exercise training can improve markers of neurodegeneration, but the underlying mechanisms remain unknown. The purpose of this study was to determine the effects of a single bout of exercise on markers of neurodegeneration and inflammation in brains from mice fed a high-fat diet. Male C57BL/6 mice were fed a low (LFD; 10% kcal from lard)- or a high-fat diet (HFD; 60% kcal from lard) for 7 wk. HFD mice underwent an acute bout of exercise (treadmill running: 15 m/min, 5% incline, 120 min) followed by a recovery period of 2 h. The HFD increased body mass and glucose intolerance (both P < 0.05). This was accompanied by an approximately twofold increase in the phosphorylation of Akt, ERK, and GSK in the cortex (P < 0.05). Following exercise, there was a decrease in beta-site amyloid precursor protein cleaving enzyme 1 (BACE1; P < 0.05) and activity (P < 0.001). This was accompanied by a reduction in AMPK phosphorylation, indicative of a decline in cellular stress (P < 0.05). Akt and ERK phosphorylation were decreased following exercise in HFD mice to a level similar to that of the LFD mice (P < 0.05). This study demonstrates that a single bout of exercise can reduce BACE1 content and activity independent of changes in adiposity. This effect is associated with reductions in Akt, ERK, and AMPK signaling in the cortex. PMID:26404616

  10. Ectopic fat storage, insulin resistance, and hypertension.

    PubMed

    Sironi, Anna Maria; Sicari, Rosa; Folli, Franco; Gastaldelli, Amalia

    2011-01-01

    Obesity, insulin resistance, glucose intolerance/type 2 diabetes and hypertension are clustered in the metabolic syndrome representing critical risk factors for increased incidence cardio-cerebro-vascular diseases, kidney failure and cancer. Ectopic fat accumulation, i.e., accumulation in the mediastinum, liver and the abdomen, as well as generalized fat accumulation are associated with arterial hypertension, either systolic or diastolic. Several mechanisms including insulin resistance, sub-inflammatory state, increased Renin- Angiotensin-Aldosterone System (RAAS) system activity, oxidative stress, autonomic dysregulation as well as mechanical compression on the kidneys are all activated by obesity. Interestingly angiotensin-converting enzyme (ACE) inhibitors and angiotensin II (ATII) receptor blockers, while correcting arterial hypertension, also have a positive effect on glucose metabolism and diabetes prevention, in high risk patients. The implementation of dietary, medical and surgical strategies to prevent and treat obesity, are cornerstones for the primary prevention as well as treatment of arterial hypertension. PMID:21861830

  11. Maternal low-protein diet up-regulates the neuropeptide Y system in visceral fat and leads to abdominal obesity and glucose intolerance in a sex- and time-specific manner

    PubMed Central

    Han, Ruijun; Li, Aiyun; Li, Lijun; Kitlinska, Joanna B.; Zukowska, Zofia

    2012-01-01

    Neuropeptide Y (NPY) mediates stress-induced obesity in adult male mice by activating its Y2 receptor (Y2R) in visceral adipose tissue (VAT). Here, we studied whether the NPY-Y2R system is also activated by maternal low-protein diet (LPD) and linked to obesity in offspring. Prenatal LPD offspring had lower birth weights compared to normal-protein diet (NPD) offspring. Female prenatal and lactation stress (PLS) offspring from mothers fed an LPD developed abdominal adiposity and glucose intolerance associated with a 5-fold up-regulation of NPY mRNA and a 6-fold up-regulation of Y2R mRNA specifically in VAT, in addition to elevated platelet-rich-plasma (PRP) NPY, compared to control females fed a high-fat diet (HFD). Conversely, PLS male offspring showed lower NPY in PRP, a 10-fold decrease of Y2R mRNA in VAT, lower adiposity, and improved glucose tolerance compared to control males. Interestingly, prenatal LPD offspring cross-fostered to control lactating mothers had completely inverse metabolic and NPY phenotypes. Taken together, these findings suggested that maternal LPD activates the VAT NPY-Y2R system and increases abdominal adiposity and glucose intolerance in a sex- and time-specific fashion, suggesting that the peripheral NPY system is a potential mediator of programming for the offspring's vulnerability to obesity and metabolic syndrome.—Han, R., Li, A., Li, L., Kitlinska, J. B., Zukowska, Z. Maternal low-protein diet up-regulates the neuropeptide Y system in visceral fat and leads to abdominal obesity and glucose intolerance in a sex- and time-specific manner. PMID:22539639

  12. Lactose intolerance.

    PubMed

    Roberson, Charlene M

    Although lactose intolerance is very common it is not a serious health condition. The diagnosis is relatively simple and minimally invasive. Treatment is geared towards a life-long plan of management. Persons who have difficulty digesting lactose will learn by trial and error what food items cause distress and learn to avoid offending milk sugars. In addition many products are available over-the-counter to aid in digestion of lactose. Often these additives enable the person to consume lactose. Adequate amounts of calcium may be consumed by eating a carefully chosen diet containing lactose free sources of calcium in order to maintain healthy bone, nerve, and muscle development. PMID:15662762

  13. Glucose indices, frank and undetected diabetes in relation to hypertension and anthropometry in a South Indian rural population.

    PubMed

    Zaman, Forhad Akhtar; Pal, Ranabir; Zaman, Gaffar Sarwar; Swati, Indupalli Amruta; Kayyum, Abdul

    2011-01-01

    Diabetes has emerged as one of the world's biggest health problems and its prevalence is increasing at an alarming rate. This study was conducted to find out the magnitude of frank and undetected diabetes mellitus, including impaired glucose tolerance (IGT) among persons in rural Karnataka, and its relationship with associated risk factors like hypertension and anthropometry. This was a population-based, cross-sectional study on 1370 participants in the field practice area of KBN Medical College, conducted from April 2009 to March, 2010. Diabetes mellitus was noted among 19.78% of the participants, with an additional 12.04% with impaired glucose tolerance. Hypertension observed among participants with diabetes and impaired glucose tolerance was 65.13 and 53.94%, respectively. Effective primary prevention strategies have to be intensified among high-risk population groups, to promote awareness through behavior change communication. PMID:21727679

  14. Lactose intolerance.

    PubMed

    Vandenplas, Yvan

    2015-01-01

    Lactose is the main carbohydrate in infant feeding, but its impact decreases as the child gets older and consumes less milk and dairy products. Congenital lactose intolerance is a very rare condition. However, lactase activity may be low and need to mature during the first weeks of life in many infants. However, the evidence that unabsorbed lactose is causing infantile crying and colic is contradictory. Unabsorbed lactose has a bifidogenic effect and improves calcium absorption. Lactose malabsorption may occur secondary and thus temporally to other etiologies such as infectious gastroenteritis, cow's milk allergy and celiac disease. One the cause is treated, lactase activity will gradually return to normal. The vast majority of Asian children will develop late onset congenital lactase deficiency. However, this entity only exceptionally causes symptoms before the age of 4-5 years. Symptoms are abdominal cramps, flatulence and watery, acid stools, and decrease the quality of life but lactose intolerance is not associated with "true disease". The diagnosis is made on clinical grounds and confirmed with a lactose breath test, if needed. These patients need to have a lifetime long reduced lactose intake to improve their quality of life. PMID:26715083

  15. What Is Lactose Intolerance?

    MedlinePlus

    ... NICHD Research Information Clinical Trials Resources and Publications Lactose Intolerance: Condition Information Skip sharing on social media links Share this: Page Content What is lactose intolerance? People who are lactose intolerant have trouble ...

  16. Allergies and Intolerance

    MedlinePlus

    ... and Intolerance The way in which celiac disease, gluten intolerance and wheat allergy are defined means a ... celiac disease may provide an incorrect diagnosis of gluten intolerance or wheat allergy. Understanding the differences between ...

  17. Glucose and the risk of hypertension in first-degree relatives of patients with type 2 diabetes.

    PubMed

    Janghorbani, Mohsen; Bonnet, Fabrice; Amini, Masoud

    2015-05-01

    To test the hypothesis that plasma glucose (PG) levels is associated with the incidence of hypertension (HT) in nondiabetic and non-hypertensive first-degree relatives (FDR) of people with type 2 diabetes (T2D). A total of 1089 FDR without diabetes and/or HT of consecutive patients with T2D 30-70 years old were examined and followed for a mean (s.d.) of 6.9 (1.7) years for HT incidence. At baseline and through follow-up, participants underwent a standard 75 gm 2-h oral glucose tolerance test. HT was defined according to the criteria of the Seventh Report of Joint National Committee. We used Cox proportional hazard models to estimate hazard ratio for incident HT and plotted a receiver operating characteristic curve to assess discrimination. The PG levels at baseline were associated with incidence of HT, independently of age, gender, obesity and high cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triglycerides, education and systolic blood pressure. Those with impaired glucose tolerance were 54% (hazard ratio 1.54; 95% confidence interval (CI) 1.33, 1.77) more likely to develop HT than those with normal glucose tolerance. Those with impaired fasting glucose were also 23% (hazard ratio 1.23; 95% CI 1.01, 1.50) more likely to develop HT. High PG levels were consistently associated with incident HT. PMID:25693857

  18. [Insulin resistance and hypertension].

    PubMed

    He, R H; Ding, G X; Chen, J W

    1994-03-01

    In this study, we have measured plasma glucose and insulin levels at fasting and following an oral glucose load (75g) in 39 non-diabetic subjects (22 untreated hypertensive, 17 normotensive subjects). We also assessed plasma cholesterol (Ch), triglyceride (TG) levels and Na(+)-K(+)-pump activity in the membranes of their erythrocytes. Overall, hypertensive subjects have hypercholesterol, hypertriglyceride, glucose intolerance and hyperinsulinemia. These changes accorded with Syndrome X proposed by Reaven. In multivariant analysis, after correcting for age, BMI, diastolic pressure (DBP) was positively related to fasting, 1/2h insulin and insulin area under cure (AUC) (P < 0.05). Both systolic pressure (SBP) and DBP were negatively correlated to Na(+)-K(+)-pump (P < 0.01, 0.001), while Na(+)-K(+)-pump was negatively fasting, 1/2h, 1h, 2h insulin levels and insulin AUC (P < 0.05, 0.05, 0.01, 0.01, respectively). These results showed that insulin may affect Na(+)-K(+)-pump activity to develop hypertension independent of age and obese. We also postulated that insulin resistance was causal in the syndrome X, also one of factors developing coronary artery disease. PMID:7805525

  19. Differentially regulated protein kinase A (PKA) activity in adipose tissue and liver is associated with resistance to diet-induced obesity and glucose intolerance in mice that lack PKA regulatory subunit type IIα.

    PubMed

    London, Edra; Nesterova, Maria; Sinaii, Ninet; Szarek, Eva; Chanturiya, Tatyana; Mastroyannis, Spyridon A; Gavrilova, Oksana; Stratakis, Constantine A

    2014-09-01

    The cAMP-dependent protein kinase A (PKA) signaling system is widely expressed and has a central role in regulating cellular metabolism in all organ systems affected by obesity. PKA has four regulatory (RIα, RIIα, RIβ, RIIβ) and four catalytic (Cα, Cβ, Cγ, Prkx) subunit isoforms that have tissue-specific expression profiles. In mice, knockout (KO) of RIIβ, the primary PKA regulatory subunit in adipose tissue or knockout of the catalytic subunit Cβ resulted in a lean phenotype that resists diet-induced obesity and associated metabolic complications. Here we report that the disruption of the ubiquitously expressed PKA RIIα subunit in mice (RIIαKO) confers resistance to diet-induced obesity, glucose intolerance, and hepatic steatosis. After 2-week high-fat diet exposure, RIIαKO mice weighed less than wild-type littermates. Over time this effect was more pronounced in female mice that were also leaner than their wild-type counterparts, regardless of the diet. Decreased intake of a high-fat diet contributed to the attenuated weight gain in RIIαKO mice. Additionally, RIIα deficiency caused differential regulation of PKA in key metabolic organs: cAMP-stimulated PKA activity was decreased in liver and increased in gonadal adipose tissue. We conclude that RIIα represents a potential target for therapeutic interventions in obesity, glucose intolerance, and nonalcoholic fatty liver disease. PMID:24914943

  20. Chemical intolerance.

    PubMed

    Dantoft, Thomas M; Andersson, Linus; Nordin, Steven; Skovbjerg, Sine

    2015-01-01

    Chemical intolerance (CI) is a term used to describe a condition in which the sufferer experiences a complex array of recurrent unspecific symptoms attributed to low-level chemical exposure that most people regard as unproblematic. Severe CI constitutes the distinguishing feature of multiple chemical sensitivity (MCS). The symptoms reported by CI subjects are manifold, involving symptoms from multiple organs systems. In severe cases of CI, the condition can cause considerable life-style limitations with severe social, occupational and economic consequences. As no diagnostic tools for CI are available, the presence of the condition can only be established in accordance to criteria definitions. Numerous modes of action have been suggested to explain CI, with the most commonly discussed theories involving the immune system, central nervous system, olfactory and respiratory systems as well as altered metabolic capacity, behavioral conditioning and emotional regulation. However, in spite of more than 50 years of research, there is still a great deal of uncertainties regarding the event(s) and underlying mechanism( s) behind symptom elicitation. As a result, patients are often misdiagnosed or offered health care solutions with limited or no effect, and they experience being met with mistrust and doubt by health care professionals, the social care system and by friends and relatives. Evidence-based treatment options are currently unavailable, however, a person-centered care model based on a multidisciplinary treatment approach and individualized care plans have shown promising results. With this in mind, further research studies and health care solutions should be based on a multifactorial and interdisciplinary approach. PMID:26088215

  1. Hypoxia-induced glucose-6-phosphate dehydrogenase overexpression and -activation in pulmonary artery smooth muscle cells: implication in pulmonary hypertension

    PubMed Central

    Chettimada, Sukrutha; Gupte, Rakhee; Rawat, Dhwajbahadur; Gebb, Sarah A.; McMurtry, Ivan F.

    2014-01-01

    Severe pulmonary hypertension is a debilitating disease with an alarmingly low 5-yr life expectancy. Hypoxia, one of the causes of pulmonary hypertension, elicits constriction and remodeling of the pulmonary arteries. We now know that pulmonary arterial remodeling is a consequence of hyperplasia and hypertrophy of pulmonary artery smooth muscle (PASM), endothelial, myofibroblast, and stem cells. However, our knowledge about the mechanisms that cause these cells to proliferate and hypertrophy in response to hypoxic stimuli is still incomplete, and, hence, the treatment for severe pulmonary arterial hypertension is inadequate. Here we demonstrate that the activity and expression of glucose-6-phosphate dehydrogenase (G6PD), the rate-limiting enzyme of the pentose phosphate pathway, are increased in hypoxic PASM cells and in lungs of chronic hypoxic rats. G6PD overexpression and -activation is stimulated by H2O2. Increased G6PD activity contributes to PASM cell proliferation by increasing Sp1 and hypoxia-inducible factor 1α (HIF-1α), which directs the cells to synthesize less contractile (myocardin and SM22α) and more proliferative (cyclin A and phospho-histone H3) proteins. G6PD inhibition with dehydroepiandrosterone increased myocardin expression in remodeled pulmonary arteries of moderate and severe pulmonary hypertensive rats. These observations suggest that altered glucose metabolism and G6PD overactivation play a key role in switching the PASM cells from the contractile to synthetic phenotype by increasing Sp1 and HIF-1α, which suppresses myocardin, a key cofactor that maintains smooth muscle cell in contractile state, and increasing hypoxia-induced PASM cell growth, and hence contribute to pulmonary arterial remodeling and pathogenesis of pulmonary hypertension. PMID:25480333

  2. What Causes Lactose Intolerance?

    MedlinePlus

    ... Information Clinical Trials Resources and Publications What causes lactose intolerance? Skip sharing on social media links Share ... lactase in the body is the cause of lactose intolerance. The names for the three types of ...

  3. Oral Supplementation with Non-Absorbable Antibiotics or Curcumin Attenuates Western Diet-Induced Atherosclerosis and Glucose Intolerance in LDLR−/− Mice – Role of Intestinal Permeability and Macrophage Activation

    PubMed Central

    Ghosh, Siddhartha S.; Bie, Jinghua; Wang, Jing; Ghosh, Shobha

    2014-01-01

    Association between circulating lipopolysaccharide (LPS) and metabolic diseases (such as Type 2 Diabetes and atherosclerosis) has shifted the focus from Western diet-induced changes in gut microbiota per se to release of gut bacteria-derived products into circulation as the possible mechanism for the chronic inflammatory state underlying the development of these diseases. Under physiological conditions, an intact intestinal barrier prevents this release of LPS underscoring the importance of examining and modulating the direct effects of Western diet on intestinal barrier function. In the present study we evaluated two strategies, namely selective gut decontamination and supplementation with oral curcumin, to modulate Western-diet (WD) induced changes in intestinal barrier function and subsequent development of glucose intolerance and atherosclerosis. LDLR−/− mice were fed WD for 16 weeks and either received non-absorbable antibiotics (Neomycin and polymyxin) in drinking water for selective gut decontamination or gavaged daily with curcumin. WD significantly increased intestinal permeability as assessed by in vivo translocation of FITC-dextran and plasma LPS levels. Selective gut decontamination and supplementation with curcumin significantly attenuated the WD-induced increase in plasma LPS levels (3.32 vs 1.90 or 1.51 EU/ml, respectively) and improved intestinal barrier function at multiple levels (restoring intestinal alkaline phosphatase activity and expression of tight junction proteins, ZO-1 and Claudin-1). Consequently, both these interventions significantly reduced WD-induced glucose intolerance and atherosclerosis in LDLR−/− mice. Activation of macrophages by low levels of LPS (50 ng/ml) and its exacerbation by fatty acids is likely the mechanism by which release of trace amounts of LPS into circulation due to disruption of intestinal barrier function induces the development of these diseases. These studies not only establish the important role of intestinal barrier function, but also identify oral supplementation with curcumin as a potential therapeutic strategy to improve intestinal barrier function and prevent the development of metabolic diseases. PMID:25251395

  4. In utero growth restriction and catch-up adipogenesis after developmental di (2-ethylhexyl) phthalate exposure cause glucose intolerance in adult male rats following a high-fat dietary challenge.

    PubMed

    Strakovsky, Rita S; Lezmi, Stphane; Shkoda, Ielyzaveta; Flaws, Jodi A; Helferich, William G; Pan, Yuan-Xiang

    2015-11-01

    Phthalates impact adipocyte morphology in vitro, but the sex-specific adipogenic signature immediately after perinatal di(2-ethylhexyl) phthalate (DEHP) exposure and adulthood physiology following a high-fat (HF) dietary challenge are unknown. In the current study, pregnant and lactating dams received DEHP (300 mg/kg body weight) or oil. At weaning [postnatal day (PND) 21], adipose tissue was sampled for real-time polymerase chain reaction. The remaining offspring consumed a control or HF diet. DEHP decreased % fat in males at birth from 13.9%0.2 to 11.8%0.6 (meanS.E.M.), representing a 15.1% decrease in fat by DEHP, and these males caught up in adiposity to controls by PND21. Adult DEHP-exposed males had a 27.5% increase in fat (12.5%0.9% in controls vs. 15.9%1.5% in the DEHP group); adipocyte perimeter was increased as well, with fewer small/medium-sized adipocytes, and decreased cell number compared to oil controls. HF diet intake in DEHP-exposed males further increased male energy intake and body weight and led to glucose intolerance. In PND21 males, DEHP increased the expression of adipogenic markers (Pparg1, Cebpa, Adipoq, Ppard, Fabp4, Fasn, Igf1), decreased Lep, and decreased markers of mesenchymal stem cell commitment to the adipogenic lineage (Bmp2, Bmp4, Stat1, Stat5a) compared to oil controls. These data suggest that DEHP may decrease the adipocyte pool at birth, which initially increases adaptive adipocyte maturation and lipid accumulation, but leads to adipose tissue dysfunction in adulthood, decreasing the capacity to adapt to a HF diet, and leading to systemic glucose intolerance. PMID:26188368

  5. Growth Hormone Receptor Antagonist Transgenic Mice Are Protected From Hyperinsulinemia and Glucose Intolerance Despite Obesity When Placed on a HF Diet

    PubMed Central

    Yang, Tianxu; Householder, Lara A.; Lubbers, Ellen R.; List, Edward O.; Troike, Katie; Vesel, Clare; Duran-Ortiz, Silvana; Kopchick, John J.

    2015-01-01

    Reduced GH levels have been associated with improved glucose metabolism and increased longevity despite obesity in multiple mouse lines. However, one mouse line, the GH receptor antagonist (GHA) transgenic mouse, defies this trend because it has reduced GH action and increased adiposity, but glucose metabolism and life span are similar to controls. Slight differences in glucose metabolism and adiposity profiles can become exaggerated on a high-fat (HF) diet. Thus, in this study, male and female GHA and wild-type (WT) mice in a C57BL/6 background were placed on HF and low-fat (LF) diets for 11 weeks, starting at 10 weeks of age, to assess how GHA mice respond to additional metabolic stress of HF feeding. On a HF diet, all mice showed significant weight gain, although GHA gained weight more dramatically than WT mice, with males gaining more than females. Most of this weight gain was due to an increase in fat mass with WT mice increasing primarily in the white adipose tissue perigonadal depots, whereas GHA mice gained in both the sc and perigonadal white adipose tissue regions. Notably, GHA mice were somewhat protected from detrimental glucose metabolism changes on a HF diet because they had only modest increases in serum glucose levels, remained glucose tolerant, and did not develop hyperinsulinemia. Sex differences were observed in many measures with males reacting more dramatically to both a reduction in GH action and HF diet. In conclusion, our findings show that GHA mice, which are already obese, are susceptible to further adipose tissue expansion with HF feeding while remaining resilient to alterations in glucose homeostasis. PMID:25406017

  6. Salivary melatonin levels and sleep-wake rhythms in pregnant women with hypertensive and glucose metabolic disorders: A prospective analysis.

    PubMed

    Shimada, Mieko; Seki, Hiroyuki; Samejima, Michikazu; Hayase, Mako; Shirai, Fumie

    2016-03-10

    In preeclampsia and gestational diabetes, the sympathetic nerves are activated, leading to disrupted sleep. Melatonin, which transmits information to regulate the sleep-wake rhythm and other such biorhythms, has been implicated in insulin resistance, antioxidant behaviors, and metabolic syndrome. In addition, its reduced secretion increases the risk of hypertension and diabetes. The aim of this study was to elucidate the features of melatonin secretion, sleep quality, and sleep-wake rhythms in pregnant women with complications. Fifty-eight pregnant women with pregnancy complications (hypertensive or glucose metabolic disorders) and 40 healthy pregnant women completed questionnaires, including sleep logs and the Pittsburgh Sleep Quality Index (PSQI), during the second to third trimesters. Their salivary melatonin levels were also measured. Pregnant women with complications had significantly lower morning (p < 0.001), daytime (p < 0.01), evening (p < 0.001), night (p < 0.01), daily mean (p < 0.001), peak (p < 0.001), and bottom (p < 0.01) melatonin values than healthy pregnant women. Pregnant women with complications also had significantly smaller melatonin amplitudes than healthy pregnant women (p < 0.001). Among pregnant women with complications, the duration (p < 0.05) and frequency (p < 0.01) of wake after sleep-onset were significantly greater in the poor sleep group than in the favorable sleep group which was divided by PSQI cutoff value. Pregnant women with hypertensive or glucose metabolic disorder complications had smaller circadian variation in salivary melatonin secretion, and their values were lower throughout the day than healthy pregnant women. PMID:26853813

  7. Synergistic effect of uricase blockade plus physiological amounts of fructose-glucose on glomerular hypertension and oxidative stress in rats

    PubMed Central

    Tapia, Edilia; Cristóbal, Magdalena; García-Arroyo, Fernando E.; Soto, Virgilia; Monroy-Sánchez, Fabiola; Pacheco, Ursino; Lanaspa, Miguel A.; Roncal-Jiménez, Carlos A.; Cruz-Robles, David; Ishimoto, Takuji; Madero, Magdalena; Johnson, Richard J.

    2013-01-01

    Fructose in sweetened beverages (SB) increases the risk for metabolic and cardiorenal disorders, and these effects are in part mediated by a secondary increment in uric acid (UA). Rodents have an active uricase, thus requiring large doses of fructose to increase plasma UA and to induce metabolic syndrome and renal hemodynamic changes. We therefore hypothesized that the effects of fructose in rats might be enhanced in the setting of uricase inhibition. Four groups of male Sprague-Dawley rats (n = 7/group) were studied during 8 wk: water + vehicle (V), water + oxonic acid (OA; 750 mg/k BW), sweetened beverage (SB; 11% fructose-glucose combination) + V, and SB + OA. Systemic blood pressure, plasma UA, triglycerides (TG), glucose and insulin, glomerular hemodynamics, renal structural damage, renal cortex and liver UA, TG, markers of oxidative stress, mitDNA, fructokinase, and fatty liver synthase protein expressions were evaluated at the end of the experiment. Chronic hyperuricemia and SB induced features of the metabolic syndrome, including hypertension, hyperuricemia, hyperglycemia, and systemic and hepatic TG accumulation. OA alone also induced glomerular hypertension, and SB alone induced insulin resistance. SB + OA induced a combined phenotype including metabolic and renal alterations induced by SB or OA alone and in addition also acted synergistically on systemic and glomerular pressure, plasma glucose, hepatic TG, and oxidative stress. These findings explain why high concentrations of fructose are required to induce greater metabolic changes and renal disease in rats whereas humans, who lack uricase, appear to be much more sensitive to the effects of fructose. PMID:23303409

  8. The effect of oral glucose loads on tissue metabolism during angiotensin II receptor and beta-receptor blockade in obese hypertensive subjects.

    PubMed

    Boschmann, M; Kreuzberg, U; Engeli, S; Adams, F; Franke, G; Klaua, S; Scholze, J; Weidinger, G; Luft, F C; Sharma, A M; Jordan, J

    2006-05-01

    AT1 receptor blockers and ACE inhibitors decrease the risk for new onset diabetes mellitus. The phenomenon could be related to a direct angiotensin II effect on tissue metabolism. To address the issue, we recruited eighteen obese hypertensive patients. Patients were randomized to double-blind treatment with either valsartan (n = 8) or atenolol (n = 10) for thirteen weeks. They underwent an oral glucose tolerance test before and during active treatment, while metabolism was monitored through subcutaneous and intramuscular microdialysis and indirect calorimetry. After glucose ingestion, venous glucose and insulin concentrations increased rapidly while systemic free fatty acid concentrations were suppressed. Dialysate glucose and lactate concentrations increased briskly in adipose tissue and in skeletal muscle. Dialysate glycerol decreased profoundly in both tissues. Respiratory quotient increased markedly after glucose ingestion. These responses were identical at baseline and during active treatment either drug. We conclude that AT1 receptor blockade in obese hypertensive patients has no effect on interstitial glucose supply, lipolysis, and substrate oxidation. One possible explanation is that angiotensin II levels in obese hypertensives are not sufficient to elicit the metabolic changes that have been observed after direct angiotensin II application. The exact mechanism by which inhibition of the renin-angiotensin-aldosterone system decreases the diabetes risk remains unresolved and requires further study. PMID:16718629

  9. Management of lactose intolerance.

    PubMed

    Tamm, A

    1994-01-01

    The management of lactose intolerance comprises two parts: (1) the basic principles of treatment in persons intolerant to a dietary dose of lactose, and (2) main manoeuvres to reduce the lactose content in food, and/or consumption of special products of milk or exogenous lactase enzyme. The tactics of management depend on the type of hypolactasia, the severity of intolerance, and on the age of the patient. Special attention is paid to the development of lactose intolerance in some patients via iatrogenic mechanisms such as certain drugs, gastric surgery and ionizing radiation. PMID:8042018

  10. Dietary fructose intolerance, fructan intolerance and FODMAPs

    PubMed Central

    Fedewa, Amy; Rao, Satish S. C.

    2014-01-01

    Dietary intolerances to fructose, fructans and FODMAPs (Fermentable Oligosaccharides, Disaccharides, Monosaccharides And Polyols) are common, yet poorly recognized and managed. Over the last decade, they have come to the forefront because of new knowledge on the mechanisms and treatment of these conditions. Patients with these problems often present with unexplained bloating, belching, distension, gas, abdominal pain or diarrhea. Here, we have examined the most up-to-date research on these food-related intolerances, discussed controversies, and have provided some guidelines for the dietary management of these conditions. Breath testing for carbohydrate intolerance appears to be standardized and essential for the diagnosis and management of these conditions, especially in the Western population. While current research shows that the FODMAP diet may be effective in treating irritable bowel syndrome, additional research is needed to identify more foods items that are high in FODMAPs, and to assess the long-term efficacy and safety of dietary interventions. PMID:24357350

  11. Effect of angiotensin receptor blockade on insulin sensitivity and endothelial function in abdominally obese hypertensive patients with impaired fasting glucose

    PubMed Central

    PERLSTEIN, Todd S.; HENRY, Robert R.; MATHER, Kieren J.; RICKELS, Michael R.; ABATE, Nicola I.; GRUNDY, Scott M.; MAI, Yabing; ALBU, Jeanine B.; MARKS, Jennifer B.; POOL, James L.; CREAGER, Mark A.

    2015-01-01

    AngII (angiotensin II) may contribute to cardiovascular risk in obesity via adverse effects on insulin sensitivity and endothelial function. In the present study, we examined the effects of ARB (angiotensin receptor blocker) therapy (losartan, 100 mg/day) on insulin sensitivity and endothelial function in 53 subjects with stage I hypertension, abdominal obesity and impaired fasting glucose. The study design was a randomized double-blinded parallel design placebo-controlled multicentre trial of 8 weeks duration. We used the hyperinsulinaemic–euglycaemic clamp technique to measure insulin sensitivity (expressed as the ‘M/I’ value) and RH-PAT (reactive hyperaemia-peripheral arterial tonometry) to measure endothelial function. Additional measures included HOMA (homoeostasis model assessment)-B, an index of pancreatic β-cell function, and markers of inflammation [e.g. CRP (C-reactive protein)] and oxidative stress (e.g. F2-isoprostanes). ARB therapy did not alter insulin sensitivity [5.2 (2.7) pre-treatment and 4.6 (1.6) post-treatment] compared with placebo therapy [6.1 (2.9) pre-treatment and 5.3 (2.7) post-treatment; P value not significant], but did improve the HOMA-B compared with placebo therapy (P = 0.05). ARB therapy also did not change endothelial function [RH-PAT, 2.15 (0.7) pre-treatment and 2.11 (0.7) post-treatment] compared with placebo therapy [RH-PAT, 1.81 (0.5) pre-treatment and 1.76 (0.7) post-treatment; P value not significant]. Markers of inflammation and oxidative stress were not significantly changed by ARB therapy. In conclusion, ARB therapy did not alter peripheral insulin sensitivity or endothelial function in this cohort of patients with essential hypertension, abdominal obesity and impaired fasting glucose, but did improve pancreatic β-cell function. PMID:21861845

  12. Prevalence of Diabetes and Impaired Fasting Glucose in Hypertensive Adults in Rural China: Far from Leveling-Off

    PubMed Central

    Yu, Shasha; Sun, Zhaoqing; Zheng, Liqiang; Guo, Xiaofan; Yang, Hongmei; Sun, Yingxian

    2015-01-01

    In recent years data from many investigations has shown a leveling–off trend in diabetes incidence. In order to explain the diabetes epidemic in rural China during the past ten years, we conducted a survey from July 2012 to August 2013. Data from comprehensive questionnaires, physical examinations, and blood tests were obtained from 5919 residents with hypertension, aged ≥ 35 years. Diabetes and impaired fasting glucose (IFG) were defined according to the American Diabetes Association (ADA) criteria. The overall prevalence of diabetes and IFG were 15.3% (13.6% in men, 16.8% in women) and 40.7% (44.1% in men, 34.7% in women) in the hypertensive rural Chinese population. The prevalence of previously diagnosed diabetes was 6.5% (4.6% in men, 8.4% in women). The prevalence of undiagnosed diabetes was 8.7% (9.0% in men, 8.5% in women). Multivariate logistic regression revealed that increasing age, drinking, overweight or obesity, systolic blood pressure, low HDL-C, high total cholesterol and triglycerides increased the risk of diabetes (p < 0.05). Diabetes is thus still prevalent in rural areas of China and is manifesting an accelerating trend. It remains an important public health problem in China, especially in rural areas and routine assessment for the early detection and treatment of diabetes should be emphasized. PMID:26610531

  13. Genetics Home Reference: lactose intolerance

    MedlinePlus

    ... Me Understand Genetics Home Health Conditions lactose intolerance lactose intolerance Enable Javascript to view the expand/collapse boxes. Print All Open All Close All Description Lactose intolerance is an impaired ability to digest lactose, ...

  14. Glucan-rich polysaccharides from Pleurotus sajor-caju (Fr.) Singer prevents glucose intolerance, insulin resistance and inflammation in C57BL/6J mice fed a high-fat diet

    PubMed Central

    2012-01-01

    Background Pleurotus sajor-caju (P. sajor-caju) has been extremely useful in the prevention of diabetes mellitus due to its low fat and high soluble fiber content for thousands of years. Insulin resistance is a key component in the development of diabetes mellitus which is caused by inflammation. In this study, we aimed to investigate the in vivo efficacy of glucan-rich polysaccharide of P. sajor-caju (GE) against diabetes mellitus and inflammation in C57BL/6J mice fed a high-fat diet. Methods Diabetes was induced in C57BL/6J mice by feeding a high-fat diet. The mice were randomly assigned to 7 groups (n=6 per group). The control groups in this study were ND (for normal diet) and HFD (for high-fat diet). The treated groups were ND240 (for normal diet) (240 mg/kg b.w) and HFD60, HFD120 and HFD240 (for high-fat), where the mice were administrated with three dosages of GE (60, 120, 240 mg GE/kg b.w respectively). Metformin (2 mg/kg b.w) served as positive control. The glucose tolerance test, glucose and insulin levels were measured at the end of 16 weeks. Expressions of genes for inflammatory markers, GLUT-4 and adiponectin in the adipose tissue of the mice were assessed. One-way ANOVA and Duncan’s multiple range tests (DMRT) were used to determine the significant differences between groups. Results GE treated groups improved the glucose tolerance, attenuated hyperglycemia and hyperinsulinemia in the mice by up-regulating the adiponectin and GLUT-4 gene expressions. The mice in GE treated groups did not develop insulin resistance. GE also down-regulated the expression of inflammatory markers (IL-6, TNF-α, SAA2, CRP and MCP-1) via attenuation of nuclear transcription factors (NF-κB). Conclusion Glucan-rich polysaccharide of P. sajor-caju can serve as a potential agent for prevention of glucose intolerance, insulin resistance and inflammation. PMID:23259700

  15. Blockade of Sphingosine 1-Phosphate Receptor 2 Signaling Attenuates High-Fat Diet-Induced Adipocyte Hypertrophy and Systemic Glucose Intolerance in Mice.

    PubMed

    Kitada, Yoshihiko; Kajita, Kazuo; Taguchi, Koichiro; Mori, Ichiro; Yamauchi, Masahiro; Ikeda, Takahide; Kawashima, Mikako; Asano, Motochika; Kajita, Toshiko; Ishizuka, Tatsuo; Banno, Yoshiko; Kojima, Itaru; Chun, Jerold; Kamata, Shotaro; Ishii, Isao; Morita, Hiroyuki

    2016-05-01

    Sphingosine 1-phosphate (S1P) is known to regulate insulin resistance in hepatocytes, skeletal muscle cells, and pancreatic β-cells. Among its 5 cognate receptors (S1pr1-S1pr5), S1P seems to counteract insulin signaling and confer insulin resistance via S1pr2 in these cells. S1P may also regulate insulin resistance in adipocytes, but the S1pr subtype(s) involved remains unknown. Here, we investigated systemic glucose/insulin tolerance and phenotypes of epididymal adipocytes in high-fat diet (HFD)-fed wild-type and S1pr2-deficient (S1pr2(-/-)) mice. Adult S1pr2(-/-) mice displayed smaller body/epididymal fat tissue weights, but the differences became negligible after 4 weeks with HFD. However, HFD-fed S1pr2(-/-) mice displayed better scores in glucose/insulin tolerance tests and had smaller epididymal adipocytes that expressed higher levels of proliferating cell nuclear antigen than wild-type mice. Next, proliferation/differentiation of 3T3-L1 and 3T3-F442A preadipocytes were examined in the presence of various S1pr antagonists: JTE-013 (S1pr2 antagonist), VPC-23019 (S1pr1/S1pr3 antagonist), and CYM-50358 (S1pr4 antagonist). S1P or JTE-013 treatment of 3T3-L1 preadipocytes potently activated their proliferation and Erk phosphorylation, whereas VPC-23019 inhibited both of these processes, and CYM-50358 had no effects. In contrast, S1P or JTE-013 treatment inhibited adipogenic differentiation of 3T3-F442A preadipocytes, whereas VPC-23019 activated it. The small interfering RNA knockdown of S1pr2 promoted proliferation and inhibited differentiation of 3T3-F442A preadipocytes, whereas that of S1pr1 acted oppositely. Moreover, oral JTE-013 administration improved glucose tolerance/insulin sensitivity in ob/ob mice. Taken together, S1pr2 blockade induced proliferation but suppressed differentiation of (pre)adipocytes both in vivo and in vitro, highlighting a novel therapeutic approach for obesity/type 2 diabetes. PMID:26943364

  16. Rationale, design, and method of the Diabetes & Women's Health study--a study of long-term health implications of glucose intolerance in pregnancy and their determinants.

    PubMed

    Zhang, Cuilin; Hu, Frank B; Olsen, Sjurdur F; Vaag, Allan; Gore-Langton, Robert; Chavarro, Jorge E; Bao, Wei; Yeung, Edwina; Bowers, Katherine; Grunnet, Louise G; Sherman, Seth; Kiely, Michele; Strøm, Marin; Hansen, Susanne; Liu, Aiyi; Mills, James; Fan, Ruzong

    2014-11-01

    Women who develop gestational diabetes mellitus or impaired glucose tolerance during pregnancy are at substantially increased risk for type 2 diabetes and comorbidities after pregnancy. Little is known about the role of genetic factors and their interactions with environmental factors in determining the transition from gestational diabetes mellitus to overt type 2 diabetes mellitus. These critical data gaps served as the impetus for this Diabetes & Women's Health study with the overall goal of investigating genetic factors and their interactions with risk factors amenable to clinical or public health interventions in relation to the transition of gestational diabetes mellitus to type 2 diabetes mellitus. To achieve the goal efficiently, we are applying a hybrid design enrolling and collecting data longitudinally from approximately 4000 women with a medical history of gestational diabetes mellitus in two existing prospective cohorts, the Nurses' Health Study II and the Danish National Birth Cohort. Women who had a medical history of gestational diabetes mellitus in one or more of their pregnancies are eligible for the present study. After enrollment, we follow study participants for an additional 2 years to collect updated information on major clinical and environmental factors that may predict type 2 diabetes mellitus risk as well as with biospecimens to measure genetic and biochemical markers implicated in glucose metabolism. Newly collected data will be appended to the relevant existing data for the creation of a new database inclusive of genetic, epigenetic and environmental data. Findings from the study are critical for the development of targeted and more effective strategies to prevent type 2 diabetes mellitus and its complications in this high-risk population. PMID:24828694

  17. CYP1B1 deficiency ameliorates obesity and glucose intolerance induced by high fat diet in adult C57BL/6J mice

    PubMed Central

    Liu, Xiaocong; Huang, Tingting; Li, Lu; Tang, Yumeng; Tian, Yatao; Wang, Suqing; Fan, Cuifang

    2015-01-01

    Cytochrome P450 1B1 (CYP1B1) expression increases in multi-potential mesenchymal stromal cells C3H10T1/2 during adipogenesis, which parallel with PPAR?, a critical transcriptional factor in adipogenic process. To assess the role of CYP1B1 in fatty acid metabolism, adult C57BL/6J wild-type and CYP1B1 deficiency mice were fed with high fat diets (HFD) for 6 weeks. CYP1B1 deficiency attenuated HFD-induced obesity when compared with their wild type counterparts, and improve glucose tolerance. The reduction in body weight gain and white adipose tissue in CYP1B1 deficient mice exhibited coordinate decreases in fatty acid synthesis (PPAR?, CD36, FAS, SCD-1) and increases in fatty acid oxidation (UCP-2, CPT-1a) when compared with wild type ones. Lower hepatocyte TG contents were consistent with hepatic Oil-Red-O staining in the CYP1B1 deficiency mice. AMPK, a nutrient sensors for energy homeostasis, was activated in both fat pad and liver by CYP1B1 deficiency. However, in vitro system, knock down CYP1B1 in C3H10T1/2 cells does not abolish adipogenesis induced by adipogenic agents IDM (Insulin, Dexamethasone, Methylisobutylxanthine). Our in vivo and in vitro findings of CYP1B1 deficiency in fat metabolism suggest a complex regulation network between CYP1B1 and energy homeostasis. PMID:26064443

  18. Relation of blood volume and blood pressure in orthostatic intolerance

    NASA Technical Reports Server (NTRS)

    Jacob, G.; Biaggioni, I.; Mosqueda-Garcia, R.; Robertson, R. M.; Robertson, D.

    1998-01-01

    A complex but crucial relationship exists between blood volume and blood pressure in human subjects; it has been recognized that in essential hypertension, renovascular hypertension, and pheochromocytoma, the relationship between plasma volume and diastolic blood pressure is an inverse one. This phenomenon has not been studied in individuals with low normal and reduced blood pressures. Orthostatic intolerance is a commonly encountered abnormality in blood pressure regulation often associated with tachycardia in the standing position. Most of these patients have varying degrees of reduced blood volume. We tested the hypothesis that the relationship previously found between plasma volume and diastolic blood pressure in pressor states would also hold in orthostatic intolerance. We studied 16 patients with a history of symptomatic orthostatic intolerance associated with an elevation in plasma norepinephrine in the upright posture and hypovolemia in 9 patients and normovolemia in 7 patients. Our studies demonstrate an inverse relationship between plasma volume and diastolic blood pressure in patients with orthostatic intolerance. This finding also holds for the change in diastolic blood pressure in response to upright posture. In this relationship, patients with orthostatic intolerance with high plasma norepinephrine resemble those with essential hypertension, renovascular hypertension, and pheochromocytoma. We conclude that in a variety of conditions at both ends of the blood pressure spectrum, the seemingly paradoxical association of hypovolemia and diastolic blood pressure is preserved.

  19. Determining the amounts of urea and glucose in urine of patients with renal complications from diabetes mellitus and hypertension by near-infrared Raman spectroscopy

    NASA Astrophysics Data System (ADS)

    Bispo, Jeyse A. M.; Silveira, Landulfo; Vieira, Elzo E. d. S.; Fernandes, Adriana B.

    2013-02-01

    Diabetes mellitus and hypertension diseases are frequently found in the same patient, which if untreated predispose to atherosclerotic and kidney diseases. The objective of this study was to identify potential biomarkers in the urine of diabetic and hypertensive patients through dispersive near-infrared Raman spectroscopy. Urine samples were collected from patients with diabetes and hypertension but no complications (LG), high degree of complications (HG), and control ones: one fraction was submitted to biochemical tests and another one was stored frozen (-20°C) until spectral analysis. Samples were warmed up and placed in an aluminum sample holder for Raman spectra collection using a dispersive spectrometer (830 nm wavelength, 300 mW laser power and 20 s exposure time). Spectra were then submitted to Principal Components Analysis. The PCA loading vectors 1 and 3 revealed spectral features of urea/creatinine and glucose, respectively; the PCA scores showed that patients with diabetes/hypertension (LG and HG) had higher amount of glucose in the urine compared to the normal group (p < 0.05), which can bring serious consequences to patients. Also, the PCA scores showed that the amount of urea decreased in the groups with diabetes/hypertension (p < 0.05), which generates the same concern as it is a marker that has a strong importance in the metabolic changes induced by such diseases. These results, applied to the analysis of urine of patients with diabetes/hypertension, can lead to early diagnostic information of complications and a possible disease prognosis in the patients where no complications from diabetes and hypertension were found.

  20. Lactose Intolerance (For Parents)

    MedlinePlus

    ... ice cream sundae or a cool glass of milk at lunch means an afternoon of cramps, gas, ... by problems digesting lactose, the main sugar in milk and milk products. Lactose intolerance happens when the ...

  1. Ethanol extract of the Prunus mume fruits stimulates glucose uptake by regulating PPAR-γ in C2C12 myotubes and ameliorates glucose intolerance and fat accumulation in mice fed a high-fat diet.

    PubMed

    Shin, Eun Ju; Hur, Haeng Jeon; Sung, Mi Jeong; Park, Jae Ho; Yang, Hye Jeong; Kim, Myung Sunny; Kwon, Dae Young; Hwang, Jin-Taek

    2013-12-15

    In this study, we performed in vitro and in vivo studies to examine whether a 70% ethanol extract of Prunus mume fruits (EMS) exhibits anti-diabetic effects. Treatment with EMS increased glucose uptake in C2C12 myotubes, and also increased PPAR-γ activity or PPAR-γ mRNA expression. To confirm these in vitro results, we next conducted an animal experiment. A high-fat diet significantly increased the body weight, fat accumulation, and glucose levels in mice. Under the same conditions, 5% EMS attenuated the high-fat diet-induced increase in body weight and fat accumulation and improved the impaired fasting glucose level and glucose tolerance. High performance liquid chromatography analysis demonstrated that EMS contained chlorogenic acid, caffeic acid, rutin, luteolin-7-glucoside, naringin, apigenin-7-glucoside, and hesperidin. Taken together, these findings suggest that EMS exerts an anti-diabetic effect both in vitro and in vivo, which is mediated, at least in part, by the activation of PPAR-γ. PMID:23993593

  2. Loop Diuretics in the Treatment of Hypertension.

    PubMed

    Malha, Line; Mann, Samuel J

    2016-04-01

    Loop diuretics are not recommended in current hypertension guidelines largely due to the lack of outcome data. Nevertheless, they have been shown to lower blood pressure and to offer potential advantages over thiazide-type diuretics. Torsemide offers advantages of longer duration of action and once daily dosing (vs. furosemide and bumetanide) and more reliable bioavailability (vs. furosemide). Studies show that the previously employed high doses of thiazide-type diuretics lower BP more than furosemide. Loop diuretics appear to have a preferable side effect profile (less hyponatremia, hypokalemia, and possibly less glucose intolerance). Studies comparing efficacy and side effect profiles of loop diuretics with the lower, currently widely prescribed, thiazide doses are needed. Research is needed to fill gaps in knowledge and common misconceptions about loop diuretic use in hypertension and to determine their rightful place in the antihypertensive arsenal. PMID:26951244

  3. Intolerance of Uncertainty

    PubMed Central

    Beier, Meghan L.

    2015-01-01

    Multiple sclerosis (MS) is a chronic and progressive neurologic condition that, by its nature, carries uncertainty as a hallmark characteristic. Although all patients face uncertainty, there is variability in how individuals cope with its presence. In other populations, the concept of “intolerance of uncertainty” has been conceptualized to explain this variability such that individuals who have difficulty tolerating the possibility of future occurrences may engage in thoughts or behaviors by which they attempt to exert control over that possibility or lessen the uncertainty but may, as a result, experience worse outcomes, particularly in terms of psychological well-being. This topical review introduces MS-focused researchers, clinicians, and patients to intolerance of uncertainty, integrates the concept with what is already understood about coping with MS, and suggests future steps for conceptual, assessment, and treatment-focused research that may benefit from integrating intolerance of uncertainty as a central feature. PMID:26300700

  4. Achievement of recommended glucose and blood pressure targets in patients with type 2 diabetes and hypertension in clinical practice – study rationale and protocol of DIALOGUE

    PubMed Central

    2012-01-01

    Background Patients with type 2 diabetes have 2–4 times greater risk for cardiovascular morbidity and mortality than those without, and this is even further aggravated if they also suffer from hypertension. Unfortunately, less than one third of hypertensive diabetic patients meet blood pressure targets, and more than half fail to achieve target HbA1c values. Thus, appropriate blood pressure and glucose control are of utmost importance. Since treatment sometimes fails in clinical practice while clinical trials generally suggest good efficacy, data from daily clinical practice, especially with regard to the use of newly developed anti-diabetic and anti-hypertensive compounds in unselected patient populations, are essential. The DIALOGUE registry aims to close this important gap by evaluating different treatment approaches in hypertensive type 2 diabetic patients with respect to their effectiveness and tolerability and their impact on outcomes. In addition, DIALOGUE is the first registry to determine treatment success based on the new individualized treatment targets recommended by the ADA and the EASD. Methods DIALOGUE is a prospective observational German multicentre registry and will enrol 10,000 patients with both diabetes and hypertension in up to 700 sites. After a baseline visit, further documentations are scheduled at 6, 12 and 24 months. There are two co-primary objectives referring to the most recent guidelines for the treatment of diabetes and hypertension: 1) individual HbA1c goal achievement with respect to anti-diabetic pharmacotherapy and 2) individual blood pressure goal achievement with different antihypertensive treatments. Among the secondary objectives the rate of major cardio-vascular and cerebro-vascular events (MACCE) and the rate of hospitalizations are the most important. Conclusion The registry will be able to gain insights into the reasons for the obvious gap between the demonstrated efficacy and safety of anti-diabetic and anti-hypertensive drugs in clinical trials and their real world balance of effectiveness and safety. PMID:23216660

  5. Orthostatic intolerance: a disorder of young women

    NASA Technical Reports Server (NTRS)

    Ali, Y. S.; Daamen, N.; Jacob, G.; Jordan, J.; Shannon, J. R.; Biaggioni, I.; Robertson, D.

    2000-01-01

    Orthostatic intolerance (OI) is a cause of significant disability in otherwise healthy women seen by gynecologists. Orthostatic tachycardia is often the most obvious hemodynamic abnormality found in OI patients, but symptoms may include dizziness, visual changes, discomfort in the head or neck, poor concentration, fatigue, palpitations, tremulousness, anxiety, and, in some cases, fainting (syncope). It is the most common disorder of blood pressure regulation after essential hypertension, and patients with OI are traditionally women of childbearing age. Estimates suggest that at least 500,000 Americans suffer from some form of OI, and such patients comprise the largest group referred to centers specialized in autonomic disorders. This article reviews recent advances made in the understanding of this condition, potential pathophysiological mechanisms contributing to orthostatic intolerance, and therapeutic alternatives currently available for the management of these patients.

  6. How Is Lactose Intolerance Diagnosed?

    MedlinePlus

    ... Information Clinical Trials Resources and Publications How is lactose intolerance diagnosed? Skip sharing on social media links ... people think that they or their children are lactose intolerant without being tested or diagnosed. 1 As ...

  7. Lactose intolerance in infants.

    PubMed

    Taylor, Cathy

    Cathy Taylor describes the pathophysiology and aetiology of lactose intolerance and how to diagnose and treat it. Management of the infant by the primary health care team is discussed, with emphasis on advice and nutritional support that can be recommended to parents. PMID:16700234

  8. Pulmonary 2-deoxy-2-[18F]-fluoro-d-glucose uptake is low in treated patients with idiopathic pulmonary arterial hypertension

    PubMed Central

    Ruiter, Gerrina; Wong, Yeun Ying

    2013-01-01

    Abstract Glucose metabolism measurement using 2-deoxy-2-[18F]-fluoro-d-glucose (18FDG) positron emission tomography (PET) could provide in vivo information about pulmonary vascular remodeling. The purpose of this study was to assess whether pulmonary 18FDG uptake in idiopathic pulmonary arterial hypertension (IPAH) patients changes and, if so, to determine whether the change is related to disease severity and survival. Sixteen IPAH patients who were treated with IPAH-specific therapy and 7 patients who had a myocardial infarction (MI) without pulmonary hypertension were included. IPAH disease severity was determined using the 6-minute walk test and right heart catheterization 2 days before 18FDG PET. Regions of interest were defined for left and right lungs, and standardized uptake values (SUVs), normalized to body weight, injected dose, and plasma glucose level, were derived. Mean SUVs for IPAH left and right lungs were and (), respectively. In MI patients, SUVs were and () in left and right lungs, respectively. Total lung SUVs were similar in IPAH and MI patients ( vs. ; ). There was no correlation between SUV and IPAH disease severity parameters. In addition, lung SUV did not predict survival in IPAH patients (hazard ratio, 1.155; 95% confidence interval, 0.16–8.26; ). In conclusion, pulmonary 18FDG uptake in treated IPAH patients is low and is not associated with disease severity and survival, thereby limiting its clinical use in patient care. PMID:24618549

  9. Continuous Glucose Monitoring in Patients with Abnormal Glucose Tolerance during Pregnancy: A Case Series.

    PubMed

    Tonoike, Mie; Kishimoto, Miyako; Yamamoto, Mayumi; Yano, Tetsu; Noda, Mitsuhiko

    2016-01-01

    Abnormal glucose tolerance during pregnancy is associated with perinatal complications. We used continuous glucose monitoring (CGM) in pregnant women with glucose intolerance to achieve better glycemic control and to evaluate the maternal glucose fluctuations. We also used CGM in women without glucose intolerance (the control cases). Furthermore, the standard deviation (SD) and mean amplitude of glycemic excursions (MAGE) were calculated for each case. For the control cases, the glucose levels were tightly controlled within a very narrow range; however, the SD and MAGE values in pregnant women with glucose intolerance were relativity high, suggesting postprandial hyperglycemia. Our results demonstrate that pregnant women with glucose intolerance exhibited greater glucose fluctuations compared with the control cases. The use of CGM may help to improve our understanding of glycemic patterns and may have beneficial effects on perinatal glycemic control, such as the detection of postprandial hyperglycemia in pregnant women. PMID:26949348

  10. Continuous Glucose Monitoring in Patients with Abnormal Glucose Tolerance during Pregnancy: A Case Series

    PubMed Central

    Tonoike, Mie; Kishimoto, Miyako; Yamamoto, Mayumi; Yano, Tetsu; Noda, Mitsuhiko

    2016-01-01

    Abnormal glucose tolerance during pregnancy is associated with perinatal complications. We used continuous glucose monitoring (CGM) in pregnant women with glucose intolerance to achieve better glycemic control and to evaluate the maternal glucose fluctuations. We also used CGM in women without glucose intolerance (the control cases). Furthermore, the standard deviation (SD) and mean amplitude of glycemic excursions (MAGE) were calculated for each case. For the control cases, the glucose levels were tightly controlled within a very narrow range; however, the SD and MAGE values in pregnant women with glucose intolerance were relativity high, suggesting postprandial hyperglycemia. Our results demonstrate that pregnant women with glucose intolerance exhibited greater glucose fluctuations compared with the control cases. The use of CGM may help to improve our understanding of glycemic patterns and may have beneficial effects on perinatal glycemic control, such as the detection of postprandial hyperglycemia in pregnant women. PMID:26949348

  11. [Metabolic intolerance to exercise].

    PubMed

    Arenas, J; Martín, M A

    2003-01-01

    Exercise intolerance (EI) is a frequent cause of medical attention, although it is sometimes difficult to come to a final diagnosis. However, there is a group of patients in whom EI is due to a metabolic dysfunction. McArdle's disease (type V glucogenosis) is due to myophosphorylase (MPL) deficiency. The ischemic exercise test shows a flat lactate curve. The most frequent mutations in the PYGM gene (MPL gene) in Spanish patients with MPL deficiency are R49X and W797R. Carnitine palmitoyltransferase (CPT) II deficiency is invariably associated to repetitive episodes of myoglobinuria triggered by exercise, cold, fever or fasting. The diagnosis depends on the demonstration of CPT II deficiency in muscle. The most frequent mutation in the CPT2 gene is the S113L. Patients with muscle adenylate deaminase deficiency usually show either a mild myopathy or no symptom. The diagnosis is based on the absence of enzyme activity in muscle and the lack of rise of ammonia in the forearm ischemic exercise test. The mutation Q12X in the AMPD1 gene is strongly associated with the disease. Exercise intolerance is a common complaint in patients with mitochondrial respiratory chain (MRC) deficiencies, although it is often overshadowed by other symptoms and signs. Only recently we have come to appreciate that exercise intolerance can be the sole presentation of defects in the mtDNA, particularly in complex I, complex III, complex IV, or in some tRNAs. In addition, myoglobinuria can be observed in patients under statin treatment, particularly if associated with fibrates, due to an alteration in the assembly of the complex IV of the MRC. PMID:12838448

  12. Eplerenone restores 24-h blood pressure circadian rhythm and reduces advanced glycation end-products in rhesus macaques with spontaneous hypertensive metabolic syndrome

    PubMed Central

    Zhang, Yan; Zheng, Wen; Liu, Yuli; Wang, Jue; Peng, Ying; Shang, Haibao; Hou, Ning; Hu, Xiaomin; Ding, Yi; Xiao, Yao; Wang, Can; Zeng, Fanxin; Mao, Jiaming; Zhang, Jun; Ma, Dongwei; Sun, Xueting; Li, Chuanyun; Xiao, Rui-Ping; Zhang, Xiuqin

    2016-01-01

    Hypertension is often associated with metabolic syndrome (MetS), and serves as a risk factor of MetS and its complications. Blood pressure circadian rhythm in hypertensive patients has been suggested to contribute to cardiovascular consequences and organ damage of hypertension. But circadian changes of BP and their response to drugs have not been clearly investigated in non-human primates (NHPs) of MetS with hypertension. Here, we identified 16 elderly, hypertensive MetS rhesus monkeys from our in-house cohort. With implanted telemetry, we investigate BP changes and its circadian rhythm, together with the effect of antihypertensive drugs on BP and its diurnal fluctuation. MetS hypertensive monkeys displayed higher BP, obesity, glucose intolerance, and dyslipidemia. We also confirmed impaired 24-h BP circadian rhythm in MetS hypertensive monkeys. Importantly, Eplerenone, a mineralocorticoid receptor blocker, exerts multiple beneficial effects in MetS hypertensive monkeys, including BP reduction, 24-h BP circadian rhythm restoration, and decreased plasma concentration of inflammation factors and advanced glycation end-products. In summary, we identified a naturally-developed hypertensive MetS NHP model, which is of great value in the studies on pathogenesis of MetS-associated hypertension and development of novel therapeutic strategies. We also provided multiple novel mechanistic insights of the beneficial effect of Eplerenone on MetS with hypertension. PMID:27032687

  13. Increased forearm blood flow during glucose clamp is related neither to insulin sensitivity nor to hyperinsulinemia in borderline hypertensive young men.

    PubMed

    Høieggen, A; Fossum, E; Moan, A; Rostrup, M; Eide, I K; Kjeldsen, S E

    1999-01-01

    It is controversial whether raised insulin within the physiological concentration range increases forearm blood flow (FBF). The aim of the present study was therefore to examine the effect of the isoglycemic hyperinsulinemic glucose clamp procedure on FBF and to relate the increase to the glucose disposal rate (GDR), i.e. insulin sensitivity. Borderline hypertensive young men were examined with the clamp technique or received saline infusion, and FBF was measured using plethysmography. It is of particular interest to study this group of subjects because their GDR correlates to a number of metabolic and hemodynamic variables, and these subjects hyperreact to stressful stimuli. There was no correlation between deltaFBF during clamp and GDR (r = -0.002, p = 0.99, n = 28). While serum insulin increased from 107 +/- 5 to 628 +/- 31 pmol/l in the hyperinsulinemic group and remained unchanged (135 +/- 11 vs 116 +/- 11 pmol/l) in the saline group, FBF increased from 3.5 +/- 0.3 to a maximum of 5.1 +/- 0.4 ml/min/100 ml (p < 0.001, n = 28) and from 2.8 +/- 0.5 to a maximum of 4.5 +/- 0.5 ml/min/100 ml (p = 0.01, n = 8), respectively. The increase in FBF (delta%) was similar in the two groups (p = 0.9). Thus, we could not demonstrate any relationship between insulin sensitivity and increments in FBF during hyperinsulinemic glucose clamp in borderline hypertensive young men. The moderate increases in FBF during insulin infusion with serum concentrations within the physiological range seem to be time-dependent and not caused by hyperinsulinemia. PMID:10697303

  14. Comparison of single and combination diuretics on glucose tolerance (PATHWAY-3): protocol for a randomised double-blind trial in patients with essential hypertension

    PubMed Central

    Brown, Morris J; Williams, Bryan; MacDonald, Thomas M; Caulfield, Mark; Cruickshank, J Kennedy; McInnes, Gordon; Sever, Peter; Webb, David J; Salsbury, Jackie; Morant, Steve; Ford, Ian

    2015-01-01

    Introduction Thiazide diuretics are associated with increased risk of diabetes mellitus. This risk may arise from K+-depletion. We hypothesised that a K+-sparing diuretic will improve glucose tolerance, and that combination of low-dose thiazide with K+-sparing diuretic will improve both blood pressure reduction and glucose tolerance, compared to a high-dose thiazide. Methods and analysis This is a parallel-group, randomised, double-blind, multicentre trial, comparing hydrochlorothiazide 25–50 mg, amiloride 10–20 mg and combination of both diuretics at half these doses. A single-blind placebo run-in of 1 month is followed by 24 weeks of blinded active treatment. There is forced dose-doubling after 3 months. The Primary end point is the blood glucose 2 h after oral ingestion of a 75 g glucose drink (OGTT), following overnight fasting. The primary outcome is the difference between 2 h glucose at weeks 0, 12 and 24. Secondary outcomes include the changes in home systolic blood pressure (BP) and glycated haemoglobin and prediction of response by baseline plasma renin. Eligibility criteria are: age 18–79, systolic BP on permitted background treatment ≥140 mm Hg and home BP ≥130 mm Hg and one component of the metabolic syndrome additional to hypertension. Principal exclusions are diabetes, estimated-glomerular filtration rate <45 mL/min, abnormal plasma K+, clinic SBP >200 mm Hg or DBP >120 mm Hg (box 2). The sample size calculation indicates that 486 patients will give 80% power at α=0.01 to detect a difference in means of 1 mmol/L (SD=2.2) between 2 h glucose on hydrochlorothiazide and comparators. Ethics and dissemination PATHWAY-3 was approved by Cambridge South Ethics Committee, number 09/H035/19. The trial results will be published in a peer-reviewed scientific journal. Trial registration numbers Eudract number 2009-010068-41 and clinical trials registration number: NCT02351973. PMID:26253567

  15. Hereditary fructose intolerance.

    PubMed Central

    Ali, M; Rellos, P; Cox, T M

    1998-01-01

    Hereditary fructose intolerance (HFI, OMIM 22960), caused by catalytic deficiency of aldolase B (fructose-1,6-bisphosphate aldolase, EC 4.1.2.13), is a recessively inherited condition in which affected homozygotes develop hypoglycaemic and severe abdominal symptoms after taking foods containing fructose and cognate sugars. Continued ingestion of noxious sugars leads to hepatic and renal injury and growth retardation; parenteral administration of fructose or sorbitol may be fatal. Direct detection of a few mutations in the human aldolase B gene on chromosome 9q facilitates the genetic diagnosis of HFI in many symptomatic patients. The severity of the disease phenotype appears to be independent of the nature of the aldolase B gene mutations so far identified. It appears that hitherto there has been little, if any, selection against mutant aldolase B alleles in the population: in the UK, approximately 1.3% of neonates harbour one copy of the prevalent A149P disease allele. The ascendance of sugar as a major dietary nutrient, especially in western societies, may account for the increasing recognition of HFI as a nutritional disease and has shown the prevalence of mutant aldolase B genes in the general population. The severity of clinical expression correlates well with the immediate nutritional environment, age, culture, and eating habits of affected subjects. Here we review the biochemical, genetic, and molecular basis of human aldolase B deficiency in HFI, a disorder which responds to dietary therapy and in which the principal manifestations of disease are thus preventable. Images PMID:9610797

  16. Lactose intolerance: a nursing perspective.

    PubMed

    Marchiondo, Kathleen

    2009-01-01

    Deficiency of intestinal lactase, the enzyme required for lactose digestion, can result in symptoms of gastrointestinal malabsorption, or lactose intolerance. The knowledge needed for accurate nursing assessment, diagnostic procedural care, teaching, and referral of affected patients is reviewed. PMID:19331294

  17. Sugar intolerance complicating acute gastroenteritis.

    PubMed Central

    Trounce, J Q; Walker-Smith, J A

    1985-01-01

    Sugar intolerance occurred in 31 of 200 children admitted to hospital with acute gastroenteritis. In 28 this was transient and settled rapidly, but in the remaining three it indicated a more serious and persistent problem. The most important predisposing factor was viral infection, in particular with rotavirus. The current regimen for the management of sugar intolerance complicating acute gastroenteritis at this hospital is outlined. PMID:4062353

  18. Lactose intolerance and health.

    PubMed Central

    Wilt, Timothy J; Shaukat, Aasma; Shamliyan, Tatyana; Taylor, Brent C; MacDonald, Roderick; Tacklind, James; Rutks, Indulis; Schwarzenberg, Sarah Jane; Kane, Robert L; Levitt, Michael

    2010-01-01

    OBJECTIVES We systematically reviewed evidence to determine lactose intolerance (LI) prevalence, bone health after dairy-exclusion diets, tolerable dose of lactose in subjects with diagnosed LI, and management. DATA SOURCES We searched multiple electronic databases for original studies published in English from 1967-November 2009. REVIEW METHODS We extracted patient and study characteristics using author's definitions of LI and lactose malabsorption. We compared outcomes in relation to diagnostic tests, including lactose challenge, intestinal biopsies of lactase enzyme levels, genetic tests, and symptoms. Fractures, bone mineral content (BMC) and bone mineral density (BMD) were compared in categories of lactose intake. Reported symptoms, lactose dose and formulation, timing of lactose ingestion, and co-ingested food were analyzed in association with tolerability of lactose. Symptoms were compared after administration of probiotics, enzyme replacements, lactose-reduced milk and increasing lactose load. RESULTS Prevalence was reported in 54 primarily nonpopulation based studies (15 from the United States). Studies did not directly assess LI and subjects were highly selected. LI magnitude was very low in children and remained low into adulthood among individuals of Northern European descent. For African American, Hispanic, Asian, and American Indian populations LI rates may be 50 percent higher in late childhood and adulthood. Small doses of lactose were well tolerated in most populations. Low level evidence from 55 observational studies of 223,336 subjects indicated that low milk consumers may have increased fracture risk. Strength and significance varied depended on exposure definitions. Low level evidence from randomized controlled trials (RCTs) of children (seven RCTs) and adult women (two RCTs) with low lactose intake indicated that dairy interventions may improve BMC in select populations. Most individuals with LI can tolerate up to 12 grams of lactose, though symptoms became more prominent at doses above 12 grams and appreciable after 24 grams of lactose; 50 grams induced symptoms in the vast majority. A daily divided dose of 24 grams was generally tolerated. We found insufficient evidence that use of lactose reduced solution/milk, with lactose content of 0-2 grams, compared to a lactose dose of greater than 12 grams, reduced symptoms of lactose intolerance. Evidence was insufficient for probiotics (eight RCTs), colonic adaptation (two RCTs) or varying lactose doses (three RCTs) or other agents (one RCT). Inclusion criteria, interventions, and outcomes were variable. Yogurt and probiotic types studied were variable and results either showed no difference in symptom scores or small differences in symptoms that may be of low clinical relevance. CONCLUSIONS There are race and age differences in LI prevalence. Evidence is insufficient to accurately assess U.S. population prevalence of LI. Children with low lactose intake may have beneficial bone outcomes from dairy interventions. There was evidence that most individuals with presumed LI or LM can tolerate 12-15 grams of lactose (approximately 1 cup of milk). There was insufficient evidence regarding effectiveness for all evaluated agents. Additional research is needed to determine LI treatment effectiveness. PMID:20629478

  19. Chronic Inhibition of 11β-Hydroxysteroid Dehydrogenase Type 1 Activity Decreases Hypertension, Insulin Resistance, and Hypertriglyceridemia in Metabolic Syndrome

    PubMed Central

    Schnackenberg, Christine G.; Costell, Melissa H.; Krosky, Daniel J.; Cui, Jianqi; Wu, Charlene W.; Hong, Victor S.; Harpel, Mark R.; Willette, Robert N.; Yue, Tian-Li

    2013-01-01

    Metabolic syndrome is a constellation of risk factors including hypertension, dyslipidemia, insulin resistance, and obesity that promote the development of cardiovascular disease. Metabolic syndrome has been associated with changes in the secretion or metabolism of glucocorticoids, which have important functions in adipose, liver, kidney, and vasculature. Tissue concentrations of the active glucocorticoid cortisol are controlled by the conversion of cortisone to cortisol by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). Because of the various cardiovascular and metabolic activities of glucocorticoids, we tested the hypothesis that 11β-HSD1 is a common mechanism in the hypertension, dyslipidemia, and insulin resistance in metabolic syndrome. In obese and lean SHR/NDmcr-cp (SHR-cp), cardiovascular, metabolic, and renal functions were measured before and during four weeks of administration of vehicle or compound 11 (10 mg/kg/d), a selective inhibitor of 11β-HSD1. Compound 11 significantly decreased 11β-HSD1 activity in adipose tissue and liver of SHR-cp. In obese SHR-cp, compound 11 significantly decreased mean arterial pressure, glucose intolerance, insulin resistance, hypertriglyceridemia, and plasma renin activity with no effect on heart rate, body weight gain, or microalbuminuria. These results suggest that 11β-HSD1 activity in liver and adipose tissue is a common mediator of hypertension, hypertriglyceridemia, glucose intolerance, and insulin resistance in metabolic syndrome. PMID:23586038

  20. Overcoming the barrier of lactose intolerance to reduce health disparities.

    PubMed Central

    Jarvis, Judith K.; Miller, Gregory D.

    2002-01-01

    Federal health goals for the public have focused on reducing health disparities that exist between whites and various racial and ethnic groups. Many of the chronic diseases for which African Americans are at greater risk- hypertension, stroke, colon cancer, and obesity-may be exacerbated by a low intake of calcium and/or other dairy-related nutrients. For example, a low intake of dairy food nutrients, such as calcium, potassium, and magnesium, may contribute to the high risk of hypertension seen in African Americans. The Dietary Approaches to Stop Hypertension (DASH) study demonstrated that a low-fat diet rich in fruits and vegetables (8 to 10 servings) and low-fat dairy foods (3 servings) significantly reduced blood pressure-and was twice as effective in African-American participants. Calcium and dairy food consumption is particularly low among African-American, Hispanic, and Asian populations. Average intakes are near the threshold of 600 to 700 mg/day, below which bone loss and hypertension can result. Although lactose intolerance may be partly to blame for the low calcium intakes due to reduced dairy food consumption by minority populations, culturally determined food preferences and dietary practices learned early in life also play a role. The high incidence figures for primary lactose maldigestion among minority groups grossly overestimates the number who will experience intolerance symptoms after drinking a glass of milk with a meal. Randomized, double-blind, controlled clinical trials have demonstrated that by using a few simple dietary strategies, those who maldigest lactose (have low levels of the lactase enzyme) can easily tolerate a dairy-rich diet that meets calcium intake recommendations. Physicians and other health professionals can help their minority patients and the general public understand how to improve calcium nutrition by overcoming the surmountable barrier of lactose intolerance. At the same time they will be helping to reduce the incidence of calcium-related chronic diseases for which minority populations are at high risk. PMID:11853047

  1. Food allergy and food intolerance.

    PubMed

    Anderson, J A

    1985-01-01

    Adverse reactions to foods and food additives include those that involve an immune mechanism of reaction (food allergies) and those that are non-immunological in nature (food intolerance). The signs and symptoms of food allergy usually involve the skin and gastrointestinal tract and are "classic" allergic symptoms. Food intolerance occurs more frequently at all ages. A number of food additives have been implicated in food intolerance, as none involve an immune mechanism of reaction. The role of food additives in food intolerance is not well established in many cases, has been discounted in others and continues to be the subject of current research. Although the history of events concerning an adverse reaction is important and gives clues to the specific type of problem (food allergy versus food intolerance), confirmation of the reaction is sometimes desirable. This can be done either by use of a standard elimination diet of non-allergic foods, followed by open challenge or by DBFC for more difficult situations. Food allergy skin testing and other in vitro immunologic tests may be helpful as supplemental information in those cases where food allergy is suspected. The best treatment for an adverse reaction to food is avoidance. Unproven and unapproved diagnostic (e.g., leukocytotoxic test) and therapeutic techniques (e.g., sublinqual neutralization) are not recommended in food allergy management. PMID:3857245

  2. FOXO1-mediated Upregulation of Pyruvate Dehydrogenase Kinase-4 (PDK4) Decreases Glucose Oxidation and Impairs Right Ventricular Function in Pulmonary Hypertension: Therapeutic Benefits of Dichloroacetate

    PubMed Central

    Piao, Lin; Sidhu, Vaninder K.; Fang, Yong-Hu; Ryan, John J.; Parikh, Kishan S.; Hong, Zhigang; Toth, Peter T.; Morrow, Erik; Kutty, Shelby; Lopaschuk, Gary D.; Archer, Stephen L.

    2012-01-01

    Introduction Pyruvate dehydrogenase kinase (PDK) is activated in right ventricular hypertrophy (RVH), causing an increase in glycolysis relative to glucose oxidation that impairs RV function. The stimulus for PDK upregulation, its isoform specificity and the long-term effects of PDK inhibition are unknown. We hypothesize that FOXO1-mediated PDK4 upregulation causes bioenergetic impairment and RV dysfunction, which can be reversed by dichloroacetate. Methods Adult male Fawn-Hooded rats (FHR) with pulmonary arterial hypertension (PAH) and RVH (age 612 months) were compared to age-matched controls. Cardiac glucose and fatty acid oxidation (GO, FAO) were measured at baseline and after acute dichloroacetate (1mM40-minutes) in isolated working-hearts and in freshly dispersed RV myocytes. The effects of chronic dichloroacetate (0.75 g/L drinking water for 6 months) on cardiac output (CO) and exercise capacity were measured in vivo. Expression of PDK4 and its regulatory transcription factor, FOXO1, were also measured in FHR and RV specimens from PAH patients (n=10). Results Microarray analysis of 168 genes related to glucose or FA metabolism showed >4-fold upregulation of PDK4, aldolase B and acyl-coenzyme A oxidase. FOXO1 was increased, in FHR RV whereas HIF-1? was unaltered. PDK4 expression was increased and the inactivated form of FOXO1 decreased in human PAH RV (P<0.01). PDH inhibition in RVH increased proton production and reduced GOs contribution to the TCA cycle. Acutely, dichloroacetate reduced RV proton production and increased GOs contribution (relative to FAO) to the TCA cycle and ATP production in FHR (P<0.01). Chronically dichloroacetate decreased PDK4 and FOXO1, thereby activating PDH and increasing GO in FHR. These metabolic changes increased CO (8414 vs. 6914 ml/min, P<0.05) and treadmill-walking distance (23920 vs. 17122 m, P<0.05). Conclusion Chronic dichloroacetate inhibits FOXO1-induced PDK4 upregulation and restores GO, leading to improved bioenergetics and RV function in RVH. PMID:23247844

  3. FOXO1-mediated upregulation of pyruvate dehydrogenase kinase-4 (PDK4) decreases glucose oxidation and impairs right ventricular function in pulmonary hypertension: therapeutic benefits of dichloroacetate.

    PubMed

    Piao, Lin; Sidhu, Vaninder K; Fang, Yong-Hu; Ryan, John J; Parikh, Kishan S; Hong, Zhigang; Toth, Peter T; Morrow, Erik; Kutty, Shelby; Lopaschuk, Gary D; Archer, Stephen L

    2013-03-01

    Pyruvate dehydrogenase kinase (PDK) is activated in right ventricular hypertrophy (RVH), causing an increase in glycolysis relative to glucose oxidation that impairs right ventricular function. The stimulus for PDK upregulation, its isoform specificity, and the long-term effects of PDK inhibition are unknown. We hypothesize that FOXO1-mediated PDK4 upregulation causes bioenergetic impairment and RV dysfunction, which can be reversed by dichloroacetate. Adult male Fawn-Hooded rats (FHR) with pulmonary arterial hypertension (PAH) and right ventricular hypertrophy (RVH; age 6-12 months) were compared to age-matched controls. Glucose oxidation (GO) and fatty acid oxidation (FAO) were measured at baseline and after acute dichloroacetate (1 mM × 40 min) in isolated working hearts and in freshly dispersed RV myocytes. The effects of chronic dichloroacetate (0.75 g/L drinking water for 6 months) on cardiac output (CO) and exercise capacity were measured in vivo. Expression of PDK4 and its regulatory transcription factor, FOXO1, were also measured in FHR and RV specimens from PAH patients (n = 10). Microarray analysis of 168 genes related to glucose or FA metabolism showed >4-fold upregulation of PDK4, aldolase B, and acyl-coenzyme A oxidase. FOXO1 was increased in FHR RV, whereas HIF-1 α was unaltered. PDK4 expression was increased, and the inactivated form of FOXO1 decreased in human PAH RV (P < 0.01). Pyruvate dehydrogenase (PDH) inhibition in RVH increased proton production and reduced GO's contribution to the tricarboxylic acid (TCA) cycle. Acutely, dichloroacetate reduced RV proton production and increased GO's contribution (relative to FAO) to the TCA cycle and ATP production in FHR (P < 0.01). Chronically dichloroacetate decreased PDK4 and FOXO1, thereby activating PDH and increasing GO in FHR. These metabolic changes increased CO (84 ± 14 vs. 69 ± 14 ml/min, P < 0.05) and treadmill-walking distance (239 ± 20 vs. 171 ± 22 m, P < 0.05). Chronic dichloroacetate inhibits FOXO1-induced PDK4 upregulation and restores GO, leading to improved bioenergetics and RV function in RVH. PMID:23247844

  4. Dietary ribonucleic acid suppresses inflammation of adipose tissue and improves glucose intolerance that is mediated by immune cells in C57BL/6 mice fed a high-fat diet.

    PubMed

    Sakai, Tohru; Taki, Tomoyo; Nakamoto, Akiko; Tazaki, Shiho; Arakawa, Mai; Nakamoto, Mariko; Tsutsumi, Rie; Shuto, Emi

    2015-01-01

    Recent evidence suggests that immune cells play an important role in differentiation of inflammatory macrophages in adipose tissue, which contributes to systemic chronic inflammation. Dietary ribonucleic acid (RNA) has been shown to modulate immune function. We hypothesized that RNA affects immune cell function in adipose tissue and then improves inflammatory response in adipose tissue. C57/BL6 mice and recombination activating gene-1 (RAG-1) knockout mice on a C57BL/6 mice background were fed a high-fat diet containing 1% RNA for 12 wk. An oral glucose tolerance test was performed. Supplementation of dietary RNA in C57BL/6 mice fed a high-fat diet resulted in a smaller area under the curve (AUC) after oral glucose administration than that for control mice. The mRNA expression levels of inflammation-related cytokines in adipose tissue and serum interleukin-6 levels were reduced by dietary RNA supplementation. Interestingly, reduction of the AUC value by RNA supplementation was abolished in T and B cell-deficient RAG-1 knockout mice. These results indicate that RNA improves inflammation in adipose tissue and reduces the AUC value following oral glucose administration in a T and B cell-dependent manner. PMID:25994141

  5. Incretins and selective renal sodium-glucose co-transporter 2 inhibitors in hypertension and coronary heart disease

    PubMed Central

    Sanchez, Ramiro A; Sanabria, Hugo; de los Santos, Cecilia; Ramirez, Agustin J

    2015-01-01

    Hyperglycemia is associated with an increased risk of cardiovascular disease, and the consequences of intensive therapy may depend on the mechanism of the anti-diabetic agent(s) used to achieve a tight control. In animal models, stable analogues of glucagon-like peptide-1 (GLP-1) were able to reduce body weight and blood pressure and also had favorable effects on ischemia following coronary reperfusion. In a similar way, dipeptidyl peptidase IV (DPP-IV) showed to have favorable effects in animal models of ischemia/reperfusion. This could be due to the fact that DPP-IV inhibitors were able to prevent the breakdown of GLP-1 and glucose-dependent insulinotropic polypeptide, but they also decreased the degradation of several vasoactive peptides. Preclinical data for GLP-1, its derivatives and inhibitors of the DPP-IV enzyme degradation suggests that these agents may be able to, besides controlling glycaemia, induce cardio-protective and vasodilator effects. Notwithstanding the many favorable cardiovascular effects of GLP-1/incretins reported in different studies, many questions remain unanswered due the limited number of studies in human beings that aim to examine the effects of GLP-1 on cardiovascular endpoints. For this reason, long-term trials searching for positive cardiovascular effects are now in process, such as the CAROLINA and CARMELINA trials, which are supported by small pilot studies performed in humans (and many more animal studies) with incretin-based therapies. On the other hand, selective renal sodium-glucose co-transporter 2 inhibitors were also evaluated in the prevention of cardiovascular outcomes in type 2 diabetes. However, it is quite early to draw conclusions, since data on cardiovascular outcomes and cardiovascular death are limited and long-term studies are still ongoing. In this review, we will analyze the mechanisms underlying the cardiovascular effects of incretins and, at the same time, we will present a critical position about the real value of these compounds in the cardiovascular system and its protection. PMID:26380062

  6. Lactose intolerance: diagnosis and management.

    PubMed

    Patel, Y T; Minocha, A

    2000-01-01

    Lactose intolerance affects hundreds of millions of people worldwide. Although the presentation is frequently atypical, it should be part of the differential diagnosis when evaluating nonspecific gastrointestinal symptoms. We review the terminology, types of lactase deficiencies, diagnostic procedures, and management. PMID:11126094

  7. Lactobacillus sakei OK67 ameliorates high-fat diet-induced blood glucose intolerance and obesity in mice by inhibiting gut microbiota lipopolysaccharide production and inducing colon tight junction protein expression.

    PubMed

    Lim, Su-Min; Jeong, Jin-Ju; Woo, Kyung Hee; Han, Myung Joo; Kim, Dong-Hyun

    2016-04-01

    A high-fat diet (HFD) induces obesity and the associated increases in blood glucose and inflammation through changes in gut microbiota, endotoxemia, and increased gut permeability. To counteract this, researchers have suggested that the use of probiotics that suppress production of proinflammatory lipopolysaccharide (LPS). Here, we tested whether Lactobacillus sakei OK67, which inhibits gut microbiota LPS production selected from among the lactic acid bacteria isolated from kimchi, exerted antihypoglycemic or anti-inflammatory effects in HFD-fed mice. Mice were randomly divided into 2 groups and fed an HFD or a low-fat diet for 4 weeks. These groups were further subdivided; 1 subgroup was treated with L sakei OK67 and fed the experimental diet for 4.5 weeks, whereas the other subgroup was fed the experimental diet alone. L sakei OK67 treatment lowered HFD-elevated LPS levels in blood and colonic fluid and significantly decreased HFD-elevated fasting blood glucose levels and the area under the curve in an oral glucose tolerance test. L sakei OK67 treatment inhibited HFD-induced body and epididymal fat weight gains, suppressed HFD-induced tumor necrosis factor-α and interleukin-1β expression and nuclear factor-κB activation in the colon, and significantly increased HFD-suppressed interleukin-10 and tight junction protein expression in the colon. Oral administration of L sakei OK67 significantly downregulated HFD-induced expression of peroxisome proliferator-activated receptor γ, fatty acid synthase, and tumor necrosis factor-α in adipose tissue. In addition, L sakei OK67 treatment strongly inhibited nuclear factor-κB activation in LPS-stimulated peritoneal macrophages. We report that L sakei OK67 ameliorates HFD-induced hyperglycemia and obesity by reducing inflammation and increasing the expression of colon tight junction proteins in mice. PMID:27001279

  8. The effect of glutathione S-transferase M1 and T1 polymorphisms on blood pressure, blood glucose, and lipid profiles following the supplementation of kale (Brassica oleracea acephala) juice in South Korean subclinical hypertensive patients

    PubMed Central

    Han, Jeong-Hwa; Lee, Hye-Jin; Kim, Tae-Seok

    2015-01-01

    BACKGROUND/OBJECTIVES Glutathione S-transferase (GST) forms a multigene family of phase II detoxification enzymes which are involved in the detoxification of reactive oxygen species. This study examines whether daily supplementation of kale juice can modulate blood pressure (BP), levels of lipid profiles, and blood glucose, and whether this modulation could be affected by the GSTM1 and GSTT1 polymorphisms. SUBJECTS/METHODS 84 subclinical hypertensive patients showing systolic BP over 130 mmHg or diastolic BP over 85 mmHg received 300 ml/day of kale juice for 6 weeks, and blood samples were collected on 0-week and 6-week in order to evaluate plasma lipid profiles (total cholesterol, triglyceride, HDL-cholesterol, and LDL-cholesterol) and blood glucose. RESULTS Systolic and diastolic blood pressure was significantly decreased in all patients regardless of their GSTM1 or GSTT1 polymorphisms after kale juice supplementation. Blood glucose level was decreased only in the GSTM1-present genotype, and plasma lipid profiles showed no difference in both the GSTM1-null and GSTM1-present genotypes. In the case of GSTT1, on the other hand, plasma HDL-C was increased and LDL-C was decreased only in the GSTT1-present type, while blood glucose was decreased only in the GSTT1-null genotype. CONCLUSIONS These findings suggest that the supplementation of kale juice affected blood pressure, lipid profiles, and blood glucose in subclinical hypertensive patients depending on their GST genetic polymorphisms, and the improvement of lipid profiles was mainly greater in the GSTT1-present genotype and the decrease of blood glucose was greater in the GSTM1-present or GSTT1-null genotypes. PMID:25671068

  9. [Intolerance reactions of the skin].

    PubMed

    Sacher, R

    1987-07-01

    Intolerance reactions of the skin in which a decision is made on allergic and toxic genesis have increased in significance in recent years. Whereas antibodies blocking bacterial or viral antigens are formed in the normergic immune reaction, nonblocking antibodies to animal, plant or chemical heterologous substances are formed in an allergy as a result of an misdirected immunological reaction. Sensitization is favored by a) large structure and protein affinity of the allergen, b) irritation of the affected part of the skin by fungi or chemicals and c) genetic predisposition. Depending on the clinical manifestation, a distinction is made between inhaled allergens (bronchial asthma, hay fever), allergens ingested with the food (food allergy) and allergens which have come in contact with the skin (immediate reaction - urticaria, late reaction - contact eczema). Intolerance reactions of the skin which can be ruled out as the cause of an allergy are designated as toxic. Acute toxic reactions are based on violent or intensively physical (heat, cold, radiation), chemical (acids, alkalis, heavy metal salts, oils, solvents) or microbial damage to the skin (infection by fungi, bacteria, viruses). The degenerative eczema as the most important form of chronic toxic intolerance reaction arises by weak but continuously acting longterm mechanical or chemical exposures. PMID:2957865

  10. Lactose intolerance and health disparities among African Americans and Hispanic Americans: an updated consensus statement.

    PubMed

    Bailey, Rahn K; Fileti, Cecelia Pozo; Keith, Jeanette; Tropez-Sims, Susanne; Price, Winston; Allison-Ottey, Sharon Denise

    2013-01-01

    Dairy foods contribute nine essential nutrients to the diet including calcium, potassium and vitamin D; nutrients identified by the 2010 Dietary Guidelines for Americans as being "of public health concern" within the U.S. population. Milk and milk product intake is associated with better diet quality and has been associated with a reduced risk of chronic diseases or conditions including hypertension, cardiovascular disease, metabolic syndrome, Type 2 Diabetes and osteoporosis. Some research also indicates dairy food intake may be linked to reduced body fat, when accompanied by energy-restriction. On average, both African Americans and Hispanic Americans consume less than the recommended levels of dairy foods, and perceived or actual lactose intolerance can be a primary reason for limiting or avoiding dairy intake. True lactose intolerance prevalence is not known because healthcare providers do not routinely measure for it, and no standardized assessment method exists. Avoiding dairy may lead to shortfalls of essential nutrients and increased susceptibility to chronic disease. This updated Consensus Statement aims to provide the most current information about lactose intolerance and health, with specific relevance to the African American and Hispanic American communities. Topics covered include diagnostic considerations, actual and recommended dairy food intake and levels of consumption of key dairy nutrients among African Americans and Hispanic Americans; prevalence of self-reported lactose intolerance among various racial/ethnic groups; the association between dairy food intake, lactose intolerance and chronic disease; and research-based management recommendations for those with lactose intolerance. PMID:24079212

  11. Hypocapnia and cerebral hypoperfusion in orthostatic intolerance

    NASA Technical Reports Server (NTRS)

    Novak, V.; Spies, J. M.; Novak, P.; McPhee, B. R.; Rummans, T. A.; Low, P. A.

    1998-01-01

    BACKGROUND AND PURPOSE: Orthostatic and other stresses trigger tachycardia associated with symptoms of tremulousness, shortness of breath, dizziness, blurred vision, and, often, syncope. It has been suggested that paradoxical cerebral vasoconstriction during head-up tilt might be present in patients with orthostatic intolerance. We chose to study middle cerebral artery (MCA) blood flow velocity (BFV) and cerebral vasoregulation during tilt in patients with orthostatic intolerance (OI). METHODS: Beat-to-beat BFV from the MCA, heart rate, CO2, blood pressure (BP), and respiration were measured in 30 patients with OI (25 women and 5 men; age range, 21 to 44 years; mean age, 31.3+/-1.2 years) and 17 control subjects (13 women and 4 men; age range, 20 to 41 years; mean age, 30+/-1.6 years); ages were not statistically different. These indices were monitored during supine rest and head-up tilt (HUT). We compared spontaneous breathing and hyperventilation and evaluated the effect of CO2 rebreathing in these 2 positions. RESULTS: The OI group had higher supine heart rates (P<0.001) and cardiac outputs (P<0.01) than the control group. In response to HUT, OI patients underwent a greater heart rate increment (P<0.001) and greater reductions in pulse pressure (P<0.01) and CO2 (P<0.001), but total systemic resistance failed to show an increment. Among the cerebrovascular indices, all BFVs (systolic, diastolic, and mean) decreased significantly more, and cerebrovascular resistance (CVR) was increased in OI patients (P<0.01) compared with control subjects. In both groups, hyperventilation induced mild tachycardia (P<0.001), a significant reduction of BFV, and a significant increase of CVR associated with a fall in CO2. Hyperventilation during HUT reproduced hypocapnia, BFV reduction, and tachycardia and worsened symptoms of OI; these symptoms and indices were improved within 2 minutes of CO2 rebreathing. The relationships between CO2 and BFV and heart rate were well described by linear regressions, and the slope was not different between control subjects and patients with OI. CONCLUSIONS: Cerebral vasoconstriction occurs in OI during orthostasis, which is primarily due to hyperventilation, causing significant hypocapnia. Hypocapnia and symptoms of orthostatic hypertension are reversible by CO2 rebreathing.

  12. [Food allergies and intolerances in children].

    PubMed

    Olives, J P; Breton, A

    1998-02-15

    Allergies and food intolerance together comprise the manifestations of "adverse food reaction". The best known and most common are: allergy to cow's milk proteins (prevalence 0.5% to 7.5%), intolerance to lactose (prevalence after weaning 5 to 100%) and gluten intolerance (prevalence 0.5%). Treatment of these conditions is based on management of the diet by exclusion (or reduction) of the responsible food or antigen. PMID:9781094

  13. Histamine, histamine intoxication and intolerance.

    PubMed

    Kovacova-Hanuskova, E; Buday, T; Gavliakova, S; Plevkova, J

    2015-01-01

    Excessive accumulation of histamine in the body leads to miscellaneous symptoms mediated by its bond to corresponding receptors (H1-H4). Increased concentration of histamine in blood can occur in healthy individuals after ingestion of foods with high contents of histamine, leading to histamine intoxication. In individuals with histamine intolerance (HIT) ingestion of food with normal contents of histamine causes histamine-mediated symptoms. HIT is a pathological process, in which the enzymatic activity of histamine-degrading enzymes is decreased or inhibited and they are insufficient to inactivate histamine from food and to prevent its passage to blood-stream. Diagnosis of HIT is difficult. Multi-faced, non-specific clinical symptoms provoked by certain kinds of foods, beverages and drugs are often attributed to different diseases, such as allergy and food intolerance, mastocytosis, psychosomatic diseases, anorexia nervosa or adverse drug reactions. Correct diagnosis of HIT followed by therapy based on histamine-free diet and supplementation of diamine oxidase can improve patient's quality of life. PMID:26242570

  14. Histamine, histamine intoxication and intolerance.

    TOXLINE Toxicology Bibliographic Information

    Kovacova-Hanuskova E; Buday T; Gavliakova S; Plevkova J

    2015-09-01

    Excessive accumulation of histamine in the body leads to miscellaneous symptoms mediated by its bond to corresponding receptors (H1-H4). Increased concentration of histamine in blood can occur in healthy individuals after ingestion of foods with high contents of histamine, leading to histamine intoxication. In individuals with histamine intolerance (HIT) ingestion of food with normal contents of histamine causes histamine-mediated symptoms. HIT is a pathological process, in which the enzymatic activity of histamine-degrading enzymes is decreased or inhibited and they are insufficient to inactivate histamine from food and to prevent its passage to blood-stream. Diagnosis of HIT is difficult. Multi-faced, non-specific clinical symptoms provoked by certain kinds of foods, beverages and drugs are often attributed to different diseases, such as allergy and food intolerance, mastocytosis, psychosomatic diseases, anorexia nervosa or adverse drug reactions. Correct diagnosis of HIT followed by therapy based on histamine-free diet and supplementation of diamine oxidase can improve patient's quality of life.

  15. Correlating the amount of urea, creatinine, and glucose in urine from patients with diabetes mellitus and hypertension with the risk of developing renal lesions by means of Raman spectroscopy and principal component analysis

    NASA Astrophysics Data System (ADS)

    Bispo, Jeyse Aliana Martins; de Sousa Vieira, Elzo Everton; Silveira, Landulfo; Fernandes, Adriana Barrinha

    2013-08-01

    Patients with diabetes mellitus and hypertension (HT) diseases are predisposed to kidney diseases. The objective of this study was to identify potential biomarkers in the urine of diabetic and hypertensive patients through Raman spectroscopy in order to predict the evolution to complications and kidney failure. Urine samples were collected from control subjects (CTR) and patients with diabetes and HT with no complications (lower risk, LR), high degree of complications (higher risk, HR), and doing blood dialysis (DI). Urine samples were stored frozen (-20°C) before spectral analysis. Raman spectra were obtained using a dispersive spectrometer (830-nm, 300-mW power, and 20-s accumulation). Spectra were then submitted to principal component analysis (PCA) followed by discriminant analysis. The first PCA loading vectors revealed spectral features of urea, creatinine, and glucose. It has been found that the amounts of urea and creatinine decreased as disease evoluted from CTR to LR/HR and DI (PC1, p<0.05), and the amount of glucose increased in the urine of LR/HR compared to CTR (PC3, p<0.05). The discriminating model showed better overall classification rate of 70%. These results could lead to diagnostic information of possible complications and a better disease prognosis.

  16. What People with Lactose Intolerance Need to Know about Osteoporosis

    MedlinePlus

    ... Osteoporosis Osteoporosis and Other Conditions What People With Lactose Intolerance Need to Know About Osteoporosis Publication available ... focus(); */ } //--> Print-Friendly Page April 2015 What Is Lactose Intolerance? Lactose intolerance is a common problem. It ...

  17. Worry, Intolerance of Uncertainty, and Statistics Anxiety

    ERIC Educational Resources Information Center

    Williams, Amanda S.

    2013-01-01

    Statistics anxiety is a problem for most graduate students. This study investigates the relationship between intolerance of uncertainty, worry, and statistics anxiety. Intolerance of uncertainty was significantly related to worry, and worry was significantly related to three types of statistics anxiety. Six types of statistics anxiety were

  18. Worry, Intolerance of Uncertainty, and Statistics Anxiety

    ERIC Educational Resources Information Center

    Williams, Amanda S.

    2013-01-01

    Statistics anxiety is a problem for most graduate students. This study investigates the relationship between intolerance of uncertainty, worry, and statistics anxiety. Intolerance of uncertainty was significantly related to worry, and worry was significantly related to three types of statistics anxiety. Six types of statistics anxiety were…

  19. [Carbohydrate intolerance during complete fasting].

    PubMed

    Göschke, H; Thölen, H

    1977-12-10

    In the first part of the study oral glucose tolerance tests (GTT) or insulin tolerance tests (ITT) were performed in 22 lean and 22 obese nondiabetics before and after fasts of at least 6 days' duration. Deterioration of glucose tolerance was greater in lean than in obese individuals. Plasma levels of factors known to influence glucose tolerance (glucagon, growth hormone, free fatty acids, ketones) were significantly higher in fasting lean than in fasting obese subjects. Furthermore, delayed insulin rise (GTT) and decreased insulin sensitivity (ITT) were observed after starvation in lean subjects but not in the obese, which could explain the greater deterioration of glucose tolerance in the lean population. In the second part of the study glucose and fructose tolerance were compared during 4-hour infusions of these substrates (0.5 g/kg/h) in 8 normal subjects before and after two 4-day fasts. After starvation, glucose as well as fructose infusion resulted in plasma levels of the infused hexose significantly higher than in control, and the rise in plasma lactate and pyruvate was delayed. These results contradict the view widely held in the literature, that fructose metabolism remains unimpaired in the fasting state. PMID:337474

  20. Space Flight Orthostatic Intolerance Protection

    NASA Technical Reports Server (NTRS)

    Luty, Wei

    2009-01-01

    This paper summarizes investigations conducted on different orthostatic intolerance protection garments. This paper emphasizes on the engineering and operational aspects of the project. The current Shuttle pneumatic Anti-G Suit or AGS at 25 mmHg (0.5 psi) and customized medical mechanical compressive garments (20-30 mmHg) were tested on human subjects. The test process is presented. The preliminary results conclude that mechanical compressive garments can ameliorate orthostatic hypotension in hypovolemic subjects. A mechanical compressive garment is light, small and works without external pressure gas source; however the current garment design does not provide an adjustment to compensate for the loss of mass and size in the lower torso during long term space missions. It is also difficult to don. Compression garments that do not include an abdominal component are less effective countermeasures than garments which do. An early investigation conducted by the Human Adaptation and Countermeasures Division at Johnson Space Center (JSC) has shown there is no significant difference between the protection function of the AGS (at 77 mmHg or 1.5 psi) and the Russian anti-g suit, Kentavr (at 25 mmHg or 0.5 psi). Although both garments successfully countered hypovolemia-induced orthostatic intolerance, the Kentavr provided protection by using lower levels of compression pressure. This more recent study with a lower AGS pressure shows that pressures at 20-30 mmHg is acceptable but protection function is not as effective as higher pressure. In addition, a questionnaire survey with flight crewmembers who used both AGS and Kentavr during different missions was also performed.

  1. Hypertension in rats deficient in copper

    SciTech Connect

    Klevay, L.M.

    1986-03-01

    Male weanling rats were matched into two groups of equal mean weight (48 g), were fed a diet low in copper and zinc and were supplemented with a drinking solution with 10..mu..gZn and 2/sup +/gCu per ml until they grew to approximately 300 g. Systolic blood pressure (mmHg) was measured without anesthesia with an Electro-Sphygmomanometer and pneumatic pulse transducer; no significant difference between groups was found (0 > 0.05). Then copper was omitted from the solution of the group with lower blood pressure in each of two experiments. Plasma cholesterol (mg/dl) was measured by fluorometry and blood pressure was measured again 53 to 86 days later; mean (SE), n = 14, 15. Hypercholesterolemia verified deficiency. Hypotension in copper deficient rats in experiments of others probably was the result of cardiac defects induced in weanling animals. Hypertension joins hypercholesterolemia, hyperuricemia, glucose intolerance and abnormal electrocardiograms as a stigma of copper deficiency. Copper deficiency is the only nutritional insult that induces all of these characteristics useful in predicting risk of ischemic heart disease.

  2. Metabolic syndrome in hypertensive patients: An unholy alliance

    PubMed Central

    Mulè, Giuseppe; Calcaterra, Ilenia; Nardi, Emilio; Cerasola, Giovanni; Cottone, Santina

    2014-01-01

    For many years, it has been recognized that hypertension tends to cluster with various anthropometric and metabolic abnormalities including abdominal obesity, elevated triglycerides, reduced high-density lipoprotein cholesterol, glucose intolerance, insulin resistance and hyperuricemia. This constellation of various conditions has been transformed from a pathophysiological concept to a clinical entity, which has been defined metabolic syndrome (MetS). The consequences of the MetS have been difficult to assess without commonly accepted criteria to diagnose it. For this reason, on 2009 the International Diabetes Federation, the American Heart Association and other scientific organizations proposed a unified MetS definition. The incidence of the MetS has been increasing worldwide in parallel with an increase in overweight and obesity. The epidemic proportion reached by the MetS represents a major public health challenge, because several lines of evidence showed that the MetS, even without type 2 diabetes, confers an increased risk of cardiovascular morbidity and mortality in different populations including also hypertensive patients. It is likely that the enhanced cardiovascular risk associated with MetS in patients with high blood pressure may be largely mediated through an increased prevalence of preclinical cardiovascular and renal changes, such as left ventricular hypertrophy, early carotid atherosclerosis, impaired aortic elasticity, hypertensive retinopathy and microalbuminuria. Indeed, many reports support this notion, showing that hypertensive patients with MetS exhibit, more often than those without it, these early signs of end organ damage, most of which are recognized as significant independent predictors of adverse cardiovascular outcomes. PMID:25276291

  3. Metabolic syndrome in hypertensive patients: An unholy alliance.

    PubMed

    Mulè, Giuseppe; Calcaterra, Ilenia; Nardi, Emilio; Cerasola, Giovanni; Cottone, Santina

    2014-09-26

    For many years, it has been recognized that hypertension tends to cluster with various anthropometric and metabolic abnormalities including abdominal obesity, elevated triglycerides, reduced high-density lipoprotein cholesterol, glucose intolerance, insulin resistance and hyperuricemia. This constellation of various conditions has been transformed from a pathophysiological concept to a clinical entity, which has been defined metabolic syndrome (MetS). The consequences of the MetS have been difficult to assess without commonly accepted criteria to diagnose it. For this reason, on 2009 the International Diabetes Federation, the American Heart Association and other scientific organizations proposed a unified MetS definition. The incidence of the MetS has been increasing worldwide in parallel with an increase in overweight and obesity. The epidemic proportion reached by the MetS represents a major public health challenge, because several lines of evidence showed that the MetS, even without type 2 diabetes, confers an increased risk of cardiovascular morbidity and mortality in different populations including also hypertensive patients. It is likely that the enhanced cardiovascular risk associated with MetS in patients with high blood pressure may be largely mediated through an increased prevalence of preclinical cardiovascular and renal changes, such as left ventricular hypertrophy, early carotid atherosclerosis, impaired aortic elasticity, hypertensive retinopathy and microalbuminuria. Indeed, many reports support this notion, showing that hypertensive patients with MetS exhibit, more often than those without it, these early signs of end organ damage, most of which are recognized as significant independent predictors of adverse cardiovascular outcomes. PMID:25276291

  4. [Progress on the research of lactose intolerance].

    PubMed

    Chen, J; Sai, X Y

    2016-02-10

    Our group generalized the research development of lactose intolerance, both internationally and nationally. We systematically reviewed the pathogenesis, genetic polymorphisms of lactase deficiency, relevant progress of diagnostic methods and treatment. Through this systematic review, we undedrstood that there were insufficient research efforts made on understanding the epidemiological feature of lactose intolerance in this country. Relevant genetic mutations of people were also not clear, neither the development of simple and effective diagnosis method made. We should continue to extensively and deeply carry out the study regarding methods for early prevention and intervention on lactose intolerance. PMID:26917535

  5. [Secondary hypertension].

    PubMed

    Yoshida, Yuichi; Shibata, Hirotaka

    2015-11-01

    Hypertension is a common disease and a crucial predisposing factor of cardiovascular diseases. Approximately 10% of hypertensive patients are secondary hypertension, a pathogenetic factor of which can be identified. Secondary hypertension consists of endocrine, renal, and other diseases. Primary aldosteronism, Cushing's syndrome, pheochromocytoma, hyperthyroidism, and hypothyroidism result in endocrine hypertension. Renal parenchymal hypertension and renovascular hypertension result in renal hypertension. Other diseases such as obstructive sleep apnea syndrome are also very prevalent in secondary hypertension. It is very crucial to find and treat secondary hypertension at earlier stages since most secondary hypertension is curable or can be dramatically improved by specific treatment. One should keep in mind that screening of secondary hypertension should be done at least once in a daily clinical practice. PMID:26619670

  6. Pulmonary Hypertension

    MedlinePlus

    ... pulmonary hypertension isn't known, it is called idiopathic pulmonary hypertension (IPH). When pulmonary hypertension develops because of ... syndrome (AIDS) Cirrhosis (a chronic liver disease) Lupus Pulmonary fibrosis (a condition that causes scarring in the lungs) ...

  7. Lactose intolerance: from diagnosis to correct management.

    PubMed

    Di Rienzo, T; D'Angelo, G; D'Aversa, F; Campanale, M C; Cesario, V; Montalto, M; Gasbarrini, A; Ojetti, V

    2013-01-01

    This review discusses one of the most relevant problems in gastrointestinal clinical practice: lactose intolerance. The role of lactase-persistence alleles the diagnosis of lactose malabsorption the development of lactose intolerance symptoms and its management. Most people are born with the ability to digest lactose, the major carbohydrate in milk and the main source of nutrition until weaning. Approximately, 75% of the world's population loses this ability at some point, while others can digest lactose into adulthood. Symptoms of lactose intolerance include abdominal pain, bloating, flatulence and diarrhea with a considerable intraindividual and interindividual variability in the severity. Diagnosis is most commonly performed by the non invasive lactose hydrogen breath test. Management of lactose intolerance consists of two possible clinical choice not mutually exclusive: alimentary restriction and drug therapy. PMID:24443063

  8. Lactose Intolerance: A Guide for Teens

    MedlinePlus

    ... Health Gynecology Medical Conditions Nutrition & Fitness Emotional Health Lactose Intolerance Posted under Health Guides . Updated 6 November ... of all races and ethnic backgrounds. What is lactose? Lactose is a natural sugar found in milk ...

  9. Mechanisms of post-flight orthostatic intolerance

    NASA Technical Reports Server (NTRS)

    Blomqvist, C. G.; Buckey, J. C.; Gaffney, F. A.; Lane, L. D.; Levine, B. D.; Watenpaugh, D. E.

    1994-01-01

    Post-flight orthostatic intolerance is a dramatic physiological consequence of human adaptation to microgravity made inappropriate by a sudden return to 1-G. The immediate mechanism is almost always a failure to maintain adequate tissue perfusion, specifically perfusion of the central nervous system, but vestibular dysfunction may occasionally be the primary cause. Orthostatic intolerance is present in a wide range of clinical disorders of the nervous and cardiovascular systems. The intolerance that is produced by spaceflight and 1-G analogs (bed rest, head-down tilt at a moderate angle, water immersion) is different from its clinical counterparts by being only transiently present in subjects who otherwise have normal cardiovascular and regulatory systems. However, the same set of basic pathophysiological elements should be considered in the analysis of any form of orthostatic intolerance.

  10. Is It Food Allergy or Food Intolerance?

    MedlinePlus

    ... Content Marketing Share this: Main Content Area Is It Food Allergy or Food Intolerance? Food allergy is ... down the sugar, bacteria in the gut break it down, which forms gas, which in turn causes ...

  11. Incidence and risk factors of isolated systolic and diastolic hypertension: a 10 year follow-up of the Tehran Lipids and Glucose Study.

    PubMed

    Asgari, Samaneh; Khalili, Davood; Mehrabi, Yadollah; Kazempour-Ardebili, Sara; Azizi, Fereidoun; Hadaegh, Farzad

    2016-06-01

    The objective of this study is to examine the incidence and risk factors of isolated systolic hypertension (ISH) and isolated diastolic hypertension (IDH) in a Middle Eastern population, during a median follow-up of 9.6 years. In total, 8573 subjects without hypertension, cardiovascular disease and known diabetes were recruited into the study. To calculate the incidence of ISH, those with diastolic blood pressure (DBP) ≥ 90 mmHg during follow-up, and for calculating IDH those with systolic blood pressure (SBP) ≥ 140 mmHg during follow-up, were excluded. During follow-up, 235 new cases of ISH were identified, with a crude incidence rate of 5.7/1000 person-years; the corresponding values for IDH were 470 and 10.9/1000 person-years. Using backward stepwise Cox regression analysis, older age, baseline SBP and body mass index were related to incident ISH. Regarding IDH, younger age, baseline DBP and waist circumference were associated with higher risk, whereas female gender and being married were associated with lower risk (all p < 0.05). The C-statistics for the prediction model were 0.91 for ISH and 0.76 for IDH. In conclusion, after a decade of follow-up of this Iranian population, we found an incidence of about 0.5% and 1% per year for ISH and IDH, respectively. PMID:26643588

  12. Frequency of methotrexate intolerance in rheumatoid arthritis patients using methotrexate intolerance severity score (MISS questionnaire).

    PubMed

    Fatimah, Nibah; Salim, Babur; Nasim, Amjad; Hussain, Kamran; Gul, Harris; Niazi, Sarah

    2016-05-01

    The objective of the study was to determine the frequency of methotrexate intolerance in rheumatoid arthritis (RA) patients by applying the methotrexate intolerance severity score (MISS) questionnaire and to see the effect of dose and concomitant use of other disease-modifying antirheumatic drugs (DMARDS) on methotrexate (MTX) intolerance. For the descriptive study, non-probability sampling was carried out in the Female Rheumatology Department of Fauji Foundation Hospital (FFH), Rawalpindi, Pakistan. One hundred and fifty diagnosed cases of RA using oral MTX were selected. The MISS questionnaire embodies five elements: abdominal pain, nausea, vomiting, fatigue and behavioural symptoms. The amplitude of each element was ranked from 0 to 3 being no complaint (0 points), mild (1 point), moderate (2 points) and severe (3 points). A cut-off score of 6 and above ascertained intolerance by the physicians. A total of 33.3 % of the subjects exhibited MTX intolerance according to the MISS questionnaire. Out of which, the most recurring symptom of all was behavioural with a value of 44 % whereas vomiting was least noticeable with a figure of 11 %. About 6.6 % of the women with intolerance were consuming DMARDs in conjunction with MTX. Those using the highest weekly dose of MTX (20 mg) had supreme intolerance with prevalence in 46.2 % of the patients. The frequency of intolerance decreased with a decrease in weekly dose to a minimum of 20 % with 7.5 mg of MTX. MTX intolerance has moderate prevalence in RA patients and if left undetected, the compliance to use of MTX as a first-line therapy will decrease. Methotrexate intolerance is directly proportional to the dose of MTX taken. Also, there is no upstroke seen in intolerance with the use of other disease-modifying agents. PMID:27053094

  13. Lactose intolerance in Indonesian children.

    PubMed

    Hegar, Badriul; Widodo, Ariani

    2015-01-01

    "Lactose intolerance (LI)" is considered a common problem in Asians, and in many parts of the world. Its prevalence and age of manifestation varies between by Asian country, for possible genetic or cultural reasons. Studies in Indonesian children 3-15 years old (y) are available within the past two decades, using a pure lactose tolerance test. The prevalences of lactose malabsorption (LM) in pre-elementary (3-5 y), elementary (6-11 y), and junior high (12-14 y) school-children were 21.3%, 57.8%, and 73%, respectively. An increasing trend for LM prevalence was seen within the pre-elementary group, from 9.1% at 3 y to 28.6% at 5 y. The most frequent symptoms of LI in junior high school (JHS) group were abdominal pain (64.1%), abdominal distention (22.6%), nausea (15.1%), flatulence (5.7%), and diarrhea (1.9%), mostly within one hour of lactose ingestion. In children with regular and irregular milk drinking, LM occurred in 81.2% and 69.6%; LI was found in 56.2% and 52.1%, respectively. Most JHS children with dairy-associated recurrent abdominal pain (RAP) symptoms proved to be malabsorbers. Dairy products most related to RAP were milk and yogurt. LI was found in 81% of RAP children with abdominal pain most frequently, followed by nausea, bloating, diarrhea, borborygmi, and flatulence. Symp-tom onset occurred 30 minutes after lactose ingestion, especially nausea, bloating, and abdominal pain. In RAP children LI symptoms mostly found in breath hydrogen concentration>20 ppm. More LI symptoms were found in lactose malabsorbers, but symptoms were mild and generally disappeared in 7 hours, and in most by 15 hours. PMID:26715082

  14. Effects of renal sympathetic denervation on blood pressure, sleep apnea course, and glycemic control in patients with resistant hypertension and sleep apnea.

    PubMed

    Witkowski, Adam; Prejbisz, Aleksander; Florczak, Elżbieta; Kądziela, Jacek; Śliwiński, Paweł; Bieleń, Przemysław; Michałowska, Ilona; Kabat, Marek; Warchoł, Ewa; Januszewicz, Magdalena; Narkiewicz, Krzysztof; Somers, Virend K; Sobotka, Paul A; Januszewicz, Andrzej

    2011-10-01

    Percutaneous renal sympathetic denervation by radiofrequency energy has been reported to reduce blood pressure (BP) by the reduction of renal sympathetic efferent and afferent signaling. We evaluated the effects of this procedure on BP and sleep apnea severity in patients with resistant hypertension and sleep apnea. We studied 10 patients with refractory hypertension and sleep apnea (7 men and 3 women; median age: 49.5 years) who underwent renal denervation and completed 3-month and 6-month follow-up evaluations, including polysomnography and selected blood chemistries, and BP measurements. Antihypertensive regimens were not changed during the 6 months of follow-up. Three and 6 months after the denervation, decreases in office systolic and diastolic BPs were observed (median: -34/-13 mm Hg for systolic and diastolic BPs at 6 months; both P<0.01). Significant decreases were also observed in plasma glucose concentration 2 hours after glucose administration (median: 7.0 versus 6.4 mmol/L; P=0.05) and in hemoglobin A1C level (median: 6.1% versus 5.6%; P<0.05) at 6 months, as well as a decrease in apnea-hypopnea index at 6 months after renal denervation (median: 16.3 versus 4.5 events per hour; P=0.059). In conclusion, catheter-based renal sympathetic denervation lowered BP in patients with refractory hypertension and obstructive sleep apnea, which was accompanied by improvement of sleep apnea severity. Interestingly, there are also accompanying improvements in glucose tolerance. Renal sympathetic denervation may conceivably be a potentially useful option for patients with comorbid refractory hypertension, glucose intolerance, and obstructive sleep apnea, although further studies are needed to confirm these proof-of-concept data. PMID:21844482

  15. Uric acid as a modulator of glucose and lipid metabolism.

    PubMed

    Lima, William Gustavo; Martins-Santos, Maria Emlia Soares; Chaves, Valria Ernestnia

    2015-09-01

    In humans, uric acid is the final oxidation product of purine catabolism. The serum uric acid level is based on the balance between the absorption, production and excretion of purine. Uric acid is similarly produced in the liver, adipose tissue and muscle and is primarily excreted through the urinary tract. Several factors, including a high-fructose diet and the use of xenobiotics and alcohol, contribute to hyperuricaemia. Hyperuricaemia belongs to a cluster of metabolic and haemodynamic abnormalities, called metabolic syndrome, characterised by abdominal obesity, glucose intolerance, insulin resistance, dyslipidaemia and hypertension. Hyperuricaemia reduction in the Pound mouse or fructose-fed rats, as well as hyperuricaemia induction by uricase inhibition in rodents and studies using cell culture have suggested that uric acid plays an important role in the development of metabolic syndrome. These studies have shown that high uric acid levels regulate the oxidative stress, inflammation and enzymes associated with glucose and lipid metabolism, suggesting a mechanism for the impairment of metabolic homeostasis. Humans lacking uricase, the enzyme responsible for uric acid degradation, are susceptible to these effects. In this review, we summarise the current knowledge of the effects of uric acid on the regulation of metabolism, primarily focusing on liver, adipose tissue and skeletal muscle. PMID:26133655

  16. [Lactose intolerance: past and present. Part 1].

    PubMed

    Buzás, György Miklós

    2015-09-20

    Lactose intolerance is the most prevalent intestinal malabsorption disorder. After presentation of its history, the author describes the emergence of lactose intolerance during the evolution of species, and the biochemistry of lactose as well as features of human and bacterial lactase enzymes are then described. The unequal distribution of lactose intolerance in different continents and population is discussed, followed by presentation of past and present prevalence data in Hungary. Adult-type hypolactasia is caused by a polymorphism of the MCM6 gene located upstream from the lactase gene on the long arm of the chromosome 2. It can be determined with the polymerase chain reaction. The intestinal symptoms of lactose intolerance are well known, but its extra-intestinal manifestations are less recognised. Invasive diagnostic methods (determination of lactase activity from small intestinal biopsies, lactose tolerance test), are accurate, but have been replaced by the non-invasive methods; their gold standard is the H2 breath test. Genetic testing is being used more and more frequently in Hungary too, and, presumably, the methane breath test will be also available in the near future. Lactose intolerance can be accompanied by inflammatory bowel diseases, coeliac disease and irritable bowel syndrome; it could be established whether this association is causal or not in order to start a correct diet and therapy. PMID:26550699

  17. [Analgesic intolerance: pathogenesis, diagnosis and treatment].

    PubMed

    Reiss, Gilfe; Reiss, Michael

    2009-12-01

    Analgesic intolerance brings on cutaneous, respiratory and/or gastrointestinal reactions. This review provides an overview of sensitivity to nonsteroidal anti-inflammatory-drugs (NSAR) and its management. The full clinical picture of analgetic intolerance--the association of bronchial asthma (with severe acute attacks), sensitivity to NSAR and nasal polyps--is commonly summarized as the "Samter triad". The symptoms include chronic rhinosinusitis with nasal polyps, asthma bronchiale, gastrointestinal ulcers, angioedema, and urticaria. The prevalence of analgetic intolerance in the general population ranges from 0.6 to 2.5%. Clinical reactions after ingestion of NSAR are often obvious in the further progress of disease. In order to initiate early therapy the diagnosis of analgesic intolerance should occur before the complete picture of analgesic intolerance is obvious. Carefully controlled challenge tests with acetyl salicylic acid or other NSAR are performed as the diagnostic but not potential undamaged tool of choice. Adaptive desensitization (Aspirin desensitization therapy) is currently the single causal therapy. Severe asthma and reactions after ingestion of NSAR are avoided. Frequency of endonasal revision surgery is reduced after desensitization. PMID:20088346

  18. Lactose intolerance in infants, children, and adolescents.

    PubMed

    Heyman, Melvin B

    2006-09-01

    The American Academy of Pediatrics Committee on Nutrition presents an updated review of lactose intolerance in infants, children, and adolescents. Differences between primary, secondary, congenital, and developmental lactase deficiency that may result in lactose intolerance are discussed. Children with suspected lactose intolerance can be assessed clinically by dietary lactose elimination or by tests including noninvasive hydrogen breath testing or invasive intestinal biopsy determination of lactase (and other disaccharidase) concentrations. Treatment consists of use of lactase-treated dairy products or oral lactase supplementation, limitation of lactose-containing foods, or dairy elimination. The American Academy of Pediatrics supports use of dairy foods as an important source of calcium for bone mineral health and of other nutrients that facilitate growth in children and adolescents. If dairy products are eliminated, other dietary sources of calcium or calcium supplements need to be provided. PMID:16951027

  19. Food allergy and food intolerance in childhood.

    PubMed

    Sullivan, P B

    1999-01-01

    Food intolerance is a reproducible adverse reaction to a specific food ingredient that is not psychologically based. Food allergy is a form of food intolerance in which there is evidence that the response is caused by an immunological reaction to food. Other mechanisms of food intolerance include enzyme defects (e.g. lactase deficiency), pharmacological effects (e.g. histamine), toxic properties (e.g. haemagglutinating lectins) and irritants (e.g. spices). Food allergy in children is a highly contentious subject and there is often a striking lack of published evidence from which to base clinical decisions. The true prevalence of food allergy in children is unknown, although there is evidence of an increasing incidence of allergic reactions to some foods, especially peanuts. Our understanding of why some children are unable to tolerate certain foods (e.g. cow's milk, egg), or how they grow out of this intolerance, is very poor. Symptoms of food allergy in children are diverse and include vomiting, poor weight gain, abdominal pain, malabsorption, cough, wheeze, rhinitis, atopic eczema, urticaria and angioedema. Despite the lack of objective data to support the notion that food intolerance contributes to behaviour in children, this is a belief firmly held by many parents and some professionals. The gold standard for diagnosing food intolerance is the double-blind placebo-controlled food challenge (DBPCFC). There is often a poor correlation between the results of food provocation tests and those of skin prick tests of radioallergosorbent tests for specific food antibodies. For proven food allergy, elimination diets are the mainstay of management. In children these must be closely supervised to avoid nutritional deficiency and compromise of growth. Some children who have had severe (anaphylactic) reactions after food need to have a supply of self-injectable adrenaline made available to their parents and teachers and must also practice strict avoidance of the offending food. PMID:11132467

  20. The Relationships between Metabolic Disorders (Hypertension, Dyslipidemia, and Impaired Glucose Tolerance) and Computed Tomography-Based Indices of Hepatic Steatosis or Visceral Fat Accumulation in Middle-Aged Japanese Men

    PubMed Central

    Yokokawa, Hirohide; Naito, Toshio; Sasabe, Noriko; Okumura, Mitsue; Iijima, Kimiko; Shibuya, Katsuhiko; Hisaoka, Teruhiko; Fukuda, Hiroshi

    2016-01-01

    Background Most studies on the relationships between metabolic disorders (hypertension, dyslipidemia, and impaired glucose tolerance) and hepatic steatosis (HS) or visceral fat accumulation (VFA) have been cross-sectional, and thus, these relationships remain unclear. We conducted a retrospective cohort study to clarify the relationships between components of metabolic disorders and HS/VFA. Methods The participants were 615 middle-aged men who were free from serious liver disorders, diabetes, and HS/VFA and underwent multiple general health check-ups at our institution between 2009 and 2013. The data from the initial and final check-ups were used. HS and VFA were assessed by computed tomography. HS was defined as a liver to spleen attenuation ratio of ≤1.0. VFA was defined as a visceral fat cross-sectional area of ≥100 cm2 at the level of the navel. Metabolic disorders were defined using Japan’s metabolic syndrome diagnostic criteria. The participants were divided into four groups based on the presence (+) or absence (-) of HS/VFA. The onset rates of each metabolic disorder were compared among the four groups. Results Among the participants, 521, 55, 24, and 15 were classified as HS(-)/VFA(-), HS(-)/VFA(+), HS(+)/VFA(-), and HS(+)/VFA(+), respectively, at the end of the study. Impaired glucose tolerance was more common among the participants that exhibited HS or VFA (p = 0.05). On the other hand, dyslipidemia was more common among the participants that displayed VFA (p = 0.01). Conclusions It is likely that VFA is associated with impaired glucose tolerance and dyslipidemia, while HS might be associated with impaired glucose tolerance. Unfortunately, our study failed to detect associations between HS/VFA and metabolic disorders due to the low number of subjects that exhibited fat accumulation. Although our observational study had major limitations, we consider that it obtained some interesting results. HS and VFA might affect different metabolic disorders. Further large-scale longitudinal studies are needed to reveal the relationships between the components of metabolic disorders and HS/VFA. PMID:26938785

  1. Pulmonary Hypertension

    MedlinePlus

    ... page from the NHLBI on Twitter. What Is Pulmonary Hypertension? Pulmonary hypertension (PULL-mun-ary HI-per-TEN-shun), or PH, is increased pressure in the pulmonary arteries. These arteries carry blood from your heart ...

  2. Renovascular hypertension

    MedlinePlus

    Renal hypertension; Hypertension - renovascular; Renal artery occlusion; Stenosis - renal artery; Renal artery stenosis ... blood pressure to rise. Risk factors for atherosclerosis: High blood pressure Smoking Diabetes High cholesterol Heavy alcohol use Cocaine ...

  3. Hypertension - overview

    MedlinePlus Videos and Cool Tools

    If left untreated, hypertension can lead to the thickening of arterial walls causing its lumen, or blood passage way, to narrow in diameter. ... the narrowed arterial openings. In addition, people with hypertension may be more susceptible to stroke.

  4. What I Need to Know about Lactose Intolerance

    MedlinePlus

    ... Alternate Language URL Español What I need to know about Lactose Intolerance Page Content On this page: ... and break easily. [ Top ] How does my doctor know if I have lactose intolerance? Your doctor will ...

  5. Milk Intolerance and the American Indian

    ERIC Educational Resources Information Center

    Indian Historian, 1973

    1973-01-01

    The intolerance of milk by American Indians and other groups (Thais, Chinese, Filipinos, Melonesians of New Guinea, Australian Aborigines, Black groups of Africa, American Blacks, and Eskimos) due to the lack of the lactose enzyme is discussed in this article. (FF)

  6. [Lactose intolerance: past and present. Part II].

    PubMed

    Buzás, György Miklós

    2015-10-25

    The author summarises the interrelations between lactose intolerance, calcium and vitamin D metabolism and osteoporosis. Lactose intolerance enhances the risk of forearm and hip fractures in some patients. Lactase gene genotype and fracture risk are related in some populations. Calcium and vitamin D supplementation increase bone mineral content and they are justified in children, during pregnancy and lactation, and in postmenopausal women. The intake of milk and milk products could increase the risk of ovarian carcinoma. CC genotype of the lactase gene increased the risk of colorectal carcinoma in Finns; no such effect was observed in British, Spanish and Italian patients. Even small quantities of lactose in drugs (10-750 mg) could elicit intolerance symptoms due to individual susceptibility. In spite of public knowledge and advertising, controlled studies did not prove the beneficial effect of either a lactose-free diet, enzyme supplementation or probiotics in an evidence-based manner. While accepted guidelines are lacking, a personalised therapy is mandatory. In spite of increasing public interest in lactose intolerance, many unknown factors must still be studied. PMID:26477616

  7. Milk Intolerance, Beta-Casein and Lactose.

    PubMed

    Pal, Sebely; Woodford, Keith; Kukuljan, Sonja; Ho, Suleen

    2015-09-01

    True lactose intolerance (symptoms stemming from lactose malabsorption) is less common than is widely perceived, and should be viewed as just one potential cause of cows' milk intolerance. There is increasing evidence that A1 beta-casein, a protein produced by a major proportion of European-origin cattle but not purebred Asian or African cattle, is also associated with cows' milk intolerance. In humans, digestion of bovine A1 beta-casein, but not the alternative A2 beta-casein, releases beta-casomorphin-7, which activates μ-opioid receptors expressed throughout the gastrointestinal tract and body. Studies in rodents show that milk containing A1 beta-casein significantly increases gastrointestinal transit time, production of dipeptidyl peptidase-4 and the inflammatory marker myeloperoxidase compared with milk containing A2 beta-casein. Co-administration of the opioid receptor antagonist naloxone blocks the myeloperoxidase and gastrointestinal motility effects, indicating opioid signaling pathway involvement. In humans, a double-blind, randomized cross-over study showed that participants consuming A1 beta-casein type cows' milk experienced statistically significantly higher Bristol stool values compared with those receiving A2 beta-casein milk. Additionally, a statistically significant positive association between abdominal pain and stool consistency was observed when participants consumed the A1 but not the A2 diet. Further studies of the role of A1 beta-casein in milk intolerance are needed. PMID:26404362

  8. Milk Intolerance, Beta-Casein and Lactose

    PubMed Central

    Pal, Sebely; Woodford, Keith; Kukuljan, Sonja; Ho, Suleen

    2015-01-01

    True lactose intolerance (symptoms stemming from lactose malabsorption) is less common than is widely perceived, and should be viewed as just one potential cause of cows’ milk intolerance. There is increasing evidence that A1 beta-casein, a protein produced by a major proportion of European-origin cattle but not purebred Asian or African cattle, is also associated with cows’ milk intolerance. In humans, digestion of bovine A1 beta-casein, but not the alternative A2 beta-casein, releases beta-casomorphin-7, which activates μ-opioid receptors expressed throughout the gastrointestinal tract and body. Studies in rodents show that milk containing A1 beta-casein significantly increases gastrointestinal transit time, production of dipeptidyl peptidase-4 and the inflammatory marker myeloperoxidase compared with milk containing A2 beta-casein. Co-administration of the opioid receptor antagonist naloxone blocks the myeloperoxidase and gastrointestinal motility effects, indicating opioid signaling pathway involvement. In humans, a double-blind, randomized cross-over study showed that participants consuming A1 beta-casein type cows’ milk experienced statistically significantly higher Bristol stool values compared with those receiving A2 beta-casein milk. Additionally, a statistically significant positive association between abdominal pain and stool consistency was observed when participants consumed the A1 but not the A2 diet. Further studies of the role of A1 beta-casein in milk intolerance are needed. PMID:26404362

  9. Cows' milk protein intolerance: a possible association with gastroenteritis, lactose intolerance, and IgA deficiency.

    PubMed Central

    Harrison, M; Kilby, A; Walker-Smith, J A; France, N E; Wood, C B

    1976-01-01

    Twenty-five children with cows' milk protein intolerance were studied. Twenty had presented with an illness clinically indistinguishable from infantile gastroenteritis; an enteropathogenic Escherichia coli was isolated from the stools in two children, and in six another member of the family simultaneously developed acute diarrhoea and vomiting. Twenty-three children had lactose intolerance secondary to cows' milk protein intolerance. Eight out of 20 children were found to be partially IgA deficient. An acute attack of gastroenteritis, in damaging the small mucosa, may act as a triggering mechanism in cows' milk protein intolerance, and a deficiency in IgA may be a predisposing factor in so far as it allows the patient to become sensitised to foreign protein. PMID:776336

  10. Pulmonary Hypertension: Types and Treatments

    PubMed Central

    Rose-Jones, Lisa J; Mclaughlin, Vallerie V

    2015-01-01

    Pulmonary arterial hypertension (PAH) is a panvasculopathy that affects the distal pulmonary arteries and leads to restricted blood flow. This increased afterload leads to adaptive mechanisms of the right ventricle, with eventual failure once it can no longer compensate. Pulmonary hypertension from associated conditions, most importantly left heart disease, i.e. heart failure, can also lead to the same sequela. Patients often experience early vague symptoms of dyspnea and exercise intolerance, and thus PH can elude clinicians until right heart failure symptoms predominate. Evidence-based treatment options with pulmo-nary vasodilators are available for those with PAH and should be employed early. It is essential that patients be accurately categorized by their etiology of PH, as treatment strategies differ, and can potentially be dangerous if employed in the wrong clinical scenario. PMID:24251459

  11. [Childhood hypertension].

    PubMed

    Takemura, Tsukasa

    2015-11-01

    For accurate diagnosis of childhood hypertension, selection of appropriate manchette size according to the child age and the circumstantial size of upper limb is essentially important. In addition, except for the emergency case of hypertension, repeated measurement of blood pressure would be desirable in several weeks interval. Recently, childhood hypertension might be closely related to the abnormality of maternal gestational period caused by the strict diet and the maternal smoking. Developmental Origins of Health and Disease(DOHaD) theory is now highlighted in the pathogenesis of adulthood hypertension. To prevent hypertension of small-for-date baby in later phase of life, maternal education for child nursing should be conducted. In children, secondary hypertension caused by renal, endocrinologic, or malignant disease is predominant rather than idiopathic hypertension. PMID:26619664

  12. Resistant Hypertension.

    PubMed

    Doroszko, Adrian; Janus, Agnieszka; Szahidewicz-Krupska, Ewa; Mazur, Grzegorz; Derkacz, Arkadiusz

    2016-01-01

    Resistant hypertension is a severe medical condition which is estimated to appear in 9-18% of hypertensive patients. Due to higher cardiovascular risk, this disorder requires special diagnosis and treatment. The heterogeneous etiology, risk factors and comorbidities of resistant hypertension stand in need of sophisticated evaluation to confirm the diagnosis and select the best therapeutic options, which should consider lifestyle modifications as well as pharmacological and interventional treatment. After having excluded pseudohypertension, inappropriate blood pressure measurement and control as well as the white coat effect, suspicion of resistant hypertension requires an analysis of drugs which the hypertensive patient is treated with. According to one definition - ineffective treatment with 3 or more antihypertensive drugs including diuretics makes it possible to diagnose resistant hypertension. A multidrug therapy including angiotensin - converting enzyme inhibitors, angiotensin II receptor blockers, beta blockers, diuretics, long-acting calcium channel blockers and mineralocorticoid receptor antagonists has been demonstrated to be effective in resistant hypertension treatment. Nevertheless, optional, innovative therapies, e.g. a renal denervation or baroreflex activation, may create a novel pathway of blood pressure lowering procedures. The right diagnosis of this disease needs to eliminate the secondary causes of resistant hypertension e.g. obstructive sleep apnea, atherosclerosis and renal or hormonal disorders. This paper briefly summarizes the identification of the causes of resistant hypertension and therapeutic strategies, which may contribute to the proper diagnosis and an improvement of the long term management of resistant hypertension. PMID:26935512

  13. Prevalence and Symptom Correlation of Lactose Intolerance in the North East Part of Bangladesh.

    PubMed

    Saha, M; Shil, B C; Saha, S K; Chowdhury, M; Perveen, I; Banik, R; Rahman, M H

    2016-01-01

    This study was designed to see the prevalence of lactose intolerance and symptom correlation following oral lactose challenge in healthy volunteers in the north east part of Bangladesh. Symptoms of abdominal pain, nausea, borborygmi, flatulence, diarrhea and others were noted for 24 hours and blood glucose was estimated at 0 hour and 30 minutes after 50gm oral lactose load to healthy volunteers. Failure to rise blood glucose level ≥1.1mmol/l at 30 minutes after lactose intake from fasting level was taken as lactose malabsorption (LM) i.e., lactose intolerance. Sensitivity and specificity of different symptoms were then found out. A total of 171 volunteers (male 123, female 48) with a mean age 34.08 years participated in this study. Lactose intolerance was found among 82.5% (n=141, M=100, F=41) subjects. Symptoms mostly experience by the lactose malabsorbers were diarrhea 93(66.0%), borborygmi 80(56.7%), abdominal pain 31(22.0%) and flatulence 32(22.7%). LM prevalence was found to increase with increasing number of symptoms up to 3 symptoms. A week positive correlation (r=0.205, P=0.007) was found between the number of symptoms and proportion of subjects having positive lactose tolerance test. Lactose intolerance among healthy adults of North East part of our country is as common as in other Asian countries including China and Malaysia. But LM is higher than that of Europeans and south Indians. Diarrhea and borborygmi were mostly associated with LM. PMID:26931253

  14. Intolerance of uncertainty in body dysmorphic disorder.

    PubMed

    Summers, Berta J; Matheny, Natalie L; Sarawgi, Shivali; Cougle, Jesse R

    2016-03-01

    Intolerance of uncertainty (IU) is a transdiagnostic construct associated with several anxiety and related disorders. Three studies were conducted to explore the potential relationship between IU and body dysmorphic disorder (BDD). Study 1 revealed a positive relationship between IU and BDD symptoms above symptoms of anxiety and depression in an unselected student sample (N=88). Study 2 demonstrated a similar relationship between IU and BDD symptoms above negative affectivity and intolerance of ambiguity in a community sample (N=116). Study 3 found that a clinical BDD sample (N=23) reported greater IU than healthy controls (N=20), though this relationship was accounted for by symptoms of anxiety and depression. Greater IU predicted functional impairment in the clinical sample above BDD symptoms and past-week anxiety and depression. The observed relationship between IU and BDD symptoms provides preliminary support for the relevance of IU to this population. PMID:26688272

  15. Lactose intolerance: diagnosis, genetic, and clinical factors

    PubMed Central

    Mattar, Rejane; de Campos Mazo, Daniel Ferraz; Carrilho, Flair José

    2012-01-01

    Most people are born with the ability to digest lactose, the major carbohydrate in milk and the main source of nutrition until weaning. Approximately 75% of the world’s population loses this ability at some point, while others can digest lactose into adulthood. This review discusses the lactase-persistence alleles that have arisen in different populations around the world, diagnosis of lactose intolerance, and its symptomatology and management. PMID:22826639

  16. Sucrose feeding in mouse pregnancy leads to hypertension, and sex-linked obesity and insulin resistance in female offspring

    PubMed Central

    Samuelsson, Anne-Maj; Matthews, Phillippa A.; Jansen, Eugene; Taylor, Paul D.; Poston, Lucilla

    2013-01-01

    Eating an unbalanced diet during pregnancy may induce long-term health consequences in offspring, in particular obesity, insulin resistance, and hypertension. We tested the hypothesis that a maternal diet rich in simple sugars predispose mouse offspring to obesity, glucose intolerance, and cardiovascular diseases in adulthood. Female C57BL/6J mice were fed either a standard chow or a sucrose-rich diet (26% of total energy) 6 weeks prior to mating, throughout pregnancy and lactation. Offspring of control dams (OC) and high sucrose fed dams (OSF) were weaned onto standard control chow, and metabolic and cardiovascular parameters determined at 3 months of age. Both male and female OSF were hyperphagic by 4 weeks of age and females were heavier than OC at 6 weeks. At 3 months, female OSF showed a significant increase in inguinal fat pad mass, whereas skeletal muscle mass (tibialis anterior) and locomotor activity were decreased relative to OC. A 10-fold increase in fasting serum insulin in female OSF vs. OC at 3 months (Insulin [pmol/L] mean ± SEM, OSF, 200.3 ± 16.1, vs. OC, 20.3 ± 1.8, n = 6 P < 0.001), was associated with impaired glucose tolerance (AUC [mmol/L min] mean ± SEM, OSF 1437.4 ± 124.2 vs. OC, 1076.8 ± 83.9, n = 6, P < 0.05). Both male and female OSF were hypertensive as assessed by radiotelemetry (night-time systolic arterial pressure (SAP) [mmHg] mean ± SEM, male OSF, 128 ± 1 vs. OC, 109 ± 1, n = 6, P < 0.01; female OSF, 130 ± 1 vs. OC, 118 ± 1, n = 6, P < 0.05). Analysis of heart rate variability (HRV) demonstrated an increased low:high frequency ratio in male and female OSF (P < 0.05), indicative of heightened sympathetic efferent tone. Renal tissue noradrenaline (NA) content was markedly raised in the OSF vs. OC (NA [pg/ml/mg tissue] mean ± SEM, male OSF, 2.28 ± 0.19 vs. OC 0.84 ± 0.09, n = 6, P < 0.01). Exposure to a maternal diet rich in sucrose led to obesity and glucose intolerance in female mice offspring, and hypertension in both sexes. PMID:23423541

  17. Seafood Allergy, Toxicity, and Intolerance: A Review.

    PubMed

    Prester, Ljerka

    2016-04-01

    Seafood allergies have been increasing their presence in the last 2 decades. Allergic reactions to seafood can range from mild urticarial and oral allergy syndrome to life-threatening anaphylactic reactions. Ingestion of seafood infested with Anisakis larvae can cause a disease known as anisakiasis with symptoms similar to true seafood allergy. Furthermore, some adverse reactions to seafood including histamine fish poisoning (HFP), and intolerance to histamine can trigger clinical symptoms, which, although nonallergic in origin, are similar to true immunoglobulin E (IgE)-mediated allergic reactions. Because seafood allergy usually remains a lifelong food allergy, this review focuses on the current knowledge on fish and shellfish allergens and emphasizes the importance of differentiating seafood allergy from other allergy-like reactions (anisakiasis, HFP, and intolerance to histamine). Key teaching points: • Fish and shellfish are potent allergens that can provoke serious IgE antibody-mediated adverse reactions in sensitive individuals. • Sensitization to seafood allergens can be achieved by ingestion, inhalation, or skin contact. • Shellfish major allergen, tropomyosin, shares significant homology to arthropods (dust mites and cockroaches). • Accidental exposures to seafood products cross-contaminated with fish or shellfish allergens (hidden allergens) during processing may present a health risk for sensitive individuals. • Allergens of fish parasite A. simplex present common hidden allergens in seafood, particularly in raw and undercooked home-made fish dishes. • Symptoms caused by HFP, histamine intolerance, and anisakiasis are similar to true seafood allergy. PMID:26252073

  18. Food intolerance and allergy--a review.

    PubMed

    Lessof, M H

    1983-01-01

    Specific food intolerance needs to be distinguished from obsessional states in which those who are affected have an aversion to numerous foods. Even in cases where specific food intolerance can be demonstrated, the diagnosis of food allergy depends on additional evidence that the patient's reaction is based on an abnormal immunological response. In food allergy, skin and laboratory tests may detect the presence of an IgE-mediated reaction, particularly in patients with asthma or eczema and especially where the foods involved are highly allergenic--such as egg, fish, nuts and milk. However, many patients with proven food intolerance have negative tests, suggesting that other immunological or non-immunological mechanisms are responsible. Laboratory tests for non-IgE reactions are unreliable. Where it is difficult to show a connection between individual foods and an allergic response--as in patients with urticaria provoked by food additives--one of the reasons for diagnostic difficulty is that the offending substances may be present in a wide range of common foods. If the diagnosis is to be firmly established in such cases, it is necessary to show that symptoms remit on an elimination diet and recur after a placebo-controlled challenge. PMID:6351151

  19. Idiopathic orthostatic intolerance and postural tachycardia syndromes

    NASA Technical Reports Server (NTRS)

    Jacob, G.; Biaggioni, I.; Robertson, D. (Principal Investigator)

    1999-01-01

    Upright posture imposes a substantial gravitational stress on the body, for which we are able to compensate, in large part because of the autonomic nervous system. Alteration in autonomic function, therefore, may lead to orthostatic intolerance. On one extreme, patients with autonomic failure caused by degenerative loss of autonomic function are severely disabled by orthostatic hypotension and may faint whenever they stand up. Fortunately, such patients are relatively rare. On the other hand, disabling orthostatic intolerance can develop in otherwise normal young people. These patients can be severely impaired by symptoms of fatigue, tachycardia, and shortness of breath when they stand up. The actual incidence of this disorder is unknown, but these patients make up the largest group of patients referred to centers that specialize in autonomic disorders. We will review recent advances made in the understanding of this condition, potential pathophysiological mechanisms that contribute to orthostatic intolerance, therapeutic alternatives currently available for the management of these patients, and areas in which more research is needed.

  20. Malignant hypertension

    MedlinePlus

    ... Arteriolar nephrosclerosis; Nephrosclerosis - arteriolar; Hypertension - malignant; High blood pressure - malignant ... a small number of people with high blood pressure, including children and adults. It is more common ...

  1. Hypovolemia in syncope and orthostatic intolerance role of the renin-angiotensin system

    NASA Technical Reports Server (NTRS)

    Jacob, G.; Robertson, D.; Mosqueda-Garcia, R.; Ertl, A. C.; Robertson, R. M.; Biaggioni, I.

    1997-01-01

    PURPOSE: Orthostatic intolerance is the cause of significant disability in otherwise normal patients. Orthostatic tachycardia is usually the dominant hemodynamic abnormality, but symptoms may include dizziness, visual changes, discomfort in the head or neck, poor concentration, fatigue, palpitations, tremulousness, anxiety and, in some cases, syncope. It is the most common disorder of blood pressure regulation after essential hypertension. There is a predilection for younger rather than older adults and for women more than men. Its cause is unknown; partial sympathetic denervation or hypovolemia has been proposed. METHODS AND MATERIALS: We tested the hypothesis that reduced plasma renin activity, perhaps from defects in sympathetic innervation of the kidney, could underlie a hypovolemia, giving rise to these clinical symptoms. Sixteen patients (14 female, 2 male) ranging in age from 16 to 44 years were studied. Patients were enrolled in the study if they had orthostatic intolerance, together with a raised upright plasma norepinephrine (> or = 600 pg/mL). Patients underwent a battery of autonomic tests and biochemical determinations. RESULTS: There was a strong positive correlation between the blood volume and plasma renin activity (r = 0.84, P = 0.001). The tachycardic response to upright posture correlated with the severity of the hypovolemia. There was also a correlation between the plasma renin activity measured in these patients and their concomitant plasma aldosterone level. CONCLUSIONS: Hypovolemia occurs commonly in orthostatic intolerance. It is accompanied by an inappropriately low level of plasma renin activity. The degree of abnormality of blood volume correlates closely with the degree of abnormality in plasma renin activity. Taken together, these observations suggest that reduced plasma renin activity may be an important pathophysiologic component of the syndrome of orthostatic intolerance.

  2. Antihypertensive drugs and glucose metabolism.

    PubMed

    Rizos, Christos V; Elisaf, Moses S

    2014-07-26

    Hypertension plays a major role in the development and progression of micro- and macrovascular disease. Moreover, increased blood pressure often coexists with additional cardiovascular risk factors such as insulin resistance. As a result the need for a comprehensive management of hypertensive patients is critical. However, the various antihypertensive drug categories have different effects on glucose metabolism. Indeed, angiotensin receptor blockers as well as angiotensin converting enzyme inhibitors have been associated with beneficial effects on glucose homeostasis. Calcium channel blockers (CCBs) have an overall neutral effect on glucose metabolism. However, some members of the CCBs class such as azelnidipine and manidipine have been shown to have advantageous effects on glucose homeostasis. On the other hand, diuretics and β-blockers have an overall disadvantageous effect on glucose metabolism. Of note, carvedilol as well as nebivolol seem to differentiate themselves from the rest of the β-blockers class, being more attractive options regarding their effect on glucose homeostasis. The adverse effects of some blood pressure lowering drugs on glucose metabolism may, to an extent, compromise their cardiovascular protective role. As a result the effects on glucose homeostasis of the various blood pressure lowering drugs should be taken into account when selecting an antihypertensive treatment, especially in patients which are at high risk for developing diabetes. PMID:25068013

  3. Antihypertensive drugs and glucose metabolism

    PubMed Central

    Rizos, Christos V; Elisaf, Moses S

    2014-01-01

    Hypertension plays a major role in the development and progression of micro- and macrovascular disease. Moreover, increased blood pressure often coexists with additional cardiovascular risk factors such as insulin resistance. As a result the need for a comprehensive management of hypertensive patients is critical. However, the various antihypertensive drug categories have different effects on glucose metabolism. Indeed, angiotensin receptor blockers as well as angiotensin converting enzyme inhibitors have been associated with beneficial effects on glucose homeostasis. Calcium channel blockers (CCBs) have an overall neutral effect on glucose metabolism. However, some members of the CCBs class such as azelnidipine and manidipine have been shown to have advantageous effects on glucose homeostasis. On the other hand, diuretics and β-blockers have an overall disadvantageous effect on glucose metabolism. Of note, carvedilol as well as nebivolol seem to differentiate themselves from the rest of the β-blockers class, being more attractive options regarding their effect on glucose homeostasis. The adverse effects of some blood pressure lowering drugs on glucose metabolism may, to an extent, compromise their cardiovascular protective role. As a result the effects on glucose homeostasis of the various blood pressure lowering drugs should be taken into account when selecting an antihypertensive treatment, especially in patients which are at high risk for developing diabetes. PMID:25068013

  4. The effect of polyphenol-rich dark chocolate on fasting capillary whole blood glucose, total cholesterol, blood pressure and glucocorticoids in healthy overweight and obese subjects.

    PubMed

    Almoosawi, Suzana; Fyfe, Lorna; Ho, Clement; Al-Dujaili, Emad

    2010-03-01

    Numerous studies indicate that polyphenol-rich chocolate reduces fasting blood glucose, blood pressure (BP) and total cholesterol in healthy individuals and hypertensives with or without glucose intolerance. The aim of the present study was to investigate the effect of two doses of polyphenol-rich dark chocolate (DC) on fasting capillary whole blood glucose, total cholesterol and BP and to examine whether improvements in these parameters are associated with changes in adrenocorticoid excretion in overweight and obese individuals. The study used a randomised, single-blind, cross-over design where fourteen overweight and obese subjects were randomised to either take 20 g DC with 500 mg polyphenols then 20 g DC with 1000 mg polyphenols or vice-versa. Participants followed each diet for 2 weeks separated by a 1-week washout period. It was observed that the 500 mg polyphenol dose was equally effective in reducing fasting blood glucose levels, systolic BP (SBP) and diastolic BP (DBP) as the 1000 mg polyphenol dose suggesting that a saturation effect might occur with increasing dose of polyphenols. There was also a trend towards a reduction in urinary free cortisone levels with both groups although it did not reach statistical significance. No changes in anthropometrical measurements were seen. We suggest that more research is required to investigate the mechanism(s) by which polyphenol-rich foods influence health. PMID:19825207

  5. Intolerance of responsibility for internal conflict.

    PubMed

    Coen, S J

    1989-01-01

    A type of patient is described, who has marked intolerance of taking responsibility for his internal conflicts so as to confront them, analyze them, and change. Defensive repetition in pathological object relations aims to avoid what is wrong within and to engage another so as to protect oneself. Genetic, dynamic, and technical aspects of such defensive, dependent relating are considered. Responsibility for oneself and for what is within oneself is held to be terrifying--more than anyone can bear on his own. How destructiveness has become, and remains, so terrifying is discussed. PMID:2632630

  6. Mechanisms of orthostatic intolerance during heat stress.

    PubMed

    Schlader, Zachary J; Wilson, Thad E; Crandall, Craig G

    2016-04-01

    Heat stress profoundly and unanimously reduces orthostatic tolerance. This review aims to provide an overview of the numerous and multifactorial mechanisms by which this occurs in humans. Potential causal factors include changes in arterial and venous vascular resistance and blood distribution, and the modulation of cardiac output, all of which contribute to the inability to maintain cerebral perfusion during heat and orthostatic stress. A number of countermeasures have been established to improve orthostatic tolerance during heat stress, which alleviate heat stress induced central hypovolemia (e.g., volume expansion) and/or increase peripheral vascular resistance (e.g., skin cooling). Unfortunately, these countermeasures can often be cumbersome to use with populations prone to syncopal episodes. Identifying the mechanisms of inter-individual differences in orthostatic intolerance during heat stress has proven elusive, but could provide greater insights into the development of novel and personalized countermeasures for maintaining or improving orthostatic tolerance during heat stress. This development will be especially impactful in occuational settings and clinical situations that present with orthostatic intolerance and/or central hypovolemia. Such investigations should be considered of vital importance given the impending increased incidence of heat events, and associated cardiovascular challenges that are predicted to occur with the ensuing changes in climate. PMID:26723547

  7. Chemical Intolerance in Primary Care Settings: Prevalence, Comorbidity, and Outcomes

    PubMed Central

    Katerndahl, David A.; Bell, Iris R.; Palmer, Raymond F.; Miller, Claudia S.

    2012-01-01

    PURPOSE This study extends previous community-based studies on the prevalence and clinical characteristics of chemical intolerance in a sample of primary care clinic patients. We evaluated comorbid medical and psychiatric disorders, functional status, and rates of health care use. METHODS A total of 400 patients were recruited from 2 family medicine clinic waiting rooms in San Antonio, Texas. Patients completed the validated Quick Environmental Exposure and Sensitivity Inventory (QEESI) to assess chemical intolerance; the Primary Care Evaluation of Mental Disorders (PRIME-MD) screen for possible psychiatric disorders; the DartmouthNorthern New England Primary Care Cooperative Information Project (Dartmouth COOP) charts for functional status; and the Healthcare Utilization Questionnaire. RESULTS Overall, 20.3% of the sample met criteria for chemical intolerance. The chemically intolerant group reported significantly higher rates of comorbid allergies and more often met screening criteria for possible major depressive disorder, panic disorder, generalized anxiety disorder, and alcohol abuse disorder, as well as somatization disorder. The total number of possible mental disorders was correlated with chemical intolerance scores (P <.001). Controlling for demographics, patients with chemical intolerance were significantly more likely to have poorer functional status, with trends toward increased medical service use when compared with nonchemically intolerant patients. After controlling for comorbid psychiatric conditions, the groups differed significantly only regarding limitations of social activities. CONCLUSIONS Chemical intolerance occurs in 1 of 5 primary care patients yet is rarely diagnosed by busy practitioners. Psychiatric comorbidities contribute to functional limitations and increased health care use. Chemical intolerance offers an etiologic explanation. Symptoms may resolve or improve with the avoidance of salient chemical, dietary (including caffeine and alcohol), and drug triggers. Given greater medication intolerances in chemical intolerance, primary care clinicians could use the QEESI to identify patients for appropriate triage to comprehensive nonpharmacologic care. PMID:22778124

  8. The role of mercury and cadmium heavy metals in vascular disease, hypertension, coronary heart disease, and myocardial infarction.

    PubMed

    Houston, Mark C

    2007-01-01

    Mercury, cadmium, and other heavy metals have a high affinity for sulfhydryl (-SH) groups, inactivating numerous enzymatic reactions, amino acids, and sulfur-containing antioxidants (NAC, ALA, GSH), with subsequent decreased oxidant defense and increased oxidative stress. Both bind to metallothionein and substitute for zinc, copper, and other trace metals reducing the effectiveness of metalloenzymes. Mercury induces mitochondrial dysfunction with reduction in ATP, depletion of glutathione, and increased lipid peroxidation; increased oxidative stress is common. Selenium antagonizes mercury toxicity. The overall vascular effects of mercury include oxidative stress, inflammation, thrombosis, vascular smooth muscle dysfunction, endothelial dysfunction, dyslipidemia, immune dysfunction, and mitochondrial dysfunction. The clinical consequences of mercury toxicity include hypertension, CHD, MI, increased carotid IMT and obstruction, CVA, generalized atherosclerosis, and renal dysfunction with proteinuria. Pathological, biochemical, and functional medicine correlations are significant and logical. Mercury diminishes the protective effect of fish and omega-3 fatty acids. Mercury, cadmium, and other heavy metals inactivate COMT, which increases serum and urinary epinephrine, norepinephrine, and dopamine. This effect will increase blood pressure and may be a clinical clue to heavy metal toxicity. Cadmium concentrates in the kidney, particularly inducing proteinuria and renal dysfunction; it is associated with hypertension, but less so with CHD. Renal cadmium reduces CYP4A11 and PPARs, which may be related to hypertension, sodium retention, glucose intolerance, dyslipidemia, and zinc deficiency. Dietary calcium may mitigate some of the toxicity of cadmium. Heavy metal toxicity, especially mercury and cadmium, should be evaluated in any patient with hypertension, CHD, or other vascular disease. Specific testing for acute and chronic toxicity and total body burden using hair, toenail, urine, serum, etc. with baseline and provoked evaluation should be done. PMID:17405690

  9. Hypertension screening

    NASA Technical Reports Server (NTRS)

    Foulke, J. M.

    1975-01-01

    An attempt was made to measure the response to an announcement of hypertension screening at the Goddard Space Center, to compare the results to those of previous statistics. Education and patient awareness of the problem were stressed.

  10. Pulmonary hypertension

    MedlinePlus

    Channick RN, Rubin LJ. Pulmonary hypertension. In: Mason RJ, Broaddus VC, Martin TR, et al., eds. Murray and Nadel's Textbook of Respiratory Medicine . 5th ed. Philadelphia, PA: Elsevier Saunders; 2010:chap ...

  11. Pulmonary Hypertension

    MedlinePlus

    Pulmonary hypertension (PH) is high blood pressure in the arteries to your lungs. It is a serious condition. If you have ... and you can develop heart failure. Symptoms of PH include Shortness of breath during routine activity, such ...

  12. [Hypertensive retinopathy].

    PubMed

    Genevois, Olivier; Paques, Michel

    2010-01-20

    Acute hypertensive retinopathy should be distinguished from retinal arteriolosclerosis. The presence of microvascular abnormalities in the ocular fundus increases the risk of heart and/or brain attack. At the clinical level, the current classification of chronic hypertensive retinopathy is based on the long-term risk of stroke. In research, a great number of studies are focused on the predictive value of retinal vascular diameters related to the general micro- and macrovascular disease. PMID:20222306

  13. Pulmonary Hypertension

    PubMed Central

    Newman, John H.

    2005-01-01

    The modern era in cardiopulmonary medicine began in the 1940s, when Cournand and Richards pioneered right-heart catheterization. Until that time, no direct measurement of central vascular pressure had been performed in humans. Right-heart catheterization ignited an explosion of insights into function and dysfunction of the pulmonary circulation, cardiac performance, ventilationperfusion relationships, lungheart interactions, valvular function, and congenital heart disease. It marked the beginnings of angiocardiography with its diagnostic implications for diseases of the left heart and peripheral circulation. Pulmonary hypertension was discovered to be the consequence of a large variety of diseases that either raised pressure downstream of the pulmonary capillaries, induced vasoconstriction, increased blood flow to the lung, or obstructed the pulmonary vessels, either by embolism or in situ fibrosis. Hypoxic vasoconstriction was found to be a major cause of acute and chronic pulmonary hypertension, and surprising vasoreactivity of the pulmonary vascular bed was discovered to be present in many cases of severe pulmonary hypertension, initially in mitral stenosis. Diseases as disparate as scleroderma, cystic fibrosis, kyphoscoliosis, sleep apnea, and sickle cell disease were found to have shared consequences in the pulmonary circulation. Some of the achievements of Cournand and Richards and their scientific descendents are discussed in this article, including success in the diagnosis and treatment of idiopathic pulmonary arterial hypertension, chronic thromboembolic pulmonary hypertension, and management of hypoxic pulmonary hypertension. PMID:15994464

  14. Intolerance of Uncertainty, Fear of Anxiety, and Adolescent Worry

    ERIC Educational Resources Information Center

    Dugas, Michel J.; Laugesen, Nina; Bukowski, William M.

    2012-01-01

    A 5 year, ten wave longitudinal study of 338 adolescents assessed the association between two forms of cognitive vulnerability (intolerance of uncertainty and fear of anxiety) and worry. Multilevel mediational analyses revealed a bidirectional and reciprocal relation between intolerance of uncertainty and worry in which change in one variable

  15. The Intolerance of Uncertainty Scale for Children: A Psychometric Evaluation

    ERIC Educational Resources Information Center

    Comer, Jonathan S.; Roy, Amy K.; Furr, Jami M.; Gotimer, Kristin; Beidas, Rinad S.; Dugas, Michel J.; Kendall, Philip C.

    2009-01-01

    Intolerance of uncertainty (IU) has contributed to our understanding of excessive worry and adult anxiety disorders, but there is a paucity of research on IU in child samples. This gap is due to the absence of a psychometrically sound measure of IU in youth. The present study adapted parallel child- and parent-report forms of the Intolerance of

  16. Intolerance of Uncertainty, Fear of Anxiety, and Adolescent Worry

    ERIC Educational Resources Information Center

    Dugas, Michel J.; Laugesen, Nina; Bukowski, William M.

    2012-01-01

    A 5 year, ten wave longitudinal study of 338 adolescents assessed the association between two forms of cognitive vulnerability (intolerance of uncertainty and fear of anxiety) and worry. Multilevel mediational analyses revealed a bidirectional and reciprocal relation between intolerance of uncertainty and worry in which change in one variable…

  17. Sediment Burial Intolerance of Marine Macroinvertebrates

    PubMed Central

    Hendrick, Vicki J.; Hutchison, Zoë L.; Last, Kim S.

    2016-01-01

    The marine environment contains suspended particulate matter which originates from natural and anthropogenic sources. Settlement of this material can leave benthic organisms susceptible to smothering, especially if burial is sudden i.e. following storms or activities such as dredging. Their survival will depend on their tolerance to, and their ability to escape from burial. Here we present data from a multi-factorial experiment measuring burial responses incorporating duration, sediment fraction and depth. Six macroinvertebrates commonly found in sediment rich environments were selected for their commercial and/or conservation importance. Assessments revealed that the brittle star (Ophiura ophiura), the queen scallop (Aequipecten opercularis) and the sea squirt (Ciona intestinalis) were all highly intolerant to burial whilst the green urchin (Psammichinus miliaris) and the anemone (Sagartiogeton laceratus), showed intermediate and low intolerance respectively, to burial. The least intolerant, with very high survival was the Ross worm (Sabellaria spinulosa). With the exception of C. intestinalis, increasing duration and depth of burial with finer sediment fractions resulted in increased mortality for all species assessed. For C. intestinalis depth of burial and sediment fraction were found to be inconsequential since there was complete mortality of all specimens buried for more than one day. When burial emergence was assessed O. ophiura emerged most frequently, followed by P. miliaris. The former emerged most frequently from the medium and fine sediments whereas P. miliaris emerged more frequently from coarse sediment. Both A. opercularis and S. laceratus showed similar emergence responses over time, with A. opercularis emerging more frequently under coarse sediments. The frequency of emergence of S. laceratus increased with progressively finer sediment and C. intestinalis did not emerge from burial irrespective of sediment fraction or depth. Finally, and perhaps unsurprisingly, the greatest ability to emerge from burial in all other species was from shallow (2 cm) burial. Although survival was consistently highly dependent on duration and depth of burial as expected, emergence behaviour was not as easily predictable thereby confounding predictions. We conclude that responses to burial are highly species specific and therefore tolerance generalisations are likely to be oversimplifications. These data may be used to inform environmental impact models that allow forecasting of the cumulative impacts of seabed disturbance and may provide mitigation measures for the sustainable use of the seabed. PMID:26901775

  18. Sediment Burial Intolerance of Marine Macroinvertebrates.

    PubMed

    Hendrick, Vicki J; Hutchison, Zoë L; Last, Kim S

    2016-01-01

    The marine environment contains suspended particulate matter which originates from natural and anthropogenic sources. Settlement of this material can leave benthic organisms susceptible to smothering, especially if burial is sudden i.e. following storms or activities such as dredging. Their survival will depend on their tolerance to, and their ability to escape from burial. Here we present data from a multi-factorial experiment measuring burial responses incorporating duration, sediment fraction and depth. Six macroinvertebrates commonly found in sediment rich environments were selected for their commercial and/or conservation importance. Assessments revealed that the brittle star (Ophiura ophiura), the queen scallop (Aequipecten opercularis) and the sea squirt (Ciona intestinalis) were all highly intolerant to burial whilst the green urchin (Psammichinus miliaris) and the anemone (Sagartiogeton laceratus), showed intermediate and low intolerance respectively, to burial. The least intolerant, with very high survival was the Ross worm (Sabellaria spinulosa). With the exception of C. intestinalis, increasing duration and depth of burial with finer sediment fractions resulted in increased mortality for all species assessed. For C. intestinalis depth of burial and sediment fraction were found to be inconsequential since there was complete mortality of all specimens buried for more than one day. When burial emergence was assessed O. ophiura emerged most frequently, followed by P. miliaris. The former emerged most frequently from the medium and fine sediments whereas P. miliaris emerged more frequently from coarse sediment. Both A. opercularis and S. laceratus showed similar emergence responses over time, with A. opercularis emerging more frequently under coarse sediments. The frequency of emergence of S. laceratus increased with progressively finer sediment and C. intestinalis did not emerge from burial irrespective of sediment fraction or depth. Finally, and perhaps unsurprisingly, the greatest ability to emerge from burial in all other species was from shallow (2 cm) burial. Although survival was consistently highly dependent on duration and depth of burial as expected, emergence behaviour was not as easily predictable thereby confounding predictions. We conclude that responses to burial are highly species specific and therefore tolerance generalisations are likely to be oversimplifications. These data may be used to inform environmental impact models that allow forecasting of the cumulative impacts of seabed disturbance and may provide mitigation measures for the sustainable use of the seabed. PMID:26901775

  19. Lactose intolerance: an unnecessary risk for low bone density.

    PubMed

    Savaiano, Dennis

    2011-01-01

    The potential for lactose intolerance causes 25-50 million Americans and an unknown number of people around the world to avoid milk. Milk avoidance is a significant risk factor for low bone density. Individuals who avoid milk, due to intolerance or learned aversion, consume significantly less calcium and have poorer bone health and probable higher risk of osteoporosis. Lactose intolerance is easily managed by: (1) regular consumption of milk that adapts the colon bacteria and facilitates digestion of lactose; (2) consumption of yogurts and cheeses and other dairy foods low in lactose; consumption of dairy foods with meals to slow transit and maximize digestion, and use of lactose-digestive aids. As dairying spreads around the world to new markets and dairy foods become the dominant source of calcium in these markets, the potential for lactose intolerance will grow. Management of lactose intolerance globally will require both education and product development. PMID:21335997

  20. [Lactose and gluten intolerance: which to suscept?].

    PubMed

    Van Gossum, M; Mascart, F; Rickaert, F; Codden, T; Colonius, V

    2000-09-01

    Lactose intolerance affects millions of people world-wide and should be suspected specially when evaluating gastrointestinal symptoms in ethnic populations in which it is prevalent. Fortunately, once a diagnosis is made, management is fairly straightforward. The authors discuss symptoms and methods of detection and offer their recommendations for helping patients with this common disorder. Coeliac disease is the end result of 3 processes that culminate in intestinal damage: genetic predisposition, environmental factors, and immunological based inflammation. Epidemiological studies based on serologic tests suggest that the prevalence of coeliac disease has been significantly underestimated. The classic sprue syndrome of steatorrhea and malnutrition may be less common than more subtle and often monosymptomatic presentations of the disease. The authors discuss the diagnostic criteria and the clinical utility of serologic tests. PMID:11068484

  1. From 'lactose intolerance' to 'lactose nutrition'.

    PubMed

    Lukito, Widjaja; Malik, Safarina G; Surono, Ingrid S; Wahlqvist, Mark L

    2015-01-01

    The concept of lactose intolerance has become embedded in Western medicine and developing economy medicine. It is based on evidence that intestinal lactase activity persists into later childhood and throughout life in only a minority of the world's population, notably northern European-derived populations. These people have the T single nucleotide polymorphism (SNP) of the rs49882359 allele (C/T), also known as C/T-13910, the MCM6 gene which positively influences the lactase LCT gene. Other lactase persistent (LP) populations are found in Africa and the Middle East with different genetic variants. These SNPs represent co-evolution with dairying since the agricultural revolution and nutrient-dependent ecological adaptation. That said, gastrointestinal symptoms considered due to small intestinal lactose malabsorption are poorly correlated with lactase non-persistence (LNP), the situation for most people. With LNP, colonic microbiome lactase enables lactose fermentation to occur so that none is found in faeces. Whether the short chain fatty acids (SCFAs) and gases (hydrogen, carbon dioxide and methane) produced cause symptoms is dose-dependent. Up to 25 g of lactose at any one time can usually be consumed by a LNP person, but its food and meal pattern context, the microbiomic characteristics, age and other factors may alter tolerance. Thus, the notion that lactose intolerance is a disorder or disease of LNP people is misplaced and has been one of cultural perspective. What actually matters is whether a particular dairy product as normally consumed give rise to symptoms. It is, therefore, proposed that lactose tolerance tests be replaced with dairy food tolerance tests. PMID:26715078

  2. [Food intolerances caused by enzyme defects and carbohydrate malassimiliations : Lactose intolerance and Co].

    PubMed

    Schäfer, Christiane

    2016-06-01

    Apart from allergic conditions, carbohydrate malassimiliations (sugar metabolism disorders) are classified within the group of food intolerances. These dose-dependent, yet non-immunological reactions require gastroenterological or internal diagnosis following nutritional therapy. Intolerances to carbohydrates such as lactose (milk sugar) and fructose (fruit sugar) in addition to sugar alcohols (sorbitol, mannitol, lactitol etc.) have been gaining increasing attention in recent decades as they are the cause of a wide range of gastrointestinal symptoms. There are currently various options for both diagnosis and therapy that differ notably in terms of effort, costs, and efficiency. Nutritional change and patient education are the bases of therapy. Non-observance of the trigger will result in increasing complaints and possibly even more infections, e.g., diverticula, rectal disorders, bacterial miscolonization, bile acid malabsorption). For an optimal therapy, the following sugar metabolism disorders have to be differentiated: hypolactasia versus lactose maldigestion, fructose malabsorption versus fructose overload, combined lactose and fructose intolerance, and isolated adverse reactions against sorbitol.For the medical conditions listed above, a three- or four-stage treatment regimen is recommended. Extensive dietary restrictions with regard to the relevant sugar, except for lactose, should not be maintained over a longer period of time. PMID:27188621

  3. Diagnosing hypertension

    PubMed Central

    Gelfer, Mark; Dawes, Martin; Kaczorowski, Janusz; Padwal, Raj; Cloutier, Lyne

    2015-01-01

    Abstract Objective To highlight the 2015 Canadian Hypertension Education Program (CHEP) recommendations for the diagnosis and assessment of hypertension. Quality of evidence A systematic search was performed current to August 2014 by a Cochrane Collaboration librarian using the MEDLINE and PubMed databases. The search results were critically appraised by the CHEP subcommittee on blood pressure (BP) measurement and diagnosis, and evidence-based recommendations were presented to the CHEP Central Review Committee for independent review and grading. Finally, the findings and recommendations were presented to the Recommendations Task Force for discussion, debate, approval, and voting. The main recommendations are based on level II evidence. Main message Based on the most recent evidence, CHEP has made 4 recommendations in 2 broad categories for 2015 to improve BP measurement and the way hypertension is diagnosed. A strong recommendation is made to use electronic BP measurement in the office setting to replace auscultatory BP measurement. For patients with elevated office readings, CHEP is recommending early use of out-of-office BP measurement, preferably ambulatory BP measurement, in order to identify early in the process those patients with white-coat hypertension. Conclusion Improvements in diagnostic accuracy are critical to optimizing hypertension management in Canada. The annual updates provided by CHEP ensure that practitioners have up-to-date evidence-based information to inform practice. PMID:26564654

  4. HIV and Pulmonary Hypertension

    MedlinePlus

    HIV Pulmonary & PH Hypertension Did you know that if you are HIV-positive, you are at risk for pulmonary hypertension? www.PHAssociation.org About Pulmonary Hypertension PULMONARY HYPERTENSION, OR PH, is complex and often misunderstood. PH means high ...

  5. Exercise Hypertension

    PubMed Central

    Schultz, Martin G.; Sharman, James E.

    2014-01-01

    Irrespective of apparent ‘normal' resting blood pressure (BP), some individuals may experience an excessive elevation in BP with exercise (i.e. systolic BP ≥210 mm Hg in men or ≥190 mm Hg in women or diastolic BP ≥110 mm Hg in men or women), a condition termed exercise hypertension or a ‘hypertensive response to exercise' (HRE). An HRE is a relatively common condition that is identified during standard exercise stress testing; however, due to a lack of information with respect to the clinical ramifications of an HRE, little value is usually placed on such a finding. In this review, we discuss both the clinical importance and underlying physiological contributors of exercise hypertension. Indeed, an HRE is associated with an increased propensity for target organ damage and also predicts the future development of hypertension, cardiovascular events and mortality, independent of resting BP. Moreover, recent work has highlighted that some of the elevated cardiovascular risks associated with an HRE may be related to high-normal resting BP (pre-hypertension) or ambulatory ‘masked' hypertension and that an HRE may be an early warning signal of abnormal BP control that is otherwise undetected with clinic BP. Whilst an HRE may be amenable to treatment via pharmacological and lifestyle interventions, the exact physiological mechanism of an HRE remains elusive, but it is likely a manifestation of multiple factors including large artery stiffness, increased peripheral resistance, neural circulatory control and metabolic irregularity. Future research focus may be directed towards determining threshold values to denote the increased risk associated with an HRE and further resolution of the underlying physiological factors involved in the pathogenesis of an HRE. PMID:26587435

  6. Exercise Hypertension.

    PubMed

    Schultz, Martin G; Sharman, James E

    2014-05-01

    Irrespective of apparent 'normal' resting blood pressure (BP), some individuals may experience an excessive elevation in BP with exercise (i.e. systolic BP ?210 mm Hg in men or ?190 mm Hg in women or diastolic BP ?110 mm Hg in men or women), a condition termed exercise hypertension or a 'hypertensive response to exercise' (HRE). An HRE is a relatively common condition that is identified during standard exercise stress testing; however, due to a lack of information with respect to the clinical ramifications of an HRE, little value is usually placed on such a finding. In this review, we discuss both the clinical importance and underlying physiological contributors of exercise hypertension. Indeed, an HRE is associated with an increased propensity for target organ damage and also predicts the future development of hypertension, cardiovascular events and mortality, independent of resting BP. Moreover, recent work has highlighted that some of the elevated cardiovascular risks associated with an HRE may be related to high-normal resting BP (pre-hypertension) or ambulatory 'masked' hypertension and that an HRE may be an early warning signal of abnormal BP control that is otherwise undetected with clinic BP. Whilst an HRE may be amenable to treatment via pharmacological and lifestyle interventions, the exact physiological mechanism of an HRE remains elusive, but it is likely a manifestation of multiple factors including large artery stiffness, increased peripheral resistance, neural circulatory control and metabolic irregularity. Future research focus may be directed towards determining threshold values to denote the increased risk associated with an HRE and further resolution of the underlying physiological factors involved in the pathogenesis of an HRE. PMID:26587435

  7. NMR measurements of intracellular ions in hypertension

    NASA Astrophysics Data System (ADS)

    Veniero, Joseph C.; Gupta, R. K.

    1993-08-01

    The NMR methods for the measurement of intracellular free Na+, K+, Mg2+, Ca2+, and H+ are introduced. The recent literature is then presented showing applications of these methods to cells and tissues from hypertensive animal model systems, and humans with essential hypertension. The results support the hypothesis of consistent derangement of the intracellular ionic environment in hypertension. The theory that this derangement may be a common link in the disease states of high blood pressure and abnormal insulin and glucose metabolism, which are often associated clinically, is discussed.

  8. Diagnosing and Treating Intolerance to Carbohydrates in Children.

    PubMed

    Berni Canani, Roberto; Pezzella, Vincenza; Amoroso, Antonio; Cozzolino, Tommaso; Di Scala, Carmen; Passariello, Annalisa

    2016-01-01

    Intolerance to carbohydrates is relatively common in childhood, but still poorly recognized and managed. Over recent years it has come to the forefront because of progresses in our knowledge on the mechanisms and treatment of these conditions. Children with intolerance to carbohydrates often present with unexplained signs and symptoms. Here, we examine the most up-to-date research on these intolerances, discuss controversies relating to the diagnostic approach, including the role of molecular analysis, and provide new insights into modern management in the pediatric age, including the most recent evidence for correct dietary treatment. PMID:26978392

  9. Diagnosing and Treating Intolerance to Carbohydrates in Children

    PubMed Central

    Berni Canani, Roberto; Pezzella, Vincenza; Amoroso, Antonio; Cozzolino, Tommaso; Di Scala, Carmen; Passariello, Annalisa

    2016-01-01

    Intolerance to carbohydrates is relatively common in childhood, but still poorly recognized and managed. Over recent years it has come to the forefront because of progresses in our knowledge on the mechanisms and treatment of these conditions. Children with intolerance to carbohydrates often present with unexplained signs and symptoms. Here, we examine the most up-to-date research on these intolerances, discuss controversies relating to the diagnostic approach, including the role of molecular analysis, and provide new insights into modern management in the pediatric age, including the most recent evidence for correct dietary treatment. PMID:26978392

  10. Neural Correlates of Intolerance of Uncertainty in Clinical Disorders.

    PubMed

    Wever, Mirjam; Smeets, Paul; Sternheim, Lot

    2015-01-01

    Intolerance of uncertainty is a key contributor to anxiety-related disorders. Recent studies highlight its importance in other clinical disorders. The link between its clinical presentation and the underlying neural correlates remains unclear. This review summarizes the emerging literature on the neural correlates of intolerance of uncertainty. In conclusion, studies focusing on the neural correlates of this construct are sparse, and findings are inconsistent across disorders. Future research should identify neural correlates of intolerance of uncertainty in more detail. This may unravel the neurobiology of a wide variety of clinical disorders and pave the way for novel therapeutic targets. PMID:26185902

  11. Chronic sulforaphane oral treatment accentuates blood glucose impairment and may affect GLUT3 expression in the cerebral cortex and hypothalamus of rats fed with a highly palatable diet.

    PubMed

    Souza, C G; Riboldi, B P; Hansen, F; Moreira, J D; Souza, D G; de Assis, A M; Brum, L M; Perry, M L S; Souza, D O

    2013-08-01

    Obesity and insulin resistance are the key factors underlying the etiology of major health problems such as hypertension, diabetes and stroke. These important health issues lead researchers to investigate new approaches to prevent and treat obesity and insulin resistance. Good candidates are the phytochemical compounds that have been extensively studied in the field. Therefore, the aim of this study was to test whether sulforaphane (SFN, 1 mg kg⁻¹, 4 months treatment), a potent inducer of antioxidant enzymes present in cruciferous vegetables, had some beneficial effects on obesity and insulin resistance induced by a highly palatable (HP) diet in male Wistar rats. Glucose tolerance, serum and hepatic lipid levels, lipid profile, ALT, AST, urea and creatinine, GLUT1 and GLUT3 levels in the cerebral cortex, hippocampus and hypothalamus were analyzed. Glucose tolerance was lower in the HP diet groups, especially in the HP group treated with SFN. Except for the liver triacylglycerols, no differences were found in serum lipids, hepatic and kidney markers of the HP diet groups. Although expression of GLUT1 was similar between groups for all three brain structures analyzed, expression of GLUT3 in the cortex and hypothalamus had a tendency to decrease in the HP diet group treated with SFN. In conclusion, SFN at the specific dose was able to accentuate glucose intolerance and may affect GLUT3 expression in the cerebral cortex and hypothalamus. PMID:23797263

  12. Hypertensive Crisis

    MedlinePlus

    ... hypertensive crisis . If you can't access the emergency medical services (EMS), have someone drive you to the hospital ... 1-1. If you can't access the emergency medical services (EMS), have someone drive you to the hospital ...

  13. Portopulmonary hypertension.

    PubMed

    Lv, Yong; Han, Guohong; Fan, Daiming

    2016-07-01

    Portopulmonary hypertension (PoPH) refers to the condition that pulmonary arterial hypertension (PAH) occur in the stetting of portal hypertension. The development of PoPH is thought to be independent of the severity of portal hypertension or the etiology or severity of liver disease. PoPH results from excessive vasoconstriction, vascular remodeling, and proliferative and thrombotic events within the pulmonary circulation that lead to progressive right ventricular failure and ultimately to death. Untreated PoPH is associated with a poor prognosis. As PoPH is frequently asymptomatic or symptoms are generally non-specific, patients should be actively screened for the presence of PoPH. Two-dimensional transthoracic echocardiography is a useful non-invasive screening tool, but a definitive diagnosis requires invasive hemodynamic confirmation by right heart catheterization. Despite a dearth of randomized, prospective data, an ever-expanding clinical experience shows that patients with PoPH benefit from therapy with PAH-specific medications including with endothelin receptor antagonists, phosphodiesterase-5 inhibitors, and/or prostanoids. Due to high perioperative mortality, transplantation should be avoided in those patients who have severe PoPH that is refractory to medical therapy. PMID:27002212

  14. Clinical evaluation, biochemistry and genetic polymorphism analysis for the diagnosis of lactose intolerance in a population from northeastern Brazil

    PubMed Central

    Ponte, Paulo Roberto Lins; de Medeiros, Pedro Henrique Quintela Soares; Havt, Alexandre; Caetano, Joselany Afio; Cid, David A C; de Moura Gondim Prata, Mara; Soares, Alberto Melo; Guerrant, Richard L; Mychaleckyj, Josyf; Lima, Aldo Ângelo Moreira

    2016-01-01

    OBJECTIVE: This work aimed to evaluate and correlate symptoms, biochemical blood test results and single nucleotide polymorphisms for lactose intolerance diagnosis. METHOD: A cross-sectional study was conducted in Fortaleza, Ceará, Brazil, with a total of 119 patients, 54 of whom were lactose intolerant. Clinical evaluation and biochemical blood tests were conducted after lactose ingestion and blood samples were collected for genotyping evaluation. In particular, the single nucleotide polymorphisms C>T-13910 and G>A-22018 were analyzed by restriction fragment length polymorphism/polymerase chain reaction and validated by DNA sequencing. RESULTS: Lactose-intolerant patients presented with more symptoms of flatulence (81.4%), bloating (68.5%), borborygmus (59.3%) and diarrhea (46.3%) compared with non-lactose-intolerant patients (p<0.05). We observed a significant association between the presence of the alleles T-13910 and A-22018 and the lactose-tolerant phenotype (p<0.05). After evaluation of the biochemical blood test results for lactose, we found that the most effective cutoff for glucose levels obtained for lactose malabsorbers was <15 mg/dL, presenting an area under the receiver operating characteristic curve greater than 80.3%, with satisfactory values for sensitivity and specificity. CONCLUSIONS: These data corroborate the association of these single nucleotide polymorphisms (C>T-13910 and G>A-22018) with lactose tolerance in this population and suggest clinical management for patients with lactose intolerance that considers single nucleotide polymorphism detection and a change in the biochemical blood test cutoff from <25 mg/dL to <15 mg/dL. PMID:26934237

  15. Upregulation of NOS by simulated microgravity, potential cause of orthostatic intolerance.

    PubMed

    Vaziri, N D; Ding, Y; Sangha, D S; Purdy, R E

    2000-07-01

    Prolonged exposure to microgravity during spaceflight or extended bed rest results in cardiovascular deconditioning, marked by orthostatic intolerance and hyporesponsiveness to vasopressors. Earlier studies primarily explored fluid and electrolyte balance and baroreceptor and vasopressor systems in search of a possible mechanism. Given the potent vasodilatory and natriuretic actions of nitric oxide (NO), we hypothesized that cardiovascular adaptation to microgravity may involve upregulation of the NO system. Male Wistar rats were randomly assigned to a control group or a group subjected to simulated microgravity by hindlimb unloading (HU) for 20 days. Tissues were harvested after death for determination of total nitrate and nitrite (NOx) as well as endothelial (e), inducible (i), and neuronal (n) NO synthase (NOS) proteins by Western blot. Separate subgroups were used to test blood pressure response to norepinephrine and the iNOS inhibitor aminoguanidine. Compared with controls, the HU group showed a significant increase in tissue NOx content and an upregulation of iNOS protein abundance in thoracic aorta, heart, and kidney and of nNOS protein expression in the brain and kidney but no discernible change in eNOS expression. This was associated with marked attenuation of hypertensive response to norepinephrine and a significant increase in hypertensive response to aminoguanidine, suggesting enhanced iNOS-derived NO generation in the HU group. Upregulation of these NOS isotypes can contribute to cardiovascular adaptation to microgravity by promoting vasodilatory tone and natriuresis and depressing central sympathetic outflow. If true in humans, short-term administration of an iNOS inhibitor may ameliorate orthostatic intolerance in returning astronauts and patients after extended bed rest. PMID:10904069

  16. Endogenous circulating sympatholytic factor in orthostatic intolerance

    NASA Technical Reports Server (NTRS)

    Shapiro, R. E.; Winters, B.; Hales, M.; Barnett, T.; Schwinn, D. A.; Flavahan, N.; Berkowitz, D. E.

    2000-01-01

    Sympathotonic orthostatic hypotension (SOH) is an idiopathic syndrome characterized by tachycardia, hypotension, elevated plasma norepinephrine, and symptoms of orthostatic intolerance provoked by assumption of an upright posture. We studied a woman with severe progressive SOH with blood pressure unresponsive to the pressor effects of alpha(1)-adrenergic receptor (AR) agonists. We tested the hypothesis that a circulating factor in this patient interferes with vascular adrenergic neurotransmission. Preincubation of porcine pulmonary artery vessel rings with patient plasma produced a dose-dependent inhibition of vasoconstriction to phenylephrine in vitro, abolished vasoconstriction to direct electrical stimulation, and had no effect on nonadrenergic vasoconstrictive stimuli (endothelin-1), PGF-2alpha (or KCl). Preincubation of vessels with control plasma was devoid of these effects. SOH plasma inhibited the binding of an alpha(1)-selective antagonist radioligand ([(125)I]HEAT) to membrane fractions derived from porcine pulmonary artery vessel rings, rat liver, and cell lines selectively overexpressing human ARs of the alpha(1B) subtype but not other AR subtypes (alpha(1A) and alpha(1D)). We conclude that a factor in SOH plasma can selectively and irreversibly inhibit adrenergic ligand binding to alpha(1B) ARs. We propose that this factor contributes to a novel pathogenesis for SOH in this patient. This patient's syndrome represents a new disease entity, and her plasma may provide a unique tool for probing the selective functions of alpha(1)-ARs.

  17. Postural Tachycardia Syndrome: Beyond Orthostatic Intolerance.

    PubMed

    Garland, Emily M; Celedonio, Jorge E; Raj, Satish R

    2015-09-01

    Postural tachycardia syndrome (POTS) is a form of chronic orthostatic intolerance for which the hallmark physiological trait is an excessive increase in heart rate with assumption of upright posture. The orthostatic tachycardia occurs in the absence of orthostatic hypotension and is associated with a >6-month history of symptoms that are relieved by recumbence. The heart rate abnormality and orthostatic symptoms should not be caused by medications that impair autonomic regulation or by debilitating disorders that can cause tachycardia. POTS is a "final common pathway" for a number of overlapping pathophysiologies, including an autonomic neuropathy in the lower body, hypovolemia, elevated sympathetic tone, mast cell activation, deconditioning, and autoantibodies. Not only may patients be affected by more than one of these pathophysiologies but also the phenotype of POTS has similarities to a number of other disorders, e.g., chronic fatigue syndrome, Ehlers-Danlos syndrome, vasovagal syncope, and inappropriate sinus tachycardia. POTS can be treated with a combination of non-pharmacological approaches, a structured exercise training program, and often some pharmacological support. PMID:26198889

  18. Systemic lactose intolerance: a new perspective on an old problem.

    PubMed

    Matthews, S B; Waud, J P; Roberts, A G; Campbell, A K

    2005-03-01

    Intolerance to certain foods can cause a range of gut and systemic symptoms. The possibility that these can be caused by lactose has been missed because of "hidden" lactose added to many foods and drinks inadequately labelled, confusing diagnosis based on dietary removal of dairy foods. Two polymorphisms, C/T13910 and G/A22018, linked to hypolactasia, correlate with breath hydrogen and symptoms after lactose. This, with a 48 hour record of gut and systemic symptoms and a six hour breath hydrogen test, provides a new approach to the clinical management of lactose intolerance. The key is the prolonged effect of dietary removal of lactose. Patients diagnosed as lactose intolerant must be advised of "risk" foods, inadequately labelled, including processed meats, bread, cake mixes, soft drinks, and lagers. This review highlights the wide range of systemic symptoms caused by lactose intolerance. This has important implications for the management of irritable bowel syndrome, and for doctors of many specialties. PMID:15749792

  19. The role of colonic metabolism in lactose intolerance.

    PubMed

    He, T; Venema, K; Priebe, M G; Welling, G W; Brummer, R-J M; Vonk, R J

    2008-08-01

    Lactose maldigestion and intolerance affect a large part of the world population. The underlying factors of lactose intolerance are not fully understood. In this review, the role of colonic metabolism is discussed, i.e. fermentation of lactose by the colonic microbiota, colonic processing of the fermentation metabolites and how these processes would play a role in the pathophysiology of lactose intolerance. We suggest that the balance between the removal and production rate of osmotic-active components (lactose, and intermediate metabolites, e.g. lactate, succinate, etc.) in the colon is a key factor in the development of symptoms. The involvement of the colon may provide the basis for designing new targeted strategies for dietary and clinical management of lactose intolerance. PMID:18573099

  20. Intolerance of Ambiguity and Student Performance in Social Work Education.

    ERIC Educational Resources Information Center

    Davis, Liane V.; Sherman, Edmund

    1987-01-01

    Social workers must assist people in coping with complex, often apparently insoluble, problems. Data are presented on the relationship between intolerance of ambiguity and a variety of performance and preference measures of 212 social work students. (Author/MH)

  1. Lactose Intolerance in Adults: Biological Mechanism and Dietary Management.

    PubMed

    Deng, Yanyong; Misselwitz, Benjamin; Dai, Ning; Fox, Mark

    2015-09-01

    Lactose intolerance related to primary or secondary lactase deficiency is characterized by abdominal pain and distension, borborygmi, flatus, and diarrhea induced by lactose in dairy products. The biological mechanism and lactose malabsorption is established and several investigations are available, including genetic, endoscopic and physiological tests. Lactose intolerance depends not only on the expression of lactase but also on the dose of lactose, intestinal flora, gastrointestinal motility, small intestinal bacterial overgrowth and sensitivity of the gastrointestinal tract to the generation of gas and other fermentation products of lactose digestion. Treatment of lactose intolerance can include lactose-reduced diet and enzyme replacement. This is effective if symptoms are only related to dairy products; however, lactose intolerance can be part of a wider intolerance to variably absorbed, fermentable oligo-, di-, monosaccharides and polyols (FODMAPs). This is present in at least half of patients with irritable bowel syndrome (IBS) and this group requires not only restriction of lactose intake but also a low FODMAP diet to improve gastrointestinal complaints. The long-term effects of a dairy-free, low FODMAPs diet on nutritional health and the fecal microbiome are not well defined. This review summarizes recent advances in our understanding of the genetic basis, biological mechanism, diagnosis and dietary management of lactose intolerance. PMID:26393648

  2. Lactose malabsorption and intolerance: pathogenesis, diagnosis and treatment.

    PubMed

    Misselwitz, Benjamin; Pohl, Daniel; Frhauf, Heiko; Fried, Michael; Vavricka, Stephan R; Fox, Mark

    2013-06-01

    Lactose malabsorption is a common condition caused by reduced expression or activity of lactase in the small intestine. In such patients, lactose intolerance is characterized by abdominal symptoms (e.g. nausea, bloating, and pain) after ingestion of dairy products. The genetic basis of lactose malabsorption is established and several tests for this condition are available, including genetic, endoscopic, and H2-breath tests. In contrast, lactose intolerance is less well understood. Recent studies show that the risk of symptoms after lactose ingestion depends on the dose of lactose, lactase expression, intestinal flora, and sensitivity of the gastrointestinal tract. Lactose intolerance has recently been defined as symptoms developing after ingestion of lactose which do not develop after placebo challenge in a person with lactose maldigestion. Such blinded testing might be especially important in those with functional gastrointestinal diseases in whom self-reported lactose intolerance is common. However, placebo-controlled testing is not part of current clinical practice. Updated protocols and high-quality outcome studies are needed. Treatment options of lactose intolerance include lactose-reduced diet and enzyme replacement. Documenting the response to multiple doses can guide rational dietary management; however, the clinical utility of this strategy has not been tested. This review summarizes the genetic basis, diagnosis, and treatment of lactose malabsorption and intolerance. PMID:24917953

  3. Lactose malabsorption and intolerance: pathogenesis, diagnosis and treatment

    PubMed Central

    Pohl, Daniel; Frühauf, Heiko; Fried, Michael; Vavricka, Stephan R; Fox, Mark

    2013-01-01

    Lactose malabsorption is a common condition caused by reduced expression or activity of lactase in the small intestine. In such patients, lactose intolerance is characterized by abdominal symptoms (e.g. nausea, bloating, and pain) after ingestion of dairy products. The genetic basis of lactose malabsorption is established and several tests for this condition are available, including genetic, endoscopic, and H2-breath tests. In contrast, lactose intolerance is less well understood. Recent studies show that the risk of symptoms after lactose ingestion depends on the dose of lactose, lactase expression, intestinal flora, and sensitivity of the gastrointestinal tract. Lactose intolerance has recently been defined as symptoms developing after ingestion of lactose which do not develop after placebo challenge in a person with lactose maldigestion. Such blinded testing might be especially important in those with functional gastrointestinal diseases in whom self-reported lactose intolerance is common. However, placebo-controlled testing is not part of current clinical practice. Updated protocols and high-quality outcome studies are needed. Treatment options of lactose intolerance include lactose-reduced diet and enzyme replacement. Documenting the response to multiple doses can guide rational dietary management; however, the clinical utility of this strategy has not been tested. This review summarizes the genetic basis, diagnosis, and treatment of lactose malabsorption and intolerance. PMID:24917953

  4. Lactose Intolerance in Adults: Biological Mechanism and Dietary Management

    PubMed Central

    Deng, Yanyong; Misselwitz, Benjamin; Dai, Ning; Fox, Mark

    2015-01-01

    Lactose intolerance related to primary or secondary lactase deficiency is characterized by abdominal pain and distension, borborygmi, flatus, and diarrhea induced by lactose in dairy products. The biological mechanism and lactose malabsorption is established and several investigations are available, including genetic, endoscopic and physiological tests. Lactose intolerance depends not only on the expression of lactase but also on the dose of lactose, intestinal flora, gastrointestinal motility, small intestinal bacterial overgrowth and sensitivity of the gastrointestinal tract to the generation of gas and other fermentation products of lactose digestion. Treatment of lactose intolerance can include lactose-reduced diet and enzyme replacement. This is effective if symptoms are only related to dairy products; however, lactose intolerance can be part of a wider intolerance to variably absorbed, fermentable oligo-, di-, monosaccharides and polyols (FODMAPs). This is present in at least half of patients with irritable bowel syndrome (IBS) and this group requires not only restriction of lactose intake but also a low FODMAP diet to improve gastrointestinal complaints. The long-term effects of a dairy-free, low FODMAPs diet on nutritional health and the fecal microbiome are not well defined. This review summarizes recent advances in our understanding of the genetic basis, biological mechanism, diagnosis and dietary management of lactose intolerance. PMID:26393648

  5. Glucose metabolism in patients with Cushing's syndrome.

    PubMed

    Bowes, S B; Benn, J J; Scobie, I N; Umpleby, A M; Lowy, C; Sönksen, P H

    1991-04-01

    Glucose intolerance, sometimes severe enough to cause frank diabetes mellitus, is a frequent feature of Cushing's syndrome. The primary cause of the hyperglycaemia, whether due to glucose over-production or under-utilization, remains unresolved. We therefore measured glucose turnover using an intravenous bolus of 3-3H glucose in 14 normoglycaemic patients with Cushing's syndrome and 14 control subjects. Seven of the patients with Cushing's syndrome were also restudied post-operatively. Plasma glucose concentrations were similar in all three groups whereas glucose metabolic clearance rate (MCR) (1.80 +/- 0.06 ml/min/kg) and glucose turnover rate (9.09 +/- 0.36 mumol/min/kg) were significantly reduced in patients with Cushing's syndrome compared to normal subjects (2.21 +/- 0.1; P less than 0.001; 10.90 +/- 0.50; P less than 0.01) and rose post-operatively to normal values (2.35 +/- 0.14 ml/min/kg; 11.07 +/- 0.48 mumol/min/kg). We conclude from these results that the hyperglycaemia sometimes found in Cushing's syndrome may be primarily due to decreased utilization rather than increased glucose production. PMID:1879061

  6. Glucose tolerance, insulin release, and insulin binding to monocytes in kidney transplant recipients

    SciTech Connect

    Briggs, W.A.; Wielechowski, K.S.; Mahajan, S.K.; Migdal, S.D.; McDonald, F.D.

    1982-03-01

    In order to evaluate glucose tolerance following renal transplantation, intravenous glucose tolerance tests (IVGTT), with evaluation of hormonal responses to the intravenous glucose load and percent specific /sup 125/I-insulin binding to peripheral blood monocytes, were studied in eight clinically stable kidney transplant recipients. For comparison purposes, identical studies were done in eight control subjects and seven clinically stable hemodialysis patients. One transplant recipient was glucose intolerant, with fasting hyperglycemia, elevated HbA1C, and abnormal glucose decay constant. Impaired pancreatic insulin release appeared to be the major factor accounting for his glucose intolerance. The seven glucose-tolerant transplant recipients had significantly increased insulin release during IVGTT compared to control subjects, and significant correlations were found among insulin release, glucose decay constant, and fasting blood sugar in those patients. Insulin binding to monocytes was significantly greater in transplant recipients than control subjects due to an increase in insulin binding capacity per cell. A significant correlation was found between percent specific /sup 125/I-insulin binding and steroid dose, expressed as mg/kg body weight/day, in those patients. Thus, chronic steroid administration does not cause glucose intolerance in transplant recipients who manifest steroid-associated increases in pancreatic insulin release and cellular insulin binding capacity.

  7. Improvement of diabetes, obesity and hypertension in type 2 diabetic KKA{sup y} mice by bis(allixinato)oxovanadium(IV) complex

    SciTech Connect

    Adachi, Yusuke; Yoshikawa, Yutaka; Yoshida, Jiro; Kodera, Yukihiro . E-mail: kodera_y@wakunaga.co.jp; Katoh, Akira . E-mail: katoh@st.seikei.ac.jp; Takada, Jitsuya . E-mail: takada@hl.rri.kyoto-u.ac.jp; Sakurai, Hiromu . E-mail: sakurai@mb.kyoto-phu.ac.jp

    2006-07-07

    Previously, we found that bis(allixinato)oxovanadium(IV) (VO(alx){sub 2}) exhibits a potent hypoglycemic activity in type 1-like diabetic mice. Since the enhancement of insulin sensitivity is involved in one of the mechanisms by which vanadium exerts its anti-diabetic effects, VO(alx){sub 2} was further tested in type 2 diabetes with low insulin sensitivity. The effect of oral administration of VO(alx){sub 2} was examined in obesity-linked type 2 diabetic KKA{sup y} mice. Treatment of VO(alx){sub 2} for 4 weeks normalized hyperglycemia, glucose intolerance, hyperinsulinemia, hypercholesterolemia and hypertension in KKA{sup y} mice; however, it had no effect on hypoadiponectinemia. VO(alx){sub 2} also improved hyperleptinemia, following attenuation of obesity in KKA{sup y} mice. This is the first example in which a vanadium compound improved leptin resistance in type 2 diabetes by oral administration. On the basis of these results, VO(alx){sub 2} is proposed to enhance not only insulin sensitivity but also leptin sensitivity, which in turn improves diabetes, obesity and hypertension in an obesity-linked type 2 diabetic animal.

  8. PAC1 receptor–deficient mice display impaired insulinotropic response to glucose and reduced glucose tolerance

    PubMed Central

    Jamen, Françoise; Persson, Kristin; Bertrand, Gyslaine; Rodriguez-Henche, Nieves; Puech, Raymond; Bockaert, Joël; Ahrén, Bo; Brabet, Philippe

    2000-01-01

    Pituitary adenylate cyclase–activating polypeptide (PACAP) is a ubiquitous neuropeptide of the vasoactive intestinal peptide (VIP) family that potentiates glucose-stimulated insulin secretion. Pancreatic β cells express two PACAP receptor subtypes, a PACAP-preferring (PAC1) and a VIP-shared (VPAC2) receptor. We have applied a gene targeting approach to create a mouse lacking the PAC1 receptor (PAC1–/–). These mice were viable and normoglycemic, but exhibited a slight feeding hyperinsulinemia. In vitro, in the isolated perfused pancreas, the insulin secretory response to PACAP was reduced by 50% in PAC1–/– mice, whereas the response to VIP was unaffected. In vivo, the insulinotropic action of PACAP was also acutely reduced, and the peptide induced impairment of glucose tolerance after an intravenous glucose injection. This demonstrates that PAC1 receptor is involved in the insulinotropic action of the peptide. Moreover, PAC1–/– mice exhibited reduced glucose-stimulated insulin secretion in vitro and in vivo, showing that the PAC1 receptor is required to maintain normal insulin secretory responsiveness to glucose. The defective insulinotropic action of glucose was associated with marked glucose intolerance after both intravenous and gastric glucose administration. Thus, these results are consistent with a physiological role for the PAC1 receptor in glucose homeostasis, notably during food intake. PMID:10792006

  9. Glucose Tests

    MedlinePlus

    ... usually with frequent urination Fatigue Blurred vision Slow-healing wounds or infections or symptoms of low blood glucose ( hypoglycemia ), such as: Sweating Hunger Trembling Anxiety Confusion Blurred vision Diabetics are often required to self-check their glucose, up to several times a ...

  10. Pulmonary Arterial Hypertension

    MedlinePlus

    ... What Is Pulmonary Hypertension? To understand pulmonary hypertension (PH) it helps to understand how blood ows throughout ... is too high, it is called pulmonary hypertension (PH). How the pressure in the right side of ...

  11. Types of Pulmonary Hypertension

    MedlinePlus

    ... Hypertension The World Health Organization divides pulmonary hypertension (PH) into five groups. These groups are organized based ... lungs. Group 2 Pulmonary Hypertension Group 2 includes PH with left heart disease. Conditions that affect the ...

  12. Osteocalcin as a hormone regulating glucose metabolism

    PubMed Central

    Kanazawa, Ippei

    2015-01-01

    The number of patients with osteoporosis and diabetes is rapidly increasing all over the world. Bone is recently recognized as an endocrine organ. Accumulating evidence has shown that osteocalcin, which is specifically expressed in osteoblasts and secreted into the circulation, regulates glucose homeostasis by stimulating insulin expression in pancreas and adiponectin expression in adipocytes, resulting in improving glucose intolerance. On the other hand, insulin and adiponectin stimulate osteocalcin expression in osteoblasts, suggesting that positive feedforward loops exist among bone, pancreas, and adipose tissue. In addition, recent studies have shown that osteocalcin enhances insulin sensitivity and the differentiation in muscle, while secreted factors from muscle, myokines, regulate bone metabolism. These findings suggest that bone metabolism and glucose metabolism are associated with each other through the action of osteocalcin. In this review, I describe the role of osteocalcin in the interaction among bone, pancreas, brain, adipose tissue, and muscle. PMID:26722618

  13. Familial aquagenic urticaria associated with familial lactose intolerance.

    PubMed

    Treudler, Regina; Tebbe, Beate; Steinhoff, Matthias; Orfanos, Constantin E

    2002-10-01

    Aquagenic urticaria is a rare disorder characterized by the occurrence of pruritus and wheals after temporary contact with water. The familial occurrence of aquagenic urticaria over 3 generations is reported here in association with familial lactose intolerance, a condition in which the enzyme lactase encoded on chromosome 2, is deficient. In two patients, a young man and his mother, we verified the appearance of pruritic hives 5 to 10 minutes after contact with water of any temperature. Other types of physical urticaria were absent, and mastocytosis was excluded by extensive laboratory investigations; lactose intolerance was confirmed in both patients by H(2)-exhalation test. In these patients the clinical symptoms did not respond to antihistamines or UV-radiation therapy. Four other members of the family had wheals from water contact, two of whom had lactose intolerance. Two other members had lactose intolerance only. Although the association of aquagenic urticaria with lactose intolerance may be coincidental, attention is drawn to the fact that the 2 conditions, known to be familial, may coexist in the same family, possibly based on an association of gene loci. PMID:12271310

  14. Dietary treatment of lactose intolerance in infants and children.

    PubMed

    Sinden, A A; Sutphen, J L

    1991-12-01

    During the past several years there have been many reports of alternative dietary therapies for primary and secondary lactose intolerance. We have learned that it is useful to feed through most episodes of mild diarrhea that previously would have been treated with clear liquid diets. Infant formulas, including both soy-protein and hydrolysate formulas with specially designed carbohydrate, protein, and fat components, are available to treat the infant with diarrheal syndromes and secondary lactase deficiency. Also, the diet can be supplemented with lactase. Specialized lactose-reduced products as well as cultured and fermented dairy products may be used in varying degrees for lactose-intolerant children. The ingestion of milk with food and fiber components in the diet has also been shown to improve symptoms of lactose intolerance. This review summarizes the essentials of diagnosis of and dietary therapy for lactose intolerance. Our findings indicate that a number of specialized formulas and products are available for successful dietary management of lactose intolerance in infants and children. PMID:1960350

  15. Left atrial volume index is an independent predictor of hypertensive response to exercise in patients with hypertension.

    PubMed

    Lee, Sang-Eun; Youn, Jong-Chan; Lee, Hye Sun; Park, Sungha; Lee, Sang-Hak; Cho, In-Jeong; Shim, Chi Young; Hong, Geu-Ru; Choi, Donghoon; Kang, Seok-Min

    2015-02-01

    A hypertensive response to exercise (HRE) is known to be associated with higher risk of heart failure and future cardiovascular events in patients with hypertension. Left atrial volume index (LAVI) is associated with the diastolic dysfunction, indicating exercise intolerance. Therefore, we investigated whether LAVI is relevant to HRE during cardiopulmonary exercise test (CPET). We studied 118 consecutive hypertensive patients (61 men, 5711 years) and 45 normotensive control subjects (16 men, 548 years). Clinical characteristics, CPET, echocardiographic and laboratory findings were assessed at the time of enrollment. HRE was defined as maximum systolic blood pressure (SBP)?210?mm?Hg in men and ?190?mm?Hg in women. HRE was more prevalent in hypertensive patients compared with normotensive control subjects (50.8% vs. 20.0%, P<0.001). Age and baseline SBP were shown to be associated with HRE in normotensive control subjects, as were baseline SBP and LAVI in hypertensive group. In multivariate analysis, LAVI was found to be an independent predictor of HRE in hypertensive patients (P=0.020) but not in normotensive control subjects (P=0.936) when controlled for age, sex, body mass index and peak oxygen consumption. Higher LAVI, reflecting the duration and severity of increased left atrial pressure is independently associated with HRE in hypertensive patients, but not in normotensive control subjects. PMID:25253581

  16. Essential Hypertension vs. Secondary Hypertension Among Children

    PubMed Central

    Banker, Ashish; Shete, Sanjay; Hashmi, Syed Sharukh; Tyson, John E.; Barratt, Michelle S.; Hecht, Jacqueline T.; Milewicz, Diane M.; Boerwinkle, Eric

    2015-01-01

    BACKGROUND The aim was to determine the proportions and correlates of essential hypertension among children in a tertiary pediatric hypertension clinic. METHODS We evaluated 423 consecutive children and collected demographic and clinical history by retrospective chart review. RESULTS We identified 275 (65%) hypertensive children (blood pressure >95th percentile per the “Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and Adolescents”) from 423 children referred to the clinic for history of elevated blood pressure. The remainder of the patients had normotension (11%), white coat hypertension (11%), prehypertension (10%), and pending diagnosis (3%). Among the 275 hypertensive children, 43% (n = 119; boys = 56%; median age = 12 years; range = 3–17 years) had essential hypertension and 57% (n = 156; boys = 66%; median age = 9 years; range = 0.08–19 years) had secondary hypertension. When compared with those with secondary hypertension, those with essential hypertension had a significantly older age at diagnosis (P = 0.0002), stronger family history of hypertension (94% vs. 68%; P < 0.0001), and lower prevalence of preterm birth (20% vs. 46%; P < 0.001). There was a bimodal distribution of age of diagnosis in those with secondary hypertension. CONCLUSIONS The phenotype of essential hypertension can present as early as 3 years of age and is the predominant form of hypertension in children after age of 6 years. Among children with hypertension, those with essential hypertension present at an older age, have a stronger family history of hypertension, and have lower prevalence of preterm birth. PMID:24842390

  17. Sodium Oxybate Intolerance Associated with Familial Serum Acylcarnitine Elevation

    PubMed Central

    Berner, Jon

    2013-01-01

    Our case describes clinical features of two families defined by joint phenotypes: sodium oxybate intolerance and elevated serum acylcarnitines. Oxybate intolerance variably presents as either cervical dystonia or sleep-related eating disorder. Our objective is to identify biological markers which predict a poor response to sodium oxybate as a treatment for disturbed sleep. Familial inheritance pattern, genotype analysis, multiorgan system involvement, and response to treatment suggest the presence of a secondary cause of fatty oxidation defect, i.e., mitochondrial disorder. Our case report supports the possible conclusion that variance in human mitochondrial metabolism may affect sodium oxybate tolerability. Citation: Berner J. Sodium oxybate intolerance associated with familial serum acylcarnitine elevation. J Clin Sleep Med 2013;9(1):71-72. PMID:23319908

  18. Management of malnourished children with acute diarrhoea and sugar intolerance.

    PubMed

    Beau, J P; Fontaine, O; Garenne, M

    1990-04-01

    A protocol of nutritional rehabilitation using fermented milk, vegetable oil and caster sugar has been tested on 54 Senegalese children, aged 6-36 months, admitted with acute diarrhoea and malnutrition. At the time of admission, 39 per cent of children were dehydrated and 26 per cent had sugar intolerance. In the course of treatment three went home against medical advice and one died from acute pneumonia with respiratory-heart failure. Among the cases of marasmus there were no differences in mean weight gain between children with sugar intolerance and others despite a longer duration of diarrhoea in the first group. Furthermore, the experimental protocol has never been compromised because of worsening diarrhoea or weight loss. These results indicate that a formula based on fermented milk together with oral rehydration can be used to treat malnourished children with acute diarrhoea and sugar intolerance. PMID:2355409

  19. Management of malnourished children with acute diarrhoea and sugar intolerance.

    PubMed

    Beau, J P; Fontaine, O; Garenne, M

    1989-12-01

    A protocol of nutritional rehabilitation using fermented milk, vegetable oil, and castor sugar has been tested on 54 Senegalese children age 6-36 months admitted with acute diarrhoea and malnutrition. At time of admission, 39 per cent of children were dehydrated and 26 per cent had sugar intolerance. In the course of treatment three absconded and one died from acute pneumonia with respiratory and heart failure. Among those with marasmus there were no differences in mean weight gains between children with sugar intolerance and others, despite a longer duration of diarrhoea in the first group. Furthermore, the treatment protocol has never been compromised because of worsening diarrhoea or weight loss. These results indicate that a formula based on fermented milk together with oral rehydration can be used to treat malnourished children with acute diarrhoea and sugar intolerance. PMID:2514280

  20. Recent advances in the management of lactose intolerance.

    PubMed

    Savaiano, D A; Kotz, C

    1989-01-01

    Lactose intolerance is a concern for the majority of the world's population. Persons who experience symptoms following the consumption of milk should consult with their physician. Symptoms may be eliminated or reduced with good dietary management that includes: Limiting milk consumption to one glass at a time. Drinking milk with other foods rather than alone. Eating yogurts instead of fluid milk. Using enzyme tablets to predigest the lactose in milk or to supplement the body's own lactase. Possibly eating small amounts of dairy foods each day to adapt the colonic bacteria. For an additional review of the research findings on lactose intolerance and milk drinking, the reader is directed to reference 4, a very recent and complete review by Scrimshaw and Murray. For information on dietary management of lactose intolerance suitable for the consumer, contact your local affiliate of the National Dairy Council. PMID:2656797

  1. When to suspect lactose intolerance. Symptomatic, ethnic, and laboratory clues.

    PubMed

    Srinivasan, R; Minocha, A

    1998-09-01

    Lactose intolerance is widespread, with adult-type hypolactasia being the predominant cause of lactose malabsorption. Daily ingestion of less than 240 mL of milk is well tolerated by most lactose-intolerant adults. Some persons with normal lactase activity may become symptomatic on consumption of products containing lactose. Lactose maldigestion may coexist in adults with irritable bowel syndrome and in children with recurrent abdominal pain. Management consists primarily of dietary changes. People who avoid dairy products should receive calcium supplementation and should be advised to read ingredient labels carefully. Several lactase replacement products are available, but their efficacy varies. PMID:9742907

  2. Dairy Intake, Dietary Adequacy, and Lactose Intolerance12

    PubMed Central

    Heaney, Robert P.

    2013-01-01

    Despite repeated emphasis in the Dietary Guidelines for Americans on the importance of calcium in the adult American diet and the recommendation to consume 3 dairy servings a day, dairy intake remains well below recommendations. Insufficient health professional awareness of the benefits of calcium and concern for lactose intolerance are among several possible reasons, This mini-review highlights both the role of calcium (and of dairy, its principal source in modern diets) in health maintenance and reviews the means for overcoming lactose intolerance (real or perceived). PMID:23493531

  3. Cardiovascular Characteristics in Subjects With Increasing Levels of Abnormal Glucose Regulation

    PubMed Central

    Capaldo, Brunella; Di Bonito, Procolo; Iaccarino, Michele; Roman, Mary J.; Lee, Elisa T.; Devereux, Richard B.; Riccardi, Gabriele; Howard, Barbara V.; de Simone, Giovanni

    2013-01-01

    OBJECTIVE To evaluate whether impaired fasting glucose (IFG) or the combination of IFG and impaired glucose tolerance (IGT) is associated with progressive abnormalities of cardiac geometry and function. RESEARCH DESIGN AND METHODS We studied 562 nondiabetic (311 women), nonhypertensive participants of the second Strong Heart Study exam, without prevalent cardiovascular (CV) disease and with estimated glomerular filtration rate ≥60 mL/min/1.73 m2 (age 46–65 years, 198 with isolated IFG [35%], and 132 with combined IFG and IGT [23%]). Anthropometric parameters, insulin resistance, fibrinogen, C-reactive protein (CRP), lipid profile, blood pressure (BP), and echocardiographic parameters were compared with 232 participants with normal glucose tolerance (NGT). RESULTS BMI, prevalence of central obesity, homeostatic model assessment index of insulin resistance, plasma triglycerides, fibrinogen, and CRP increased progressively across categories of glucose intolerance (P < 0.0001), with the IFG+IGT group having higher values than those with isolated IFG (0.05 < P < 0.0001). Compared with NGT, both IFG and IFG+IGT exhibited greater left ventricular (LV) mass (P < 0.0001) and lower Doppler early peak rapid filling velocity to peak atrial filling velocity ratio (P < 0.005), without differences in LV systolic function. The odds of LV hypertrophy (LV mass index >46.7 in women or >49.2 g/m2.7 in men) was 3.5 in IFG participants (95% CI 0.68–17.76; P = NS) and 9.76 (2.03–46.79; P = 0.004) in IFG+IGT, compared with NGT, after adjustment for age, sex, heart rate, systolic BP, and waist circumference (WC). In the overall sample, LV mass index was associated with WC (P = 0.033), CRP (P = 0.027), and 2-h oral glucose tolerance test (P = 0.001) independently of confounders. CONCLUSIONS Cardiometabolic profile and markers of inflammation are more severely altered in men and women with both IFG and IGT compared with those with IFG alone. These individuals, in the absence of hypertension, have a 10-fold greater probability of preclinical CV disease (LV hypertrophy). PMID:23223343

  4. How Many People Are Affected or At Risk for Lactose Intolerance?

    MedlinePlus

    ... many people are affected or at risk for lactose intolerance? Skip sharing on social media links Share this: Page Content How many people are lactose intolerant? The true number of people with lactose ...

  5. [Insulin resistance--a physiopathological condition with numerous sequelae: non-insulin-dependent diabetes mellitus (NIDDM), android obesity, essential hypertension, dyslipidemia and atherosclerosis].

    PubMed

    Pedersen, O

    1992-05-11

    Recent research has demonstrated that reduced insulin-stimulated glucose metabolism in skeletal muscle (insulin resistance) and hyperinsulinism are common features in widespread diseases such as essential hypertension, android obesity, non-insulin dependent diabetes mellitus, dyslipidemia (in the form of raised serum triglyceride and reduced serum high-density lipoprotein (HDL) cholesterol) and arteriosclerosis. Simultaneously, investigations in a comprehensive group of healthy middle-aged men have revealed insulin resistance in one fourth. On the basis of these observations, a working hypothesis is suggested which postulates that genetic abnormalities in one or more of the candidate genes in the modes of action of insulin occur in a great proportion of the population. These may result in insulin resistance (primary genetic insulin resistance). Primary insulin resistance may be potentiated by a series of circumstances such as ageing, high-fat diet, lack of physical activity, hormonal and metabolic abnormalities or drugs (secondary insulin resistance). As a consequence of the reduced effect of insulin on muscle tissue, compensatory hyperinsulinism develops. Depending on the remaining vulnerability of the individual the hyperinsulinism is presumed to result in development of one or more phenotypes. For example if the beta-cells of the pancreas are unable to secrete sufficient insulin to compensate the insulin resistance on account of genetic defects, glucose intolerance will develop. In a similar manner, hyperinsulinism in insulin-resistant individuals who are predisposed to essential hypertension is presumed to reveal genetic defects in the blood pressure regulating mechanisms and thus contribute to development of the disease.(ABSTRACT TRUNCATED AT 250 WORDS) PMID:1631967

  6. The five glucose-6-phosphatase paralogous genes are differentially regulated by insulin alone or combined with high level of amino acids and/or glucose in trout hepatocytes.

    PubMed

    Lucie, Marandel; Weiwei, Dai; Stéphane, Panserat; Sandrine, Skiba-Cassy

    2016-04-01

    A recent analysis of the newly sequenced rainbow trout (Oncorhynchus mykiss) genome suggested that duplicated gluconeogenic g6pc paralogues, fixed in this genome after the salmonid-specific 4th whole genome duplication, may have a role in the setting up of the glucose-intolerant phenotype in this carnivorous species. This should be due to the sub- or neo-functionalization of their regulation. In the present short communication we thus addressed the question of the regulation of these genes by insulin, hormone involved in the glucose homeostasis, and its interaction with glucose and amino acids in vitro. The stimulation of trout hepatocytes with insulin revealed an atypical up-regulation of g6pcb2 ohnologues and confirmed the sub- or neo-functionalization of the five g6pc genes at least at the regulatory level. Intriguingly, when hepatocytes were cultured with high levels of glucose and/or AAs in presence of insulin, most of the g6pc paralogues were up-regulated. It strongly suggested a cross-talk between insulin and nutrients for the regulation of these genes. Moreover these results strengthened the idea that g6pc duplicated genes may significantly contribute to the setting up of the glucose-intolerant phenotype in trout via their atypical regulation by insulin alone or in interaction with nutrients. These findings open new perspectives to better understand in vivo glucose-intolerant phenotype in trout fed a high carbohydrate diet. PMID:26896939

  7. Clinical role of a fixed combination of standardized Berberis aristata and Silybum marianum extracts in diabetic and hypercholesterolemic patients intolerant to statins

    PubMed Central

    Di Pierro, Francesco; Bellone, Iaele; Rapacioli, Giuliana; Putignano, Pietro

    2015-01-01

    Background Statin intolerance is a medical condition often leading patients to nonadherence to the prescribed therapy or to a relevant reduction of the statin dosage. Both situations determine a totally or partially uncontrolled lipid profile, and these conditions unquestionably increase the risk of cardiovascular events. Methods We enrolled hypercholesterolemic, type 2 diabetic patients complaining of intolerance to statins. Some of them had reduced the statin dose ‘until the disappearance of symptoms’; others had opted for treatment with ezetimibe; and yet others were not undergoing any treatment at all. All patients of the three groups were then given a fixed combination of berberine and silymarin (Berberol®), known from previous papers to be able to control both lipidic and glycemic profiles. Results The tested product both as a single therapy and as add-on therapy to low-dose statin or to ezetimibe reduced triglycerides, low-density lipoprotein cholesterol, fasting blood glucose, and glycosylated hemoglobin in a significant manner without inducing toxicity conditions that might be somehow ascribed to a statin-intolerant condition. Conclusion Our study demonstrates that use of Berberol®, administered as a single or add-on therapy in statin-intolerant subjects affected by diabetes and hypercholesterolemia is a safe and effective tool capable of improving the patients’ lipidic and glycemic profiles. PMID:25678808

  8. Orthostatic Intolerance and Motion Sickness After Parabolic Flight

    NASA Technical Reports Server (NTRS)

    Schlegel, Todd T.; Brown, Troy E.; Wood, Scott J.; Benavides, Edgar W.; Bondar, Roberta L.; Stein, Flo; Moradshahi, Peyman; Harm, Deborah L.; Low, Phillip A.

    1999-01-01

    Orthostatic intolerance is common in astronauts after prolonged space flight. However, the "push-pull effect" in military aviators suggests that brief exposures to transitions between hypo- and hypergravity are sufficient to induce untoward autonomic cardiovascular physiology in susceptible individuals. We therefore investigated orthostatic tolerance and autonomic cardiovascular function in 16 healthy test subjects before and after a seated 2-hr parabolic flight. At the same time, we also investigated relationships between parabolic flight-induced vomiting and changes in orthostatic and autonomic cardiovascular function. After parabolic flight, 8 of 16 subjects could not tolerate a 30-min upright tilt test, compared to 2 of 16 before flight. Whereas new intolerance in non-Vomiters resembled the clinical postural tachycardia syndrome (POTS), new intolerance in Vomiters was characterized by comparatively isolated upright hypocapnia and cerebral vasoconstriction. As a group, Vomiters also had evidence for increased postflight fluctuations in efferent vagal-cardiac nerve traffic occurring independently of any superimposed change in respiration. Results suggest that syndromes of orthostatic intolerance resembling those occurring after space flight can occur after a brief (i.e., 2-hr) parabolic flight.

  9. Preliminary Investigation of Intolerance of Uncertainty Treatment for Anxiety Disorders

    ERIC Educational Resources Information Center

    Hewitt, Sarah N.; Egan, Sarah; Rees, Clare

    2009-01-01

    Intolerance of uncertainty (IU) is the tendency to react negatively to uncertain situations or events, and it has been found to be an important maintaining factor in a number of different anxiety disorders. It is often included as a part of cognitive behavioural interventions for anxiety disorders but its specific contribution to treatment outcome…

  10. Tolerance of Intolerance: Values and Virtues at Stake in Education

    ERIC Educational Resources Information Center

    Orlenius, Kennert

    2008-01-01

    The article addresses the issue of the tolerance of intolerance in an educational context. It concerns a real case in a Swedish upper secondary school some years ago, when a student was suspended from school owing to his sympathies with Nazi ideas. One hundred and twenty student teachers' responses to this decision were analysed in respect of the…

  11. Lactose intolerance. Recognizing the link between diet and discomfort.

    PubMed

    Aurisicchio, L N; Pitchumoni, C S

    1994-01-01

    Lactose intolerance is a common disorder encountered in clinical practice. Evaluation involves obtaining a thorough nutritional history and recognizing associations between diet and gastrointestinal complaints. Lack of suspicion of the problem can lead to expensive and invasive diagnostic procedures, which may further aggravate patients' anxiety and result in iatrogenic complications. Once the diagnosis is confirmed, simple dietary management may resolve symptoms completely. PMID:8278293

  12. Rainbow Visibility: How One Catholic University Responded to Intolerance.

    ERIC Educational Resources Information Center

    Getz, Cheryl; Kirkley, Evelyn A.

    2002-01-01

    When intolerance of gays and lesbians at the University of San Diego became a problem, a group of students, staff, and faculty decided to do something about it. The result was a project called Rainbow Visibility that works on many forms to educate the campus community. (Author)

  13. The effects of combined vitamin D and calcium supplementation on fasting plasma glucose in non-diabetic adults age 65 and older

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Altered vitamin D and calcium homeostasis may play a role in the development of glucose intolerance. In a 3-year randomized controlled trial, we compared the effects of combined vitamin D and calcium supplementation vs. placebo on fasting plasma glucose (FPG) in healthy adults 65 years of age or old...

  14. Perioperative hypertensive emergencies.

    PubMed

    Aronson, Solomon

    2014-07-01

    The concept of "perioperative hypertensive emergency" must be defined differently from that of ambulatory hypertensive emergency in view of its unique clinical considerations in an atypical setting. It should be noted that moderately high normal blood pressure (BP) values in the perioperative setting often trigger situations requiring immediate treatment in what would otherwise be a "BP-acceptable" non-surgical condition. Commonly recognized circumstances that may result in a perioperative hypertensive emergency include exacerbation of severe mitral insufficiency, hypertension resulting in acute decompensated heart failure, hypertension caused by acute catecholamine excess, rebound hypertension after withdrawal of antihypertensive medications, hypertension resulting in bleeding from vascular surgery suture lines, intracerebral hemorrhage, aortic dissection, hypertension associated with preeclampsia, and hypertension associated with autonomic dysreflexia. In addition, perioperative BP lability has been reported to increase the risk for stroke, acute kidney injury, and 30-day mortality in patients undergoing cardiac surgery. PMID:24852830

  15. Glucose toxicity.

    PubMed

    Rossetti, L; Giaccari, A; DeFronzo, R A

    1990-06-01

    Glucose toxicity is a well-established entity that has been shown in animal models of diabetes to contribute to development of insulin resistance and impaired insulin secretion. In type II (non-insulin-dependent) diabetes in humans, a considerable body of evidence has accumulated indicating that a chronic physiological increment in the plasma glucose concentration leads to progressive impairment in insulin secretion and may contribute to insulin resistance as well. The precise biochemical mechanism(s) responsible for the hyperglycemia-induced defect in insulin secretion remains to be defined but may be related to a defect in phosphoinositide metabolism. In animal models of diabetes, development of insulin resistance is related to downregulation of the glucose-transport system, and a similar phenomenon is also likely to occur in humans. In addition, hyperglycemia in humans may lead to a defect in glycogen synthesis. In this respect, humans may be different from rats. In type I (insulin-dependent) diabetic patients who are poorly controlled, insulin resistance is a characteristic feature and can be ameliorated by tight glycemic control, suggesting that hyperglycemia is responsible for the insulin resistance. Evidence also has accumulated to implicate glucose toxicity in the functional impairment in insulin secretion that occurs during the initial presentation of patients with type I diabetes, and this may explain the honeymoon period so commonly observed after the institution of insulin therapy. PMID:2192847

  16. Consumption of honey, sucrose, and high fructose corn syrup produce similar metabolic effects in glucose tolerant and glucose intolerant individuals

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Background: Current public health recommendations call for reduction of added sugars; however, controversy exits over whether all nutritive sweeteners produce similar metabolic effects. Objective: To compare effects of chronic consumption of three nutritive sweeteners (honey, sucrose and high fructo...

  17. Glutathionylation of hepatic and visceral adipose proteins decreases in obese-prone, glucose intolerant rats

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Obesity and insulin resistance are associated with increases in oxidative stress and lipid peroxidation. On the other hand, adipocytes from obese animals have elevated GSH content, and insulin resistance can be reversed by GSH depletion. Oxidation of active site cysteines of protein tyrosine phospha...

  18. Liver Disease and Pulmonary Hypertension

    MedlinePlus

    Liver Disease Pulmonary & PH Hypertension Did you know that if you have liver disease, you are at risk for pulmonary hypertension? www.PHAssociation.org About Pulmonary Hypertension PULMONARY HYPERTENSION, OR PH, is complex and often misunderstood. PH means high ...

  19. Age- and gender-related changes in glucose homeostasis in glucocorticoid-treated rats.

    PubMed

    dos Santos, Cristiane; Ferreira, Francielle Batista D; Gonalves-Neto, Luiz M; Taboga, Sebastio Roberto; Boschero, Antonio Carlos; Rafacho, Alex

    2014-10-01

    The disruption to glucose homeostasis upon glucocorticoid (GC) treatment in adult male rats has not been fully characterized in older rats or in females. Thus, we evaluated the age- and gender-related changes in glucose homeostasis in GC-treated rats. We injected male and female rats at 3 months and 12 months of age with either dexamethasone (1.0 mg/kg body mass, intraperitoneally) or saline, daily for 5 days. All of the GC-treated rats had decreased body mass and food intake, and adrenal hypotrophy. Increased glycemia was observed in all of the GC-treated groups and only the 3-month-old female rats were not glucose intolerant. Dexamethasone treatment resulted in hyperinsulinemia and hypertriacylglyceridemia in all of the GC-treated rats. The glucose-stimulated insulin secretion (GSIS) was higher in all of the dexamethasone-treated animals, but it was less pronounced in the older animals. The ?-cell mass was increased in the younger male rats treated with dexamethasone. We conclude that dexamethasone treatment induces glucose intolerance in both the 3- and 12-month-old male rats as well as hyperinsulinemia and augmented GSIS. Three-month-old female rats are protected from glucose intolerance caused by GC, whereas 12-month-old female rats developed the same complications that were present in 3- and 12-month-old male rats. PMID:25272090

  20. Rictor/mTORC2 facilitates central regulation of energy and glucose homeostasis

    PubMed Central

    Kocalis, Heidi E.; Hagan, Scott L.; George, Leena; Turney, Maxine K.; Siuta, Michael A.; Laryea, Gloria N.; Morris, Lindsey C.; Muglia, Louis J.; Printz, Richard L.; Stanwood, Gregg D.; Niswender, Kevin D.

    2014-01-01

    Insulin signaling in the central nervous system (CNS) regulates energy balance and peripheral glucose homeostasis. Rictor is a key regulatory/structural subunit of the mTORC2 complex and is required for hydrophobic motif site phosphorylation of Akt at serine 473. To examine the contribution of neuronal Rictor/mTORC2 signaling to CNS regulation of energy and glucose homeostasis, we utilized Cre-LoxP technology to generate mice lacking Rictor in all neurons, or in either POMC or AgRP expressing neurons. Rictor deletion in all neurons led to increased fat mass and adiposity, glucose intolerance and behavioral leptin resistance. Disrupting Rictor in POMC neurons also caused obesity and hyperphagia, fasting hyperglycemia and pronounced glucose intolerance. AgRP neuron specific deletion did not impact energy balance but led to mild glucose intolerance. Collectively, we show that Rictor/mTORC2 signaling, especially in POMC-expressing neurons, is important for central regulation of energy and glucose homeostasis. PMID:24944899

  1. Pulsatile insulin secretion, impaired glucose tolerance and type 2 diabetes

    PubMed Central

    Satin, Leslie S.; Butler, Peter C.; Ha, Joon; Sherman, Arthur S.

    2015-01-01

    Type 2 diabetes (T2DM) results when increases in beta cell function and/or mass cannot compensate for rising insulin resistance. Numerous studies have documented the longitudinal changes in metabolism that occur during the development of glucose intolerance and lead to T2DM. However, the role of changes in insulin secretion, both amount and temporal pattern has been understudied. Most of the insulin secreted from pancreatic beta cells of the pancreas is released in a pulsatile pattern, which is disrupted in T2DM. Here we review the evidence that changes in beta cell pulsatility occur during the progression from glucose intolerance to T2DM in humans, and contribute significantly to the etiology of the disease. We review the evidence that insulin pulsatility improves the efficacy of secreted insulin on its targets, particularly hepatic glucose production, but also examine evidence that pulsatility alters or is altered by changes in peripheral glucose uptake. Finally, we summarize our current understanding of the biophysical mechanisms responsible for oscillatory insulin secretion. Understanding how insulin pulsatility contributes to normal glucose homeostasis and is altered in metabolic disease states may help improve the treatment of T2DM. PMID:25637831

  2. Effect of a single dose of lactase on symptoms and expired hydrogen after lactose challenge in lactose-intolerant subjects.

    PubMed

    Sanders, S W; Tolman, K G; Reitberg, D P

    1992-06-01

    The effect of a single dose or oral lactase on symptoms, breath hydrogen concentration, and glucose absorption in lactose-intolerant subjects challenged with lactose was studied. Volunteers underwent a lactose challenge test; those whose breath hydrogen concentrations increased 20 ppm or more and who met other criteria were admitted as subjects. After fasting, the subjects were given three chewable lactase tablets (total lactase dose, 9900 FCC units) or placebo tablets in a randomized, double-blind, crossover manner. The subjects also consumed 8 oz of whole milk in which 37.5 g of lactose powder was dissolved (total lactose content, 50 g). The washout period between lactose challenges was at least one week. Breath hydrogen and plasma glucose concentrations were measured before and at intervals after the challenges, and the subjects completed symptom-evaluation questionnaires every eight hours for four days. Twenty-four subjects completed the study. The maximum mean breath hydrogen concentration was significantly lower after lactase treatment than after placebo treatment. In 21 subjects, the area under the hydrogen concentration-time curve (AUC) was lower after lactase than after placebo; three subjects had hydrogen AUCs more than 300 ppm.hr lower. There were no significant differences in plasma glucose levels. Subjective ratings of the severity of abdominal cramping, belching, flatulence, and diarrhea were lower during the first eight hours after challenge in lactase-treated subjects; ratings for bloating were lower during the next eight hours. Single doses of a chewable lactase tablet reduced the concentration of expired hydrogen and symptoms of lactose intolerance after a lactose challenge. PMID:1534729

  3. Hypertension and Spina Bifida

    MedlinePlus

    ... hypertension has to be identiled lrst, particularly in young people. The following healthy lifestyles changes can signilcantly improve blood pressure: For adults, Internal Medicine specialists are experts at diagnosing and treating hypertension. ...

  4. Gestational Hypertension and Preeclampsia

    MedlinePlus Videos and Cool Tools

    ... Your e-mail was sent. Save to my dashboard Sign in or Sign up to save this ... saved this page It's been added to your dashboard . Gestational hypertension and preeclampsia 4:17 Gestational hypertension ...

  5. Hypertension and aging.

    PubMed

    Buford, Thomas W

    2016-03-01

    Hypertension is a highly prevalent condition with numerous health risks, and the incidence of hypertension is greatest among older adults. Traditional discussions of hypertension have largely focused on the risks for cardiovascular disease and associated events. However, there are a number of collateral effects, including risks for dementia, physical disability, and falls/fractures which are increasingly garnering attention in the hypertension literature. Several key mechanisms - including inflammation, oxidative stress, and endothelial dysfunction - are common to biologic aging and hypertension development and appear to have key mechanistic roles in the development of the cardiovascular and collateral risks of late-life hypertension. The objective of the present review is to highlight the multi-dimensional risks of hypertension among older adults and discuss potential strategies for treatment and future areas of research for improving overall care for older adults with hypertension. PMID:26835847

  6. Drug-induced hypertension

    MedlinePlus

    ... blood pressure caused by using a chemical substance, drug, or medication. ... of secondary hypertension caused by a response to medication. Drugs that can cause hypertension include: Acetaminophen Alcohol, amphetamines, ...

  7. Pulmonary hypertension - at home

    MedlinePlus

    Pulmonary hypertension (PAH) is abnormally high blood pressure in the arteries of the lungs. With PAH, the right ... Chin K, Channick RN. Pulmonary hypertension. In: Broaddus VC, ... Nadel's Textbook of Respiratory Medicine . 6th ed. Philadelphia, ...

  8. Cirrhosis and Portal Hypertension

    MedlinePlus

    MENU Return to Web version Cirrhosis and Portal Hypertension Overview What is cirrhosis? In people who have ... lead to coma and death. What is portal hypertension? Normally, blood is carried to the liver by ...

  9. What Causes Pulmonary Hypertension?

    MedlinePlus

    ... on Twitter. What Causes Pulmonary Hypertension? Pulmonary hypertension (PH) begins with inflammation and changes in the cells ... also can affect the pulmonary arteries and cause PH. For example, the condition may develop if: The ...

  10. Living with Pulmonary Hypertension

    MedlinePlus

    ... on Twitter. Living With Pulmonary Hypertension Pulmonary hypertension (PH) has no cure. However, you can work with ... your doctor advises. Call your doctor if your PH symptoms worsen or change. The earlier symptoms are ...

  11. Towards an Ontological Theory of Substance Intolerance and Hypersensitivity

    PubMed Central

    Hogan, William R.

    2010-01-01

    A proper ontological treatment of intolerance—including hypersensitivity—to various substances is critical to patient care and research. However, existing methods and standards for documenting these conditions have flaws that inhibit these goals, especially translational research that bridges the two activities. In response, I outline a realist approach to the ontology of substance intolerance, including hypersensitivity conditions. I defend a view of these conditions as a subtype of disease. Specifically, a substance intolerance is a disease whose pathological process(es) are realized upon exposure to a quantity of substance of a particular type, and this quantity would normally not cause the realization of the pathological process(es). To develop this theory, it was necessary to build pieces of a theory of pathological processes. Overall, however, the framework of the Ontology for General Medical Science (which uses Basic Formal Ontology as its uppermost level) was a more-than-adequate foundation on which to build the theory. PMID:20152933

  12. Intolerance of uncertainty and decisions about delayed, probabilistic rewards.

    PubMed

    Luhmann, Christian C; Ishida, Kanako; Hajcak, Greg

    2011-09-01

    Worry is the inflated concern about potential future threats and is a hallmark feature of generalized anxiety disorder. Previous theoretical work has suggested that worry may be a consequence of intolerance of uncertainty (IU). The current study seeks to explore the behavioral consequences of IU. Specifically, we examine how IU might be associated with aspects of reward-based decision making. We utilized a simple laboratory gambling task in which participants chose between small, low-probability rewards available immediately at the beginning of each trial and large, high-probability rewards only available after some variable delay. Results demonstrate that higher levels of intolerance of uncertainty were associated with a tendency to select the immediately available, but less valuable and less probable rewards. IU also predicted decision-makers' sensitivity to outcomes. We discuss the cognitive and affective mechanisms that are likely to underlie the observed decision-making behavior and the implications for anxiety disorders. PMID:21658521

  13. Exercise Intolerance in Heart Failure: Did We Forget the Brain?

    PubMed

    Brassard, Patrice; Gustafsson, Finn

    2016-04-01

    Exercise tolerance is affected in patients with heart failure (HF). Although the inability of the heart to pump blood to the working muscle has been the conventional mechanism proposed to explain the lowered capacity of patients with HF to exercise, evidence suggests that the pathophysiological mechanisms associated with their exercise intolerance is more complex. Recent findings indicate that lowered cerebral blood flow (CBF) and oxygenation likely represent limiting factors for exercise capacity in patients with HF. After an overview of cardiac and peripheral responses during acute and chronic exercise in healthy individuals, we succinctly review cardiac and noncardiac mechanisms by which HF influences exercise tolerance. We then consider how HF, comorbidity, and HF treatment influence CBF and oxygenation at rest and during exercise. Finally, we provide suggestions for further research to improve our understanding of the role of the brain in exercise intolerance in HF. PMID:26875016

  14. Orthostatic intolerance and tachycardia associated with norepinephrine-transporter deficiency

    NASA Technical Reports Server (NTRS)

    Shannon, J. R.; Flattem, N. L.; Jordan, J.; Jacob, G.; Black, B. K.; Biaggioni, I.; Blakely, R. D.; Robertson, D.

    2000-01-01

    BACKGROUND: Orthostatic intolerance is a syndrome characterized by lightheadedness, fatigue, altered mentation, and syncope and associated with postural tachycardia and plasma norepinephrine concentrations that are disproportionately high in relation to sympathetic outflow. We tested the hypothesis that impaired functioning of the norepinephrine transporter contributes to the pathophysiologic mechanism of orthostatic intolerance. METHODS: In a patient with orthostatic intolerance and her relatives, we measured postural blood pressure, heart rate, plasma catecholamines, and systemic norepinephrine spillover and clearance, and we sequenced the norepinephrine-transporter gene and evaluated its function. RESULTS: The patient had a high mean plasma norepinephrine concentration while standing, as compared with the mean (+/-SD) concentration in normal subjects (923 vs. 439+/-129 pg per milliliter [5.46 vs. 2.59+/-0.76 nmol per liter]), reduced systemic norepinephrine clearance (1.56 vs. 2.42+/-0.71 liters per minute), impairment in the increase in the plasma norepinephrine concentration after the administration of tyramine (12 vs. 56+/-63 pg per milliliter [0.07 vs. 0.33+/-0.37 pmol per liter]), and a disproportionate increase in the concentration of plasma norepinephrine relative to that of dihydroxyphenylglycol. Analysis of the norepinephrine-transporter gene revealed that the proband was heterozygous for a mutation in exon 9 (encoding a change from guanine to cytosine at position 237) that resulted in more than a 98 percent loss of function as compared with that of the wild-type gene. Impairment of synaptic norepinephrine clearance may result in a syndrome characterized by excessive sympathetic activation in response to physiologic stimuli. The mutant allele in the proband's family segregated with the postural heart rate and abnormal plasma catecholamine homeostasis. CONCLUSIONS: Genetic or acquired deficits in norepinephrine inactivation may underlie hyperadrenergic states that lead to orthostatic intolerance.

  15. Depression in hypertensive subjects.

    PubMed

    Ramachandran, V; Parikh, G J; Srinivasan, V

    1983-10-01

    168 patients attending hypertension clinic were randomly selected for the study. They were thoroughly investigated using E.C.G., X-ray chest, Urine analysis, Blood sugar, Blood urea, Serum cholesterol, Serum K, Serum Na, Scrum creatinine and Uric acid level. Detailed psychiatric case history and mental examination was carried out. Beck Rating Scale was used to measure the depression. 25% of hypertensive subjects exhibited depressive features and their mean score in Beck Rating scale is 21.76. The mean score of non-depressives is 4.46. All patients were receiving methyl dopa.25 mg. twice or thrice daily with thiazide diuretic. No significant difference in the incidence of depression with the duration of medication was observed.The hypertension was classified into mild, moderate and severe depending on the diastolic pressure. Depression was more frequent in severe hypertensives but not to the statistically significant level.Further hypertensives were classified into:1. Hypertension without organ involvement2. Hypertension with LVH only3. Hypertension with additional organ involvement4. Malignant hypertensionDepression was significantly more frequent in hypertensives with complications and also hypertensives in whom the B.P. remained uncontrolled. As all the patients were on the same drug, the drug effect is common to all; hence, the higher incidence of depression in hypertensives with complications is due to the limitation and distress caused by the illness. PMID:21847301

  16. Adrenocortical Causes of Hypertension

    PubMed Central

    Moraitis, Andreas; Stratakis, Constantine

    2011-01-01

    Primary aldosteronism is the most common cause of secondary hypertension. In the past, screening for primary aldosteronism was offered only in patients with hypertension associated with hypokalemia. Recent studies showed that hypokalemia is seen in only 25% of the patients with primary aldosteronism, which has increased the prevalence of primary aldosteronism to 10–15% of all cases with new onset hypertension. PMID:21423682

  17. Orthostatic intolerance and motion sickness after parabolic flight

    NASA Technical Reports Server (NTRS)

    Schlegel, T. T.; Brown, T. E.; Wood, S. J.; Benavides, E. W.; Bondar, R. L.; Stein, F.; Moradshahi, P.; Harm, D. L.; Fritsch-Yelle, J. M.; Low, P. A.

    2001-01-01

    Because it is not clear that the induction of orthostatic intolerance in returning astronauts always requires prolonged exposure to microgravity, we investigated orthostatic tolerance and autonomic cardiovascular function in 16 healthy subjects before and after the brief micro- and hypergravity of parabolic flight. Concomitantly, we investigated the effect of parabolic flight-induced vomiting on orthostatic tolerance, R-wave-R-wave interval and arterial pressure power spectra, and carotid-cardiac baroreflex and Valsalva responses. After parabolic flight 1) 8 of 16 subjects could not tolerate 30 min of upright tilt (compared to 2 of 16 before flight); 2) 6 of 16 subjects vomited; 3) new intolerance to upright tilt was associated with exaggerated falls in total peripheral resistance, whereas vomiting was associated with increased R-wave-R-wave interval variability and carotid-cardiac baroreflex responsiveness; and 4) the proximate mode of new orthostatic failure differed in subjects who did and did not vomit, with vomiters experiencing comparatively isolated upright hypocapnia and cerebral vasoconstriction and nonvomiters experiencing signs and symptoms reminiscent of the clinical postural tachycardia syndrome. Results suggest, first, that syndromes of orthostatic intolerance resembling those developing after space flight can develop after a brief (i.e., 2-h) parabolic flight and, second, that recent vomiting can influence the results of tests of autonomic cardiovascular function commonly utilized in returning astronauts.

  18. Drug effects on orthostatic intolerance induced by bedrest

    NASA Technical Reports Server (NTRS)

    Vernikos, J.; Dallman, M. F.; Van Loon, G.; Keil, L. C.

    1991-01-01

    Effective and practical preventive procedures for postflight orthostatic intolerance are highly desirable. The current practice of attempts to expand plasma volume by ingestion of salt and fluids before reentry has proven benefits. This study evaluated alternative options using fludrocortisone (F) to expand plasma volume (PV), dextroamphetamine (Dex) to enhance norepinephrine (NE) release, and atropine (A) to reduce the effects of vagal stimulation. Seven subjects with proven post-bedrest orthostatic intolerance returned for a 7-day 6-deg head-down bedrest study. F (0.2 mg) was given at 8:00 AM and 8:00 PM the day before and 8:00 AM the day the subjects got out of bed (2 hours before standing). PV was measured before and 1 hour after the last dose of F. Dex (5 mg) and A (0.8 mg) were then taken orally 1 hour before the stand test. F expanded PV by 16 percent and caused sodium retention. Four of the 7 subjects stood for 1 hour post-bedrest and heart rate, plasma NE and plasma renin responses to standing were greatly enhanced and sustained. Although there was a narrowing of pulse pressure, the ability to overcome orthostatic intolerance with these countermeasures was largely due to vasoconstriction and sustained high heart rate.

  19. [Food Allergy and Intolerance : Distinction, Definitions and Delimitation].

    PubMed

    Kleine-Tebbe, Jörg; Waßmann-Otto, Anja; Mönnikes, Hubert

    2016-06-01

    Immunologically mediated hypersensitivity to foods is defined as food allergy, mainly due to immunglobulins of class E (IgE) triggering immediate reactions (type I hypersensitivity) with possible involvement of mucosa, skin, airways, intestinal tract, and the vascular system. Primary food allergy is based on (early) IgE sensitization against animal (e. g., cow's milk, hen's eggs) or plant proteins (e. g. peanut, hazelnut or wheat). In the case of secondary food allergies, IgE against pollen proteins (e. g., birch) reacts to structurally related food proteins (with cross-reactions to stone and pit fruits). Non-immunological food intolerance reactions are mostly based on carbohydrate malassimilation (e. g., lactose intolerance, fructose malabsorption) and are rarely due to pseudo-allergies (e. g., flavors, dyes, preservatives) primarily in patients with chronic urticaria. Common intestinal symptoms are mainly due to functional disorders (e. g., irritable bowel disease), rarely because of inflammatory intestinal diseases (e. g., celiac disease). Histamine intolerance, gluten hypersensitivity, and so-called food type III hypersensitivities are controversial diagnoses. The aforementioned disease entities/models are of variable importance for the affected individuals, the public health system, and society in general. PMID:27215624

  20. Are ambiguity aversion and ambiguity intolerance identical? A neuroeconomics investigation

    PubMed Central

    Tanaka, Yusuke; Fujino, Junya; Ideno, Takashi; Okubo, Shigetaka; Takemura, Kazuhisa; Miyata, Jun; Kawada, Ryosaku; Fujimoto, Shinsuke; Kubota, Manabu; Sasamoto, Akihiko; Hirose, Kimito; Takeuchi, Hideaki; Fukuyama, Hidenao; Murai, Toshiya; Takahashi, Hidehiko

    2015-01-01

    In recent years, there has been growing interest in understanding a person's reaction to ambiguous situations, and two similar constructs related to ambiguity, “ambiguity aversion” and “ambiguity intolerance,” are defined in different disciplines. In the field of economic decision-making research, “ambiguity aversion” represents a preference for known risks relative to unknown risks. On the other hand, in clinical psychology, “ambiguity intolerance” describes the tendency to perceive ambiguous situations as undesirable. However, it remains unclear whether these two notions derived from different disciplines are identical or not. To clarify this issue, we combined an economic task, psychological questionnaires, and voxel-based morphometry (VBM) of structural brain magnetic resonance imaging (MRI) in a sample of healthy volunteers. The individual ambiguity aversion tendency parameter, as measured by our economic task, was negatively correlated with agreeableness scores on the self-reported version of the Revised NEO Personality Inventory. However, it was not correlated with scores of discomfort with ambiguity, one of the subscales of the Need for Closure Scale. Furthermore, the ambiguity aversion tendency parameter was negatively correlated with gray matter (GM) volume of areas in the lateral prefrontal cortex and parietal cortex, whereas ambiguity intolerance was not correlated with GM volume in any region. Our results suggest that ambiguity aversion, described in decision theory, may not necessarily be identical to ambiguity intolerance, referred to in clinical psychology. Cautious applications of decision theory to clinical neuropsychiatry are recommended. PMID:25698984

  1. Drug effects on orthostatic intolerance induced by bedrest.

    PubMed

    Vernikos, J; Dallman, M F; Van Loon, G; Keil, L C

    1991-10-01

    Effective and practical preventive procedures for postflight orthostatic intolerance are highly desirable. The current practice of attempts to expand plasma volume by ingestion of salt and fluids before reentry has proven benefits. This study evaluated alternative options using fludrocortisone (F) to expand plasma volume (PV), dextroamphetamine (Dex) to enhance norepinephrine (NE) release and atropine (A) to reduce the effects of vagal stimulation. Seven subjects with proven post-bedrest orthostatic intolerance returned for a 7-day 6 degrees head-down bedrest study. F (0.2 mg) was given at 8:00 AM and 8:00 PM the day before and 8:00 AM the day the subjects got out of bed (2 hours before standing). PV was measured before and 1 hour after the last dose of F. D (5 mg) and A (0.8 mg) were then taken orally 1 hour before the stand test. F expanded PV by 16% and caused sodium retention. Four of the 7 subjects stood for 1 hour post-bedrest and HR, plasma NE and PRA responses to standing were greatly enhanced and sustained. Although there was a narrowing of pulse pressure, the ability to overcome orthostatic intolerance with these countermeasures was largely due to vasoconstriction and sustained high heart rate. The existing literature on pharmacologic countermeasures for post-flight and post-bedrest orthostatic hypotension is reviewed, and the results are discussed in that context. PMID:1761730

  2. Effect of amiloride, or amiloride plus hydrochlorothiazide, versus hydrochlorothiazide on glucose tolerance and blood pressure (PATHWAY-3): a parallel-group, double-blind randomised phase 4 trial

    PubMed Central

    Brown, Morris J; Williams, Bryan; Morant, Steve V; Webb, David J; Caulfield, Mark J; Cruickshank, J Kennedy; Ford, Ian; McInnes, Gordon; Sever, Peter; Salsbury, Jackie; Mackenzie, Isla S; Padmanabhan, Sandosh; MacDonald, Thomas M

    2016-01-01

    Summary Background Potassium depletion by thiazide diuretics is associated with a rise in blood glucose. We assessed whether addition or substitution of a potassium-sparing diuretic, amiloride, to treatment with a thiazide can prevent glucose intolerance and improve blood pressure control. Methods We did a parallel-group, randomised, double-blind trial in 11 secondary and two primary care sites in the UK. Eligible patients were aged 18–80 years; had clinic systolic blood pressure of 140 mm Hg or higher and home systolic blood pressure of 130 mmHg or higher on permitted background drugs of angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, β blockers, calcium-channel blockers, or direct renin inhibitors (previously untreated patients were also eligible in specific circumstances); and had at least one component of the metabolic syndrome in addition to hypertension. Patients with known diabetes were excluded. Patients were randomly assigned (1:1:1) to 24 weeks of daily oral treatment with starting doses of 10 mg amiloride, 25 mg hydrochlorothiazide, or 5 mg amiloride plus 12·5 mg hydrochlorothiazide; all doses were doubled after 12 weeks. Random assignment was done via a central computer system. Both participants and investigators were masked to assignment. Our hierarchical primary endpoints, assessed on a modified intention-to-treat basis at 12 and 24 weeks, were the differences from baseline in blood glucose measured 2 h after a 75 g oral glucose tolerance test (OGTT), compared first between the hydrochlorothiazide and amiloride groups, and then between the hydrochlorothiazide and combination groups. A key secondary endpoint was change in home systolic blood pressure at 12 and 24 weeks. This trial is registered with ClinicalTrials.gov, number NCT00797862, and the MHRA, Eudract number 2009-010068-41, and is now complete. Findings Between Nov 18, 2009, and Dec 15, 2014, 145 patients were randomly assigned to amiloride, 146 to hydrochlorothiazide, and 150 to the combination group. 132 participants in the amiloride group, 134 in the hydrochlorothiazide group, and 133 in the combination group were included in the modified intention-to-treat analysis. 2 h glucose concentrations after OGTT, averaged at 12 and 24 weeks, were significantly lower in the amiloride group than in the hydrochlorothiazide group (mean difference −0·55 mmol/L [95% CI −0·96 to −0·14]; p=0·0093) and in the combination group than in the hydrochlorothiazide group (−0·42 mmol/L [–0·84 to −0·004]; p=0·048). The mean reduction in home systolic blood pressure during 24 weeks did not differ significantly between the amiloride and hydrochlorothiazide groups, but the fall in blood pressure in the combination group was significantly greater than that in the hydrochlorothiazide group (p=0·0068). Hyperkalaemia was reported in seven (4·8%) patients in the amiloride group and three (2·3%) patients in the combination group; the highest recorded potassium concentration was 5·8 mmol/L in a patient in the amiloride group. 13 serious adverse events occurred but the frequency did not differ significantly between groups. Interpretation The combination of amiloride with hydrochlorothiazide, at doses equipotent on blood pressure, prevents glucose intolerance and improves control of blood pressure compared with montherapy with either drug. These findings, together with previous data about morbidity and mortality for the combination, support first-line use of amiloride plus hydrochlorothiazide in hypertensive patients who need treatment with a diuretic. Funding British Heart Foundation and National Institute for Health Research. PMID:26489809

  3. Chronic placental ischemia alters amniotic fluid milieu and results in impaired glucose tolerance, insulin resistance and hyperleptinemia in young rats.

    PubMed

    Heltemes, Alaina; Gingery, Anne; Soldner, Emma L B; Bozadjieva, Nadejda; Jahr, Kristen N; Johnson, Britt K; Gilbert, Jeffrey S

    2010-07-01

    Although small size at birth is associated with hypertension and associated co-morbidities such as insulin resistance and type II diabetes mellitus, many of the animal models employed to simulate this phenomenon do not closely mimic the ontogeny of growth restriction observed clinically. While intrauterine growth restriction (IUGR) is often detected near mid-pregnancy in women and persists until term, most rodent models of IUGR employ ligation of uterine arteries for a brief period during late gestation (days 19-21 of pregnancy). We hypothesized that IUGR associated with chronic reduction in uteroplacental perfusion (RUPP) and placental ischemia during the third trimester of pregnancy in the rat alters the amniotic fluid (AF) environment and results in hypertensive offspring presenting with metabolic abnormalities such as glucose intolerance and insulin resistance. Insulin-like growth factor-1 (IGF-1), IGF-2, Na(+) concentration and oxidative stress in the AF were increased, while K(+) concentration was decreased in the RUPP compared with normal pregnant (NP) fetuses. RUPP-offspring (RUPP-O) were smaller (6.1 +/- 0.2 versus 6.7 +/- 0.2 g; P < 0.05) at birth compared with NP-offspring (NP-O) groups. At nine weeks of age, mean arterial pressure (121 +/- 3 versus 107 +/- 5 mmHg; P < 0.05), fasting insulin (0.71 +/- 0.014 versus 0.30 +/- 0.08 ng/mL; P < 0.05), glucose (4.4 +/- 0.2 versus 3.1 +/- 0.3 mmol/L; P < 0.05), leptin (3.8 +/- 0.5 versus 2.3 +/- 0.3 ng/mL; P < 0.05) and the homeostasis model assessment of insulin resistance index was greater (2.9 +/- 0.6 versus 1.0 +/- 0.3; P < 0.05) in the RUPP-O compared with the NP-O rats. These data indicate that chronic placental ischemia results in numerous alterations to the fetal environment that contributes to the development of impaired glucose metabolism, insulin resistance and hyperleptinemia in young offspring. PMID:20558843

  4. [Metabolic changes in patients with hereditary fructose intolerance. A contribution to the topic of fructose administration for parenteral feeding].

    PubMed

    Sachs, M; Asskali, F; Encke, A; Förster, H

    1991-11-15

    The literature contains a number of reports of death following the intravenous administration of fructose in patients with hereditary fructose intolerance (HFI). The aim of the present study was, therefore, to investigate the metabolic changes occurring during intravenous administration of fructose to patients with HFI, with the aim of identifying metabolic parameters that would permit the early diagnosis of HFI. Also, the deaths reported in the literature were analyzed. In three of our own patients with fruit intolerance known since childhood, and in volunteers with normal metabolism, a one-hour intravenous fructose tolerance test (1.7 g fructose/min) was performed. An analysis was done using the usual enzymatic and chemical methods: blood glucose, fructose, lactic acid, serum uric acid, ammonia, free fatty acids, inorganic phosphate, and serum amino acids (ion exchange chromatography). During fructose infusion, the following metabolic changes were detected: hypoglycemia (20 to 60 mg/dl), increase in blood fructose levels (up to 350 mg/dl), hypophosphatemia (2 to 3 mg/dl), hyperlacticacidemia (up to 60 mg/dl), elevation of plasma ammonia levels (up to 120 mg/dl), increased serum glutamate, and a decrease in serum glutamine, as also hyperuricemia (up to 10 mg/dl). On termination of the fructose infusion, these changes were completely reversible. Analysis of the deaths reported in the literature revealed a known intolerance to fruit or sweets, and that no regular metabolic studies were apparently performed. Although HFI is rare, use should be made of the known advantages of sugar substitutes in post-aggression metabolism.(ABSTRACT TRUNCATED AT 250 WORDS) PMID:1770897

  5. HIV-related Social Intolerance and Risky Sexual Behavior in a High HIV Prevalence Environment

    PubMed Central

    Delavande, Adeline; Sampaio, Mafalda

    2014-01-01

    Although most countries state that fighting social intolerance against persons with HIV is part of their national HIV strategy, the impact of reducing intolerance on risky sexual behavior is largely unknown. In this paper, we estimate the effect of social intolerance against HIV+ persons on risky sexual behavior in rural Malawi using data from roughly 2,000 respondents from the 2004 and 2006 waves of the Malawi Longitudional Study of Families and Health (MLSFH). The effect of social intolerance on risky behavior is a priori ambiguous. On the one hand, higher social intolerance or stigma can lead people to disassociate from the stigmatized group and hence promote risky behavior. On the other hand, intolerance can be viewed as a social tax on being HIV+ and thus higher intolerance may reduce risky behavior. We find that a decrease in social intolerance is associated with a decrease in risky behavior, including fewer partners and a lower likelihood of having extra-marital relations. This effect is mainly driven by the impact of social intolerance on men. Overall the results suggests that reducing social intolerance might not only benefit the HIV positive but might also forestall the spread of HIV. PMID:24768779

  6. HIV-related social intolerance and risky sexual behavior in a high HIV prevalence environment.

    PubMed

    Delavande, Adeline; Sampaio, Mafalda; Sood, Neeraj

    2014-06-01

    Although most countries state that fighting social intolerance against persons with HIV is part of their national HIV strategy, the impact of reducing intolerance on risky sexual behavior is largely unknown. In this paper, we estimate the effect of social intolerance against HIV+ persons on risky sexual behavior in rural Malawi using data from roughly 2000 respondents from the 2004 and 2006 waves of the Malawi Longitudinal Study of Families and Health (MLSFH). The effect of social intolerance on risky behavior is a priori ambiguous. On the one hand, higher social intolerance or stigma can lead people to disassociate from the stigmatized group and hence promote risky behavior. On the other hand, intolerance can be viewed as a social tax on being HIV+ and thus higher intolerance may reduce risky behavior. We find that a decrease in social intolerance is associated with a decrease in risky behavior, including fewer partners and a lower likelihood of having extra-marital relations. This effect is mainly driven by the impact of social intolerance on men. Overall the results suggests that reducing social intolerance might not only benefit the HIV positive but might also forestall the spread of HIV. PMID:24768779

  7. Understanding and treating hypertension in diabetic populations.

    PubMed

    Volpe, Massimo; Battistoni, Allegra; Savoia, Carmine; Tocci, Giuliano

    2015-10-01

    Hypertension and diabetes frequently occurs in the same individuals in clinical practice. Moreover, the presence of hypertension does increase the risk of new-onset diabetes, as well as diabetes does promote development of hypertension. Whatever the case, the concomitant presence of these conditions confers a high risk of major cardiovascular complications and promotes the use integrated pharmacological interventions, aimed at achieving the recommended therapeutic targets. While the benefits of lowering abnormal fasting glucose levels in patients with hypertension and diabetes have been consistently demonstrated, the blood pressure (BP) targets to be achieved to get a benefit in patients with diabetes have been recently reconsidered. In the past, randomized clinical trials have, indeed, demonstrated that lowering BP levels to less than 140/90 mmHg was associated to a substantial reduction of the risk of developing macrovascular and microvascular complications in hypertensive patients with diabetes. In addition, epidemiological and clinical reports suggested that "the lower, the better" for BP in diabetes, so that levels of BP even lower than 130/80 mmHg have been recommended. Recent randomized clinical trials, however, designed to evaluate the potential benefits obtained with an intensive antihypertensive therapy, aimed at achieving a target systolic BP level below 120 mmHg as compared to those obtained with less stringent therapy, have challenged the previous recommendations from international guidelines. In fact, detailed analyses of these trials showed a paradoxically increased risk of coronary events, mostly myocardial infarction, in those patients who achieved the lowest BP levels, particularly in the high-risk subsets of hypertensive populations with diabetes. In the light of these considerations, the present article will briefly review the common pathophysiological mechanisms, the potential sites of therapeutic interactions and the currently recommended BP targets to be achieved under pharmacological treatment in hypertension and diabetes. PMID:26543822

  8. Understanding and treating hypertension in diabetic populations

    PubMed Central

    Battistoni, Allegra; Savoia, Carmine; Tocci, Giuliano

    2015-01-01

    Hypertension and diabetes frequently occurs in the same individuals in clinical practice. Moreover, the presence of hypertension does increase the risk of new-onset diabetes, as well as diabetes does promote development of hypertension. Whatever the case, the concomitant presence of these conditions confers a high risk of major cardiovascular complications and promotes the use integrated pharmacological interventions, aimed at achieving the recommended therapeutic targets. While the benefits of lowering abnormal fasting glucose levels in patients with hypertension and diabetes have been consistently demonstrated, the blood pressure (BP) targets to be achieved to get a benefit in patients with diabetes have been recently reconsidered. In the past, randomized clinical trials have, indeed, demonstrated that lowering BP levels to less than 140/90 mmHg was associated to a substantial reduction of the risk of developing macrovascular and microvascular complications in hypertensive patients with diabetes. In addition, epidemiological and clinical reports suggested that “the lower, the better” for BP in diabetes, so that levels of BP even lower than 130/80 mmHg have been recommended. Recent randomized clinical trials, however, designed to evaluate the potential benefits obtained with an intensive antihypertensive therapy, aimed at achieving a target systolic BP level below 120 mmHg as compared to those obtained with less stringent therapy, have challenged the previous recommendations from international guidelines. In fact, detailed analyses of these trials showed a paradoxically increased risk of coronary events, mostly myocardial infarction, in those patients who achieved the lowest BP levels, particularly in the high-risk subsets of hypertensive populations with diabetes. In the light of these considerations, the present article will briefly review the common pathophysiological mechanisms, the potential sites of therapeutic interactions and the currently recommended BP targets to be achieved under pharmacological treatment in hypertension and diabetes. PMID:26543822

  9. Determination of fructose metabolic pathways in normal and fructose-intolerant children: A sup 13 C NMR study using (U- sup 13 C)fructose

    SciTech Connect

    Gopher, A.; Lapidot, A. ); Vaisman, N. ); Mandel, H. )

    1990-07-01

    An inborn deficiency in the ability of aldolase B to split fructose 1-phosphate is found in humans with hereditary fructose intolerance (HFI). A stable isotope procedure to elucidate the mechanism of conversion of fructose to glucose in normal children and in HFI children has been developed. A constant infusion of D-(U-{sup 13}C)fructose was given nasogastrically to control and to HFI children. Hepatic fructose conversion to glucose was estimated by examination of {sup 13}C NMR spectra of plasma glucose. Significantly lower values ({approx}3-fold) for fructose conversion to glucose were obtained for the HFI patients as compared to the controls. A quantitative determination of the metabolic pathways of fructose conversion to glucose was derived from {sup 13}C NMR measurement of plasma ({sup 13}C)glucose isotopomer populations. The finding of isotopomer populations of three adjacent {sup 13}C atoms at glucose C-4 ({sup 13}C{sub 3}-{sup 13}C{sub 4}-{sup 13}C{sub 5}) suggests that there is a direct pathway from fructose, by-passing fructose-1-phosphate aldolase, to fructose 1,6-bisphosphate. The metabolism of fructose by fructose-1-phosphate aldolase activity accounts for only {approx}50% of the total amount of hepatic fructose conversion to glucose. In view of the marked decline by 67% in synthesis of glucose from fructose in HFI subjects found in this study, the extent of ({sup 13}C)glucose formation from a trace amount of (U-{sup 13}C)fructose infused into the patient can be used as a safe and noninvasive diagnostic test for inherent faulty fructose metabolism.

  10. Synthetic Oligodeoxynucleotides Containing Multiple Telemeric TTAGGG Motifs Suppress Inflammasome Activity in Macrophages Subjected to Oxygen and Glucose Deprivation and Reduce Ischemic Brain Injury in Stroke-Prone Spontaneously Hypertensive Rats.

    PubMed

    Zhao, Jing; Mou, Yongshan; Bernstock, Joshua D; Klimanis, Dace; Wang, Sixian; Spatz, Maria; Maric, Dragan; Johnson, Kory; Klinman, Dennis M; Li, Xiaohong; Li, Xinhui; Hallenbeck, John M

    2015-01-01

    The immune system plays a fundamental role in both the development and pathobiology of stroke. Inflammasomes are multiprotein complexes that have come to be recognized as critical players in the inflammation that ultimately contributes to stroke severity. Inflammasomes recognize microbial and host-derived danger signals and activate caspase-1, which in turn controls the production of the pro-inflammatory cytokine IL-1?. We have shown that A151, a synthetic oligodeoxynucleotide containing multiple telemeric TTAGGG motifs, reduces IL-1? production by activated bone marrow derived macrophages that have been subjected to oxygen-glucose deprivation and LPS stimulation. Further, we demonstrate that A151 reduces the maturation of caspase-1 and IL-1?, the levels of both the iNOS and NLRP3 proteins, and the depolarization of mitochondrial membrane potential within such cells. In addition, we have demonstrated that A151 reduces ischemic brain damage and NLRP3 mRNA levels in SHR-SP rats that have undergone permanent middle cerebral artery occlusion. These findings clearly suggest that the modulation of inflammasome activity via A151 may contribute to a reduction in pro-inflammatory cytokine production by macrophages subjected to conditions that model brain ischemia and modulate ischemic brain damage in an animal model of stroke. Therefore, modulation of ischemic pathobiology by A151 may have a role in the development of novel stroke prevention and therapeutic strategies. PMID:26473731

  11. Synthetic Oligodeoxynucleotides Containing Multiple Telemeric TTAGGG Motifs Suppress Inflammasome Activity in Macrophages Subjected to Oxygen and Glucose Deprivation and Reduce Ischemic Brain Injury in Stroke-Prone Spontaneously Hypertensive Rats

    PubMed Central

    Bernstock, Joshua D.; Klimanis, Dace; Wang, Sixian; Spatz, Maria; Maric, Dragan; Johnson, Kory; Klinman, Dennis M.; Li, Xiaohong; Li, Xinhui; Hallenbeck, John M.

    2015-01-01

    The immune system plays a fundamental role in both the development and pathobiology of stroke. Inflammasomes are multiprotein complexes that have come to be recognized as critical players in the inflammation that ultimately contributes to stroke severity. Inflammasomes recognize microbial and host-derived danger signals and activate caspase-1, which in turn controls the production of the pro-inflammatory cytokine IL-1?. We have shown that A151, a synthetic oligodeoxynucleotide containing multiple telemeric TTAGGG motifs, reduces IL-1? production by activated bone marrow derived macrophages that have been subjected to oxygen-glucose deprivation and LPS stimulation. Further, we demonstrate that A151 reduces the maturation of caspase-1 and IL-1?, the levels of both the iNOS and NLRP3 proteins, and the depolarization of mitochondrial membrane potential within such cells. In addition, we have demonstrated that A151 reduces ischemic brain damage and NLRP3 mRNA levels in SHR-SP rats that have undergone permanent middle cerebral artery occlusion. These findings clearly suggest that the modulation of inflammasome activity via A151 may contribute to a reduction in pro-inflammatory cytokine production by macrophages subjected to conditions that model brain ischemia and modulate ischemic brain damage in an animal model of stroke. Therefore, modulation of ischemic pathobiology by A151 may have a role in the development of novel stroke prevention and therapeutic strategies. PMID:26473731

  12. Neuronal LRP1 Regulates Glucose Metabolism and Insulin Signaling in the Brain

    PubMed Central

    Liu, Chia-Chen; Hu, Jin; Tsai, Chih-Wei; Yue, Mei; Melrose, Heather L.; Kanekiyo, Takahisa

    2015-01-01

    Alzheimer's disease (AD) is a neurological disorder characterized by profound memory loss and progressive dementia. Accumulating evidence suggests that Type 2 diabetes mellitus, a metabolic disorder characterized by insulin resistance and glucose intolerance, significantly increases the risk for developing AD. Whereas amyloid-β (Aβ) deposition and neurofibrillary tangles are major histological hallmarks of AD, impairment of cerebral glucose metabolism precedes these pathological changes during the early stage of AD and likely triggers or exacerbates AD pathology. However, the mechanisms linking disturbed insulin signaling/glucose metabolism and AD pathogenesis remain unclear. The low-density lipoprotein receptor-related protein 1 (LRP1), a major apolipoprotein E receptor, plays critical roles in lipoprotein metabolism, synaptic maintenance, and clearance of Aβ in the brain. Here, we demonstrate that LRP1 interacts with the insulin receptor β in the brain and regulates insulin signaling and glucose uptake. LRP1 deficiency in neurons leads to impaired insulin signaling as well as reduced levels of glucose transporters GLUT3 and GLUT4. Consequently, glucose uptake is reduced. By using an in vivo microdialysis technique sampling brain glucose concentration in freely moving mice, we further show that LRP1 deficiency in conditional knock-out mice resulted in glucose intolerance in the brain. We also found that hyperglycemia suppresses LRP1 expression, which further exacerbates insulin resistance, glucose intolerance, and AD pathology. As loss of LRP1 expression is seen in AD brains, our study provides novel insights into insulin resistance in AD. Our work also establishes new targets that can be explored for AD prevention or therapy. PMID:25855193

  13. Neuronal LRP1 regulates glucose metabolism and insulin signaling in the brain.

    PubMed

    Liu, Chia-Chen; Hu, Jin; Tsai, Chih-Wei; Yue, Mei; Melrose, Heather L; Kanekiyo, Takahisa; Bu, Guojun

    2015-04-01

    Alzheimer's disease (AD) is a neurological disorder characterized by profound memory loss and progressive dementia. Accumulating evidence suggests that Type 2 diabetes mellitus, a metabolic disorder characterized by insulin resistance and glucose intolerance, significantly increases the risk for developing AD. Whereas amyloid-β (Aβ) deposition and neurofibrillary tangles are major histological hallmarks of AD, impairment of cerebral glucose metabolism precedes these pathological changes during the early stage of AD and likely triggers or exacerbates AD pathology. However, the mechanisms linking disturbed insulin signaling/glucose metabolism and AD pathogenesis remain unclear. The low-density lipoprotein receptor-related protein 1 (LRP1), a major apolipoprotein E receptor, plays critical roles in lipoprotein metabolism, synaptic maintenance, and clearance of Aβ in the brain. Here, we demonstrate that LRP1 interacts with the insulin receptor β in the brain and regulates insulin signaling and glucose uptake. LRP1 deficiency in neurons leads to impaired insulin signaling as well as reduced levels of glucose transporters GLUT3 and GLUT4. Consequently, glucose uptake is reduced. By using an in vivo microdialysis technique sampling brain glucose concentration in freely moving mice, we further show that LRP1 deficiency in conditional knock-out mice resulted in glucose intolerance in the brain. We also found that hyperglycemia suppresses LRP1 expression, which further exacerbates insulin resistance, glucose intolerance, and AD pathology. As loss of LRP1 expression is seen in AD brains, our study provides novel insights into insulin resistance in AD. Our work also establishes new targets that can be explored for AD prevention or therapy. PMID:25855193

  14. Energy Excess, Glucose Utilization, and Skeletal Remodeling: New Insights.

    PubMed

    Lecka-Czernik, Beata; Rosen, Clifford J

    2015-08-01

    Skeletal complications have recently been recognized as another of the several comorbidities associated with diabetes. Clinical studies suggest that disordered glucose and lipid metabolism have a profound effect on bone. Diabetes-related changes in skeletal homeostasis result in a significant increased risk of fractures, although the pathophysiology may differ from postmenopausal osteoporosis. Efforts to understand the underlying mechanisms of diabetic bone disease have focused on the direct interaction of adipose tissue with skeletal remodeling and the potential influence of glucose utilization and energy uptake on these processes. One aspect that has emerged recently is the major role of the central nervous system in whole-body metabolism, bone turnover, adipose tissue remodeling, and beta cell secretion of insulin. Importantly, the skeleton contributes to the metabolic balance inherent in physiologic states. New animal models have provided the insights necessary to begin to dissect the effects of obesity and insulin resistance on the acquisition and maintenance of bone mass. In this Perspective, we focus on potential mechanisms that underlie the complex interactions between adipose tissue and skeletal turnover by focusing on the clinical evidence and on preclinical studies indicating that glucose intolerance may have a significant impact on the skeleton. In addition, we raise fundamental questions that need to be addressed in future studies to resolve the conundrum associated with glucose intolerance, obesity, and osteoporosis. PMID:26094610

  15. Treatment of 51 pregnancies with danaparoid because of heparin intolerance.

    PubMed

    Lindhoff-Last, Edelgard; Kreutzenbeck, Hans-Joachim; Magnani, Harry N

    2005-01-01

    Pregnant patients with acute venous thrombosis or a history of thrombosis may need alternative anticoagulation, when heparin intolerance occurs. Only limited data on the use of the heparinoid danaparoid are available in literature. We reviewed the use of danaparoid in 51 pregnancies of 49 patients identified in literature between 1981 and 2004. All patients had developed heparin intolerance (32 due to heparin-induced thrombocytopenia, 19 mainly due to heparin-induced skin rashes) and had a current and/or past history of thromboembolic complications. The initial danaparoid dose regimens ranged from 1000 to 7500 U/day administered s.c. or i.v.. The median duration of danaparoid use was 10 weeks. Danaparoid was used until delivery of a healthy infant in 37 pregnancies. In the remaining 14 pregnancies it was stopped earlier, because anticoagulant treatment was no longer required (3/14) or an adverse event led to a treatment discontinuation (11/14). Four maternal bleeding events were recorded during pregnancy, delivery or postpartum, two of them were fatal due to placental problems. Three fetal deaths were recorded, all associated with maternal complications antedating danaparoid use. Danaparoid cross-reactivity was suspected in 4 HIT patients and 5 non-HIT patients with skin reactions and was confirmed serologically in one of the two HIT patients tested. In none of five fetal cord blood- and three maternal breast milksamples anti-Xa activity transfer was observed. In conclusion danaparoid can be used as an alternative antithrombotic agent in pregnant women with high thrombotic risk and intolerance to heparins. PMID:15630492

  16. Down on heights? One in three has visual height intolerance.

    PubMed

    Huppert, Doreen; Grill, Eva; Brandt, Thomas

    2013-02-01

    The distressing phenomenon of visual height intolerance (vHI) occurs when a visual stimulus causes apprehension of losing control of balance and falling from some height. Epidemiological data of this condition in the general population are lacking. Assignment of prevalence, determinants, and compensation of vHI was performed in a cross-sectional epidemiological study of 3,517 individuals representing the German population. Life-time prevalence of vHI is 28 % (females 32 %). A higher prevalence is associated independently with a family history of vHI, anxiety disorders, migraine, or motion sickness susceptibility. Women aged 50-59 have a higher prevalence than younger women or men of all ages. Initial attacks occur most often (30 %) in the second decade; however, attacks can manifest throughout life. The main symptoms are fearfulness, inner agitation, a queasy-stomach feeling, subjective postural instability with to-and-fro vertigo, and weakness in the knees. Climbing a tower is the first most common precipitating stimulus; the spectrum of such stimuli widens with time in more than 50 % of afflicted individuals. The most frequent reaction to vHI is to avoid the triggering stimuli (>50 %); 11 % of susceptible individuals consult a doctor, most often a general practitioner, neurologist, ENT doctor, or psychiatrist. In brief, visual height intolerance affects one-third of the general population, considerably restricting the majority of these individuals in their daily activities. The data show that the two terms do not indicate a categorical distinction but rather a continuum from slight forms of visual height intolerance to the specific phobia of fear of heights. PMID:23070463

  17. Autogenic-feedback training: A countermeasure for orthostatic intolerance

    NASA Technical Reports Server (NTRS)

    Cowings, Patricia S.; Toscano, William B.; Kamiya, Joe; Miller, Neal E.; Pickering, Thomas G.

    1991-01-01

    NASA has identified cardiovascular deconditioning as a serious biomedical problem associated with long-duration exposure to microgravity in space. High priority has been given to the development of countermeasures for this disorder and the resulting orthostatic intolerance experienced by crewmembers upon their return to the 1g norm of Earth. The present study was designed to examine the feasibility of training human subjects to control their own cardiovascular responses to gravitational stimulation (i.e., a tilt table). Using an operant conditioning procedure, Autogenic-Feedback Training (AFT), we would determine if subjects could learn to increase their own blood pressure voluntarily.

  18. Hypertension in young adults.

    PubMed

    De Venecia, Toni; Lu, Marvin; Figueredo, Vincent M

    2016-03-01

    Hypertension remains a major societal problem affecting 76 million, or approximately one third, of US adults. While more prevalent in the older population, an increasing incidence in the younger population, including athletes, is being observed. Active individuals, like the young and athletes, are viewed as free of diseases such as hypertension. However, the increased prevalence of traditional risk factors in the young, including obesity, diabetes mellitus, and renal disease, increase the risk of developing hypertension in younger adults. Psychosocial factors may also be contributing factors to the increasing incidence of hypertension in the younger population. Increased left ventricular wall thickness and mass are increasingly found in young adults on routine echocardiograms and predict future cardiovascular events. This increasing incidence of hypertension in the young calls for early surveillance and prompt treatment to prevent future cardiac events. In this review we present the current epidemiological data, potential mechanisms, clinical implications, and treatment of hypertension in young patients and athletes. PMID:26821528

  19. Hypertension and medical informatics.

    PubMed Central

    McBride, William; Ferrario, Carlos; Lyle, Paulette A.

    2003-01-01

    BACKGROUND: Only about 27% of Americans with hypertension have their disease under control. Hypertension in the African-American population has a higher prevalence (32%) and is less likely to be treated or controlled compared with that in the caucasian population. Hypertension places a significant burden on patients and health care systems. Applications of medical informatics can facilitate the management of hypertension. Examples that illustrate the utility, status, and future potential of medical informatics applications in the treatment of hypertension are presented. METHODS: Relevant studies and review articles were accessed through a PubMed search of the English-language literature and for current Internet-based information for the time period of 1993-2002. Search terms included, but were not limited to, hypertension, medical informatics, medical information science, electronic medical records, Internet, and managed care. RESULTS: There is evidence that medical informatics has a favorable impact on health care issues as it relates to patients and physicians. Although the use of computers to assist in managing hypertension is in its infancy, there are examples where informatics applications have a demonstrated clinical value. CONCLUSIONS: Management of hypertension needs much improvement. The use of computers and the Internet in health care is expanding and expected to have a positive impact on the management of chronic diseases, such as hypertension. PMID:14651371

  20. [Hypertension and the eye].

    PubMed

    Ambresin, Aude; Borruat, François Xavier

    2015-12-16

    Systemic hypertension is widely spread in the general population. It is recognised as a major risk factor for cardiovascular morbidity and mortality. Hypertensive retinopathy is the most common manifestation. Initial changes are retinal arteriolar vasoconstriction and findings such as flame or blot hemorrhages, cotton wool spots and hard exsudates resulting from localised retinal ischemia. Ocular complications of high blood pressure (HBP) are subconjunctival hemorrhages and retinal vein occlusions. Hypertensive retinopathy contributes to worsening of diabetic retinopathy. Less common but more threatening are ischemic optic neuropathy and retinal arterial occlusions. Screening is recommended in case of severe systemic hypertension, diabetes, or any complain of recent visual disturbances. PMID:26852552

  1. Blood Test: Glucose

    MedlinePlus

    ... Kids Up for Sports Pregnant? Your Baby's Growth Cerebral Palsy: Caring for Your Child All About Food Allergies ... Ketoacidosis Blood Glucose Record Getting a Blood Test (Video) Diabetes Center Definition: Blood Glucose Level Blood Glucose ...

  2. Variability of gluten intolerance in treated childhood coeliac disease.

    PubMed Central

    McNicholl, B; Egan-Mitchell, B; Fottrell, P F

    1979-01-01

    Fifty children consecutively attending a clinic for coeliac disease co-operated in a trial; 10 found to have flat mucosa were excluded. Forty children of mean age 9.8 years, whose duodenal or jejunal mucosa had returned to normal or near normal appearance after a mean of 5.8 years on gluten-free diets, were put back on normal diets. In 37, mucosal occurred in a mean of 16.9 months (four to 74 months). Four of the 37 had serial biopsies, in which mucosal enzymes (particularly lactase) fell and interepithelial lymphocyte counts rose before the mucosal morphology was regarded as definitely 'coeliac'. Three children had normal mucosal appearance after 58 to 73 months on normal diets, one of whom showed temporary mucosal abnormalities, another having occasionally low enzymes, in both suggesting underlying gluten sensitivity. Lactase suppression and raised IEL counts appear to be sensitive indicators of gluten intolerance. In our experience, a diagnosis of coeliac disease based on severe mucosal damage and a satisfactory response to a gluten-free but milk-containing diet implies a very strong likelihood of permanent or prolonged gluten intolerance, but with a striking variability in its expression. Images Figure PMID:428824

  3. Carbohydrate intolerance and kidney stones in children in the Goldfields.

    PubMed

    Baldwin, D N; Spencer, J L; Jeffries-Stokes, C A

    2003-07-01

    Renal stones have been reported as a common finding in Australian Aboriginal children. The stones are predominantly urate in composition. We report on five children with nephrolithiasis from the Goldfields region of Western Australia. All were diagnosed when under 5 years of age, the majority being under 3 years. All five children also had lactose intolerance, and we postulate that carbohydrate malabsorption, together with the ensuing chronic diarrhoea and intraluminal breakdown of sugars by enteric bacteria may result in a situation of chronic metabolic acidosis. Chronic metabolic acidosis can lead to protein catabolism, increased urate excretion and the formation of renal stones. Carbohydrate intolerance may be an aetiological factor in the development of renal stones and possibly chronic renal disease, particularly in Aboriginal Australians. Renal disease represents one of the most significant factors affecting the health of Australian Aboriginal people. The incidence of end stage renal failure in this population exceeds that of non-Aboriginals by a factor of 13:1, and this disproportionate figure is increasing. It is likely that chronic renal damage is multifactorial; however, it is probable that at least some aetiological factors have their onset during childhood. PMID:12887672

  4. Intolerance of sexy peers: intrasexual competition among women.

    PubMed

    Vaillancourt, Tracy; Sharma, Aanchal

    2011-01-01

    Intrasexual competition among males of different species, including humans, is well documented. Among females, far less is known. Recent nonexperimental studies suggest that women are intolerant of attractive females and use indirect aggression to derogate potential rivals. In Study 1, an experimental design was used to test the evolutionary-based hypothesis that women would be intolerant of sexy women and would censure those who seem to make sex too readily available. Results provide strong empirical support for intrasexual competition among women. Using independent raters, blind to condition, we found that almost all women were rated as reacting negatively ("bitchy") to an attractive female confederate when she was dressed in a sexually provocative manner. In contrast, when she was dressed conservatively, the same confederate was barely noticed by the participants. In Study 2, an experimental design was used to assess whether the sexy female confederate from Study 1 was viewed as a sexual rival by women. Results indicated that as hypothesized, women did not want to introduce her to their boyfriend, allow him to spend time alone with her, or be friends with her. Findings from both studies are discussed in terms of evolutionary theory. PMID:21932332

  5. Self-reported intolerance of uncertainty and behavioural decisions.

    PubMed

    Carleton, R Nicholas; Duranceau, Sophie; Shulman, Elizabeth P; Zerff, Marissa; Gonzales, Josh; Mishra, Sandeep

    2016-06-01

    Intolerance of Uncertainty (IU) appears to be a robust transdiagnostic risk factor related to anxiety and depression. Most transdiagnostic IU research has used the self-report Intolerance of Uncertainty Scale-Short Form; however, there is comparatively little research exploring presumed behavioral correlates of IU. The current study was designed to assess relationships between self-reported IU and decisions in uncertainty-based behavioral tasks (specifically, the Wisconsin Card Sorting Task, the Risky Gains Task, and the Modified Iowa Gambling Task). Participants comprised compensated community members (n = 108; 69% women) and undergraduates (n = 98; 78% women). Community member compensation was not contingent on performance, but undergraduate compensation was partially contingent on performance. Results replicated prior research, with both samples producing small (r = .19) to moderate (r = -.29) correlations (ps < .05) between self-reported IU and outcome variables from each of the behavioral tasks. The relationships were larger in the undergraduate sample, likely due to the compensation incentive. In general, the results suggest that increasing IU is associated with increasingly risk adverse behaviors; however, the relationship appears complex and in need of substantial additional research to understand how clinically-significant IU would impact pathology-related behaviours. PMID:26788617

  6. [Histamine intolerance - are the criteria of an adverse reaction met?].

    PubMed

    Reese, Imke

    2016-06-01

    Searching the internet for an explaination of recurring symptoms, many people come across the so-called histamine intolerance disorder. Also many practitioners like to diagnose this disorder without making sure that reproducibility, a prerequisite for an adverse reaction, is present. Consequently, presumably affected persons are often advised to follow a low-histamine diet. Depending on the source of information, these diets often avoid a huge variety of foods containing more or less histamine, which has a considerable impact on patient quality of life. While most persons benefit from such a diet in the beginning - this might be due to the change in dietary habits or the expectation of symptom improvement by dieting - in the long run the expected loss of symptoms will not happen. Underlying a diminished capacity for histamine degradation, the lack of partial or complete symptom improvement might be due to the fact that endogenous histamine release is responsible for reactions. The role of ingested histamine is discussed controversially. However, it is more than obvious that the histamine content of a certain food alone is not enough to predict its tolerance.If histamine intolerance is suspected, an individual diagnostic and therapeutic procedure is mandatory in order to minimize avoidance and to preserve a high quality of life. Ideally this is done in a close cooperation between allergologists and nutritionists/dieticians. PMID:27177895

  7. Efficacy of Garcinia Cambogia on Body Weight, Inflammation and Glucose Tolerance in High Fat Fed Male Wistar Rats

    PubMed Central

    Sripradha, Ramalingam

    2015-01-01

    Introduction: Obesity leads to derangements in lipid and glucose homeostasis resulting in various metabolic complications. Plants containing vital phytochemicals are known to posses anti obesity properties and have proved to exert beneficial effects in obesity. Objectives: The present study was aimed to investigate the effects of Garcinia Cambogia on body weight, glucose tolerance and inflammation in high fat diet fed male Wistar rats. Materials and Methods: Five month old male wistar rats (n=40) were divided into four groups. Two groups were fed with standard rodent diet and the remaining two with 30% high fat diet. One group in each of the two sets received the crude ethanolic extract of Garcinia Cambogia at a dose of 400mg/kg body weight/day for ten weeks. Body weight, intraperitoneal glucose tolerance test, leptin, tumour necrosis factor-α (TNF-α) and renal function (urea, creatinine, uric acid) were studied. Results: High fat diet fed rats showed increased body weight gain, glucose intolerance, elevated levels of plasma leptin and TNF-α. Supplementation of Garcinia Cambogia extract (GE) along with high fat diet significantly decreased body weight gain, glucose intolerance, plasma leptin and TNF-α level. No significant changes were observed in the renal function parameters in any of the groups. Conclusion: Supplementation of the Garcinia Cambogia extract with high fat diet reduced body weight gain, inflammation and glucose intolerance. PMID:25859449

  8. Idiopathic Intracranial Hypertension (Pseudotumor Cerebri)

    MedlinePlus

    ... Asked Questions Español Condiciones Chinese Conditions Idiopathic Intracranial Hypertension (Pseudotumor Cerebri) En Español Read in Chinese What is idiopathic intracranial hypertension? Idiopathic intracranial hypertension (IIH) is a disorder that ...

  9. Effects of Estrogen on Glucose Uptake by Rat Muscle 1

    PubMed Central

    Shamoon, Harry; Felig, Philip

    1974-01-01

    The isolated rat diaphragm was used to study the effects of 17β-estradiol on basal and insulin-mediated glucose uptake. Rats were injected with estradiol for 2 wk in daily doses of 10 μg/100 g of body weight and were compared to untreated control animals. Estrogen treatment resulted in a 16% decrease in basal glucose uptake by diaphragm muscle as compared to controls. In contrast, in the presence of insulin, glucose uptake by muscle increased 103% above basal in estradiol-treated animals as compared to a 38% rise in the control group. The absolute rate of glucose uptake induced by insulin in the estradiol treated animals (5.8 mg/g/hr) was 22% higher than in controls. These findings were not accompanied by changes in weight gain, plasma glucose and plasma immunoreactive insulin concentrations in the treated animals. In vitro incubation of diaphragm muscle with estradiol did not have an effect on basal or insulin-mediated glucose uptake. The data indicate that treatment with naturally occurring estrogens increases muscle sensitivity to insulin-stimulated glucose uptake. These findings suggest that the carbohydrate intolerance associated with the administration of oral contraceptives may be related to the use of synthetic rather than natural estrogens and/or progestins in such preparations. PMID:4456835

  10. Stress and hypertension.

    PubMed

    Kulkarni, S; O'Farrell, I; Erasi, M; Kochar, M S

    1998-12-01

    Stress can cause hypertension through repeated blood pressure elevations as well as by stimulation of the nervous system to produce large amounts of vasoconstricting hormones that increase blood pressure. Factors affecting blood pressure through stress include white coat hypertension, job strain, race, social environment, and emotional distress. Furthermore, when one risk factor is coupled with other stress producing factors, the effect on blood pressure is multiplied. Overall, studies show that stress does not directly cause hypertension, but can have an effect on its development. A variety of non-pharmacologic treatments to manage stress have been found effective in reducing blood pressure and development of hypertension, examples of which are meditation, acupressure, biofeedback and music therapy. Recent results from the National Health and Nutrition Examination Survey indicate that 50 million American adults have hypertension (defined to be a systolic blood pressure of greater than 139 mm Hg or a diastolic blood pressure of greater than 89 mm Hg). In 95% of these cases, the cause of hypertension is unknown and they are categorized as "essential" hypertension. Although a single cause may not be identified, the general consensus is that various factors contribute to blood pressure elevation in essential hypertension. In these days of 70 hour work weeks, pagers, fax machines, and endless committee meetings, stress has become a prevalent part of people's lives; therefore the effect of stress on blood pressure is of increasing relevance and importance. Although stress may not directly cause hypertension, it can lead to repeated blood pressure elevations, which eventually may lead to hypertension. In this article we explore how stress can cause hypertension and what can be done about it. PMID:9894438

  11. A glucose-centric perspective of hyperglycemia.

    PubMed

    Ramasarma, T; Rafi, M

    2016-02-01

    Digestion of food in the intestines converts the compacted storage carbohydrates, starch and glycogen, to glucose. After each meal, a flux of glucose (> 200 g) passes through the blood pool (4-6 g) in a short period of 2 h, keeping its concentration ideally in the range of 80-120 mg/100 mL. Tissue-specific glucose transporters (GLUTs) aid in the distribution of glucose to all tissues. The balance glucose after meeting the immediate energy needs is converted into glycogen and stored in liver (up to 100 g) and skeletal muscle (up to 300 g) for later use. High blood glucose gives the signal for increased release of insulin from pancreas. Insulin binds to insulin receptor on the plasma membrane and activates its autophosphorylation. This initiates the post-insulin-receptor signal cascade that accelerates synthesis of glycogen and triglyceride. Parallel control by phos-dephos and redox regulation of proteins exists for some of these steps. A major action of insulin is to inhibit gluconeogensis in the liver decreasing glucose output into blood. Cases with failed control of blood glucose have alarmingly increased since 1960 coinciding with changed life-styles and large scale food processing. Many of these turned out to be resistant to insulin, usually accompanied by dysfunctional glycogen storage. Glucose has an extended stay in blood at 8 mM and above and then indiscriminately adds on to surface protein-amino groups. Fructose in common sugar is 10-fold more active. This random glycation process interferes with the functions of many proteins (e.g., hemoglobin, eye lens proteins) and causes progressive damage to heart, kidneys, eyes and nerves. Some compounds are known to act as insulin mimics. Vanadium-peroxide complexes act at post-receptor level but are toxic. The fungus-derived 2,5-dihydroxybenzoquinone derivative is the first one known to act on the insulin receptor. The safe herbal products in use for centuries for glucose control have multiple active principles and targets. Some are effective in slowing formation of glucose in intestines by inhibiting α-glucosidases (e.g., salacia/saptarangi). Knowledge gained from French lilac on active guanidine group helped developing Metformin (1,1-dimethylbiguanide) one of the popular drugs in use. One strategy of keeping sugar content in diets in check is to use artificial sweeteners with no calories, no glucose or fructose and no effect on blood glucose (e.g., steviol, erythrytol). However, the three commonly used non-caloric artificial sweeteners, saccharin, sucralose and aspartame later developed glucose intolerance, the very condition they are expected to evade. Ideal way of keeping blood glucose under 6 mM and HbA1c, the glycation marker of hemoglobin, under 7% in blood is to correct the defects in signals that allow glucose flow into glycogen, still a difficult task with drugs and diets. PMID:26934776

  12. Noncirrhotic Portal Hypertension

    PubMed Central

    Rajekar, Harshal; Vasishta, Rakesh K; Chawla, Yogesh K; Dhiman, Radha K

    2011-01-01

    Portal hypertension is characterized by an increase in portal pressure (> 10 mmHg) and could be a result of cirrhosis of the liver or of noncirrhotic diseases. When portal hypertension occurs in the absence of liver cirrhosis, noncirrhotic portal hypertension (NCPH) must be considered. The prognosis of this disease is much better than that of cirrhosis. Noncirrhotic diseases are the common cause of portal hypertension in developing countries, especially in Asia. NCPH is a heterogeneous group of diseases that is due to intrahepatic or extrahepatic etiologies. In general, the lesions in NCPH are vascular in nature and can be classified based on the site of resistance to blood flow. In most cases, these disorders can be explained by endothelial cell lesions, intimal thickening, thrombotic obliterations, or scarring of the intrahepatic portal or hepatic venous circulation. Many different conditions can determine NCPH through the association of these various lesions in various degrees. Many clinical manifestations of NCPH result from the secondary effects of portal hypertension. Patients with NCPH present with upper gastrointestinal bleeding, splenomegaly, ascites after gastrointestinal bleeding, features of hypersplenism, growth retardation, and jaundice due to portal hypertensive biliopathy. Other sequelae include hyperdynamic circulation, pulmonary complications, and other effects of portosystemic collateral circulation like portosystemic encephalopathy. At present, pharmacologic and endoscopic treatments are the treatments of choice for portal hypertension. The therapy of all disorders causing NCPH involves the reduction of portal pressure by pharmacotherapy or portosystemic shunting, apart from prevention and treatment of complications of portal hypertension. PMID:25755321

  13. Studies on Intolerance in American Life. Program in American History and Civilization.

    ERIC Educational Resources Information Center

    Tufts Univ., Medford, MA. Lincoln Filene Center for Citizenship and Public Affairs.

    The narrative selected for this unit on intolerance illustrates the perennial and universal methods for scapegoating. The general teaching objectives are to lead the students: 1) to feelings of tolerance toward individuals and groups who are different; 2) to investigate intolerance in terms of some of its causes: fear, deprivation, threatened…

  14. The Intolerance of Uncertainty Index: Replication and Extension with an English Sample

    ERIC Educational Resources Information Center

    Carleton, R. Nicholas; Gosselin, Patrick; Asmundson, Gordon J. G.

    2010-01-01

    Intolerance of uncertainty (IU) is related to anxiety, depression, worry, and anxiety sensitivity. Precedent IU measures were criticized for psychometric instability and redundancy; alternative measures include the novel 45-item measure (Intolerance of Uncertainty Index; IUI). The IUI was developed in French with 2 parts, assessing general…

  15. Prevalence of self-reported lactose intolerance in multiethnic sample of adults

    Technology Transfer Automated Retrieval System (TEKTRAN)

    According to the National Institute of Diabetes and Digestive and Kidney Diseases, between 30 and 50 million Americans have the potential for lactose-intolerance symptoms. However, lactose-intolerance prevalence rates in practical life settings may be lower than originally suggested. The goal of thi...

  16. Lactose Intolerance: Exploring Reaction Kinetics Governing Lactose Conversion of Dairy Products within the Undergraduate Laboratory

    ERIC Educational Resources Information Center

    Smart, Jimmy L.

    2008-01-01

    Lactose intolerance is a condition suffered by an estimated 50 million Americans. Certain ethnic and racial populations are more widely affected than others. As many as 75 percent of all African-American, Jewish, Native American, and Mexican-American adults, and 90 percent of Asian-American adults are lactose intolerant. Some populations in Africa…

  17. Promoting Good Campus Relations: Dealing with Hate Crimes and Intolerance. Guidelines

    ERIC Educational Resources Information Center

    Universities UK, 2005

    2005-01-01

    This guidance has been produced to help higher education institutions (HEIs) deal with hate crimes and intolerance. Aiming to replace the previous Committee of Vice-Chancellors and Principals' guidance on extremism and intolerance, this publication provides an overview of the ways in which HEIs can encourage tolerance and respect and ensure that

  18. Lactose Intolerance: Exploring Reaction Kinetics Governing Lactose Conversion of Dairy Products within the Undergraduate Laboratory

    ERIC Educational Resources Information Center

    Smart, Jimmy L.

    2008-01-01

    Lactose intolerance is a condition suffered by an estimated 50 million Americans. Certain ethnic and racial populations are more widely affected than others. As many as 75 percent of all African-American, Jewish, Native American, and Mexican-American adults, and 90 percent of Asian-American adults are lactose intolerant. Some populations in Africa

  19. Relationships among Perceived Racial Stress, Intolerance of Uncertainty, and Worry in a Black Sample

    ERIC Educational Resources Information Center

    Rucker, LaTanya S.; West, Lindsey M.; Roemer, Lizabeth

    2010-01-01

    The purpose of this study was to explore the relationships among chronic worry, perceived racial stress, and intolerance of uncertainty in a sample of adults who racially identify as Black. Intolerance of uncertainty has been associated with worry and generalized anxiety disorder in predominantly White samples. Given that racial stress is likely…

  20. The Intolerance of Uncertainty Index: Replication and Extension with an English Sample

    ERIC Educational Resources Information Center

    Carleton, R. Nicholas; Gosselin, Patrick; Asmundson, Gordon J. G.

    2010-01-01

    Intolerance of uncertainty (IU) is related to anxiety, depression, worry, and anxiety sensitivity. Precedent IU measures were criticized for psychometric instability and redundancy; alternative measures include the novel 45-item measure (Intolerance of Uncertainty Index; IUI). The IUI was developed in French with 2 parts, assessing general

  1. Relationships among Perceived Racial Stress, Intolerance of Uncertainty, and Worry in a Black Sample

    ERIC Educational Resources Information Center

    Rucker, LaTanya S.; West, Lindsey M.; Roemer, Lizabeth

    2010-01-01

    The purpose of this study was to explore the relationships among chronic worry, perceived racial stress, and intolerance of uncertainty in a sample of adults who racially identify as Black. Intolerance of uncertainty has been associated with worry and generalized anxiety disorder in predominantly White samples. Given that racial stress is likely

  2. Promoting Good Campus Relations: Dealing with Hate Crimes and Intolerance. Guidelines

    ERIC Educational Resources Information Center

    Universities UK, 2005

    2005-01-01

    This guidance has been produced to help higher education institutions (HEIs) deal with hate crimes and intolerance. Aiming to replace the previous Committee of Vice-Chancellors and Principals' guidance on extremism and intolerance, this publication provides an overview of the ways in which HEIs can encourage tolerance and respect and ensure that…

  3. Discomfort Intolerance: Evaluation of a Potential Risk Factor for Anxiety Psychopathology

    ERIC Educational Resources Information Center

    Schmidt, Norman B.; Richey, J. Anthony; Cromer, Kiara R.; Buckner, Julia D.

    2007-01-01

    Discomfort intolerance, defined as an individual difference in the capacity to tolerate unpleasant bodily sensations, is a construct recently posited as a risk factor for panic and anxiety psychopathology. The present report used a biological challenge procedure to evaluate whether discomfort intolerance predicts fearful responding beyond the…

  4. Hypertension in the elderly

    PubMed Central

    Lionakis, Nikolaos; Mendrinos, Dimitrios; Sanidas, Elias; Favatas, Georgios; Georgopoulou, Maria

    2012-01-01

    The elderly are the most rapidly growing population group in the world. Data collected over a 30-year period have demonstrated the increasing prevalence of hypertension with age. The risk of coronary artery disease, stroke, congestive heart disease, chronic kidney insufficiency and dementia is also increased in this subgroup of hypertensives. Hypertension in the elderly patients represents a management dilemma to cardiovascular specialists and other practioners. During the last years and before the findings of the Systolic Hypertension in Europe Trial were published, the general medical opinion considered not to decrease blood pressure values similarly to other younger patients, in order to avoid possible ischemic events and poor oxygenation of the organs (brain, heart, kidney). The aim of this review article is to highlight the importance of treating hypertension in aged population in order to improve their quality of life and lower the incidence of the cardiovascular complications. PMID:22655162

  5. Malignant or Accelarated Hypertension

    PubMed Central

    Vaziri, N. D.

    1984-01-01

    Malignant or accelarated hypertension is a life-threatening medical emergency that is a possible complication of practically any hypertensive disorder. If not promptly treated it can cause severe, rapidly progressive target-organ damage and death. While the histo-pathologic features of malignant hypertension are well recognized, the pathogenesis of the associated vascular lesions and the transition from a benign to a malignant phase are unclear. With adequate control of hypertension, progression to the accelarated or malignant phase can be prevented. Moreover, promptly and effectively reducing the blood pressure during the malignant phase can prevent, minimize or even reverse serious target organ injury. Malignant hypertension, therefore, is both preventable and treatable. PMID:6372248

  6. [Hypertension in pregnancy].

    PubMed

    Cífková, R

    2006-03-01

    Hypertension in pregnancy is one of the main causes of maternal, fetal and newborn morbidity and mortality in civilised countries. Current recommendations of the European Society for Hypertension prefer definition of hypertension in pregnancy based on absolute values of blood pressure, i.e. systolic blood pressure > or = 140 mm Hg or diastolic blood pressure > or = 90 mm Hg. The most important task of classification of hypertension in pregnancy is to distinguish whether hypertension comes before pregnancy (the so called pre-existing hypertension) or whether it is a pregnancy-induced condition (the so called gestational hypertension). Pre-existing hypertension is diagnosed either before pregnancy or within the first 20 weeks of pregnancy. Gestational hypertension is characterised with poor blood circulation in many body organs, higher value of blood pressure usually being just one of the characteristic features. Non-pharmacological treatment of hypertension must be considered in pregnant women with systolic blood pressure 140-150 mm Hg or diastolic blood pressure 90-99 mm Hg. Salt restriction is not recommended, as well as weight reduction in obese women. Systolic blood pressure > or = 170 mm Hg or diastolic blood pressure > or = 110 mm Hg in pregnant women must be considered serious condition necessitating hospitalisation. Pharmacological therapy should include labetalol i.v. or metyldopa or nifedipin administered orally. Intravenous administration of dihydralazine is no longer a therapy of choice, for its use is connected with increased occurrence of adverse effects. The threshold values for commencement of anti-hypertension therapy are systolic blood pressure 140 mm Hg or diastolic blood pressure 90 mm Hg in females with gestational hypertension without proteinuria or with pre-existing hypertension before commencement of 28th week of pregnancy. Drug administration to reduce hypertension is instituted after reaching the same threshold values in females with gestational hypertension and proteinuria or after occurrence of the symptoms any time during pregnancy, with the same threshold values of blood pressure in the case of pre-existing hypertension at the presence of accompanying diseases or organ malfunction and further in the case of pre-existing hypertension and gestational hypertension. In other cases drug treatment of hypertension is recommended at systolic blood pressure values of 150 mm Hg or diastolic blood pressure values of 95 mm Hg. Unless serious hypertension is involved, the drugs of choice include metyldope, labetalol, calcium channel blockers and beta-blockers. Calcium channel blockers are considered safe, unless administered concurrently with magnesium sulphate (risk of hypotension in the case of potential synergism). ACE inhibitors and angiotensine blockers II (AT1-blockers) are contraindicated in pregnancy. Treatment with diuretics is not substantiated, unless oliguria is present. I.v. magnesium sulphate is recommended for prevention of eclampsia and spasm treatment. PMID:16722158

  7. Mild fasting hyperglycemia shifts fuel reliance toward fat during exercise in adults with impaired glucose tolerance

    PubMed Central

    Malin, Steven K.; Viskochil, Richard; Oliver, Corianne

    2013-01-01

    Impaired glucose tolerance (IGT) is characterized by decreased oxidative capacity and reduced carbohydrate utilization during exercise. However, it is unclear if the presence of impaired fasting glucose (IFG) affects fuel utilization during exercise in adults with IGT. We tested the hypothesis that the presence of IFG in adults with IGT decreases reliance on carbohydrate during exercise. Middle-aged, obese, sedentary individuals (n = 6, IGT and n = 6, IFG+IGT) were compared during exercise at 60% peak O2 consumption for 45 min on a cycle ergometer. Glucose rates of appearance and disposal and muscle glycogen were assessed by stable isotope dilution methods, and fat utilization was estimated via indirect calorimetry. A 75-g oral glucose tolerance test was used to determine fasting and 2-h glucose concentrations. A glucose intolerance severity z-score was calculated from the oral glucose tolerance test. Glucose flux (i.e., rates of appearance and disposal) was not different between groups. However, individuals with IFG+IGT had lower muscle glycogen use (P < 0.05) and elevated fat oxidation (P < 0.01) during exercise compared with those with isolated IGT. Plasma nonesterified fatty acids and glucose were significantly higher during exercise in subjects with IFG+IGT vs. IGT alone (P < 0.05). Fat utilization during exercise correlated with fasting glucose (r = 0.57, P = 0.05), glucose intolerance severity z-score (r = 0.66, P = 0.01), and nonesterified fatty acids (trend; r = 0.55, P = 0.08). The presence of IFG shifts fuel selection toward increased fat oxidation and decreased muscle glycogen utilization during exercise in adults with IGT. Whether these differences in substrate use contribute to, or are the result of, movement along the continuum from prediabetes to type 2 diabetes awaits further work. PMID:23599396

  8. Predictors of Hypertension Among Filipino Immigrants in the Northeast US

    PubMed Central

    Islam, Nadia Shilpi; Aguilar, David E.; Wyatt, Laura C.; Tandon, S. Darius; Abesamis-Mendoza, Noilyn; Nur, Potri Ranka Manis Queano; Rago-Adia, Josephine; Ileto, Benjamin; Rey, Mariano J.; Trinh-Shevrin, Chau

    2013-01-01

    Hypertension remains disproportionately high among Filipinos compared to other racial and ethnic minority populations, and little research on cardiovascular disease risk factors has been conducted among Filipino immigrants in the Northeastern part of the United States. To determine hypertension prevalence and risk factors among Filipino Americans in the New York City area, blood pressure and other clinical measurements were taken from a sample of Filipino Americans during 119 community health screenings conducted between 2006 and 2010. Additional socio-demographic and health-related characteristics were also collected via a cross-sectional survey. A total of 1,028 Filipino immigrants completed the survey and had clinical readings collected. Bivariate analyses and logistic regression were performed in order to predict and assess risk factors for hypertension among our sample. Fifty-three percent of individuals were hypertensive, and half of hypertensive individuals were uninsured. Logistic regression indicated that older age, male gender, living in the United States for over 5 years, a BMI greater than 23.0 kg/m2, an elevated glucose reading, a family history of hypertension, and fair or poor self-reported health status were predictors of hypertension. There is a great need to develop more effective community-based interventions in the Filipino community to address cardiovascular health disparities. PMID:23553685

  9. Four faces of baroreflex failure: hypertensive crisis, volatile hypertension, orthostatic tachycardia, and malignant vagotonia

    NASA Technical Reports Server (NTRS)

    Ketch, Terry; Biaggioni, Italo; Robertson, RoseMarie; Robertson, David

    2002-01-01

    BACKGROUND: The baroreflex normally serves to buffer blood pressure against excessive rise or fall. Baroreflex failure occurs when afferent baroreceptive nerves or their central connections become impaired. In baroreflex failure, there is loss of buffering ability, and wide excursions of pressure and heart rate occur. Such excursions may derive from endogenous factors such as stress or drowsiness, which result in quite high and quite low pressures, respectively. They may also derive from exogenous factors such as drugs or environmental influences. METHODS AND RESULTS: Impairment of the baroreflex may produce an unusually broad spectrum of clinical presentations; with acute baroreflex failure, a hypertensive crisis is the most common presentation. Over succeeding days to weeks, or in the absence of an acute event, volatile hypertension with periods of hypotension occurs and may continue for many years, usually with some attenuation of pressor surges and greater prominence of depressor valleys during long-term follow-up. With incomplete loss of baroreflex afferents, a mild syndrome of orthostatic tachycardia or orthostatic intolerance may appear. Finally, if the baroreflex failure occurs without concomitant destruction of the parasympathetic efferent vagal fibers, a resting state may lead to malignant vagotonia with severe bradycardia and hypotension and episodes of sinus arrest. CONCLUSIONS: Although baroreflex failure is not the most common cause of the above conditions, correct differentiation from other cardiovascular disorders is important, because therapy of baroreflex failure requires specific strategies, which may lead to successful control.

  10. Hypertension in Malaysia

    PubMed Central

    Naing, Cho; Yeoh, Peng Nam; Wai, Victor Nyunt; Win, Ni Ni; Kuan, Lai Pei; Aung, Kyan

    2016-01-01

    Abstract This study aimed to determine trends in prevalence, awareness, and control of hypertension in Malaysia and to assess the relationship between socioeconomic determinants and prevalence of hypertension in Malaysia. The distribution of hypertension in Malaysia was assessed based on available data in 3 National Health and Morbidity Surveys (NHMSs) and 1 large scale non-NHMS during the period of 1996 to 2011. Summary statistics was used to characterize the included surveys. Differences in prevalence, awareness, and control of hypertension between any 2 surveys were expressed as ratios. To assess the independent associations between the predictors and the outcome variables, regression analyses were employed with prevalence of hypertension as an outcome variable. Overall, there was a rising trend in the prevalence of hypertension in adults ≥30 years: 32.9% (30%–35.8%) in 1996, 42.6% (37.5%–43.5%) in 2006, and 43.5% (40.4%–46.6%) in 2011. There were significant increase of 32% from 1996 to 2011 (P < 0.001) and of 29% from 1996 to 2006 (P < 0.05), but only a small change of 1% from 2006 to 2011 (P = 0.6). For population ≥18 years, only a 1% increase in prevalence of hypertension occurred from the 2006 NHMS (32.2%) to the 2011 NHMS (32.7%) (P = 0.25). A relative increase of 13% occurred in those with primary education (P < 0.001) and a 15% increase was seen in those with secondary education (P < 0.001). The rate of increase in the prevalence of hypertension in the population with income level RM 3000–3999 was the highest (18%) during this period. In general, the older age group had higher prevalence of hypertension in the 2006 and 2011 NHMSs. The prevalence peaked at 74.1% among population aged 65 to 69 years in the 2011 NHMS. Both the proportion of awareness and the control of hypertension in Malaysia improved from 1996 to 2006. A change in the control of hypertension was 13% higher in women than in men. The findings suggest that the magnitude of hypertension in Malaysia needs additional attention. Strengthening the screening for hypertension in primary health-care settings in the high-risk groups and frequent health promotion to the community to enhance individual awareness and commitment to healthy living would be of immense value. PMID:26765422

  11. [Old age and illness--destroying the intolerable?].

    PubMed

    Heinrich, K

    1991-05-01

    The spectacular criminal case of a nurse who because of killing seven old patients in an intensive care ward had been sentenced to jail for 11 years is shown as example of radical thinking in the face of intolerability of serious illness and age. The deficit model of age is on the one hand justly criticized and called invalid, on the other hand negative aspects of age may not be concealed in the face of hedonistic principles of the present epoch. There is no doubt about the monstrosity of the case of the guilty nurse but it may be exemplary for a frequent defensive behaviour against the phenomena of age. If this is right this singular case may be characteristic of common thinking on the unbearable presumption of age. Self defense turning into aggressivity because of foreseeing the own fate of hopeless illness in moribund aged would then have to be seen as a socially significant attitude. PMID:1869232

  12. Fruit-induced FPIES masquerading as hereditary fructose intolerance.

    PubMed

    Fiocchi, Alessandro; Dionisi-Vici, Carlo; Cotugno, Giovanna; Koch, Pierluigi; Dahdah, Lamia

    2014-08-01

    Hereditary fructose intolerance (HFI) symptoms develop at first introduction of fruit during weaning. We report on an infant with suspected HFI who presented with repeated episodes of vomiting and hypotension after ingestion of fruit-containing meals. The first episode occurred at age 4 months. Despite negative genetic testing for HFI, strict avoidance of fruit ingestion resulted in lack of recurrence of symptoms. Oral-fructose-tolerance testing conducted with an apple mousse did not determine hypoglycemia or fructosuria but caused severe hypotension. Allergy evaluations were negative, and the history was diagnostic for fruit-induced food protein-induced enterocolitis syndrome. Because this non-immunoglobulin E-mediated gastrointestinal food hypersensitivity manifests as profuse, repetitive vomiting, often with diarrhea, leading to acute dehydration and lethargy, it may be misinterpreted as HFI. We advise pediatricians to consider food protein-induced enterocolitis syndrome in the differential diagnosis when there is a suspicion of HFI. PMID:25002667

  13. Mechanisms of Orthostatic Intolerance During Real and Simulated Microgravity

    NASA Technical Reports Server (NTRS)

    1997-01-01

    Session MP1 includes short reports on: (1) Orthostatic Tests after 42 Days of Simulated Weightlessness; (2) Effects of 12 Days Exposure to Simulated Microgravity on Central Circulatory Hemodynamics in the Rhesus Monkey; (3) Increased Sensitivity and Resetting of Baroflex Control of Exercise Heart Rate After Prolonged Bed-Rest; (4) Complex Cardiovascular Dynamics and Deconditioning During Head-down Bed Rest; (5) The Cardiovascular Effects of 6 Hours of Head-down Tilt Upon Athletes and Non-athletes; (6) Individual Susceptibility to Post-spaceflight Orthostatic Intolerance: Contributions of Gender-related and Microgravity-related Factors; (7) Cassiopee Mission 1996: Comparison of Cardiovascular Alteration after Short and Long-term Spaceflights; (8) Cerebral and Femoral Flow Response to LBNP during 6 Month MIR Spaceflights (93-95); and (9) Cerebrovascular Changes due to Spaceflight and Postflight Presyncope.

  14. Vascular responsiveness to norepinephrine in sympathicotonic orthostatic intolerance.

    PubMed

    Miller, J W; Streeten, D H

    1990-05-01

    Sympathicotonic orthostatic intolerance (hypotension, tachycardia, or both) is associated with normal or excessive orthostatic increases in plasma norepinephrine concentration and is reversible by the inflation of a military anti-shock trouser suit enveloping the lower limbs and abdomen. These facts suggest that one possible mechanism of the disorder might be a defect in alpha-adrenergic receptor or postreceptor responsiveness of the veins or arterioles. We have investigated in 11 patients and 15 healthy controls the blood pressure and heart rate responses to increasing rates of intravenous norepinephrine infusion (1 to 16 micrograms/min), the dorsal hand vein contractile responses to increasing rates of norepinephrine infusion (1 to 256 ng/min) with a linear variable differential transformer, and the platelet alpha 2-adrenergic receptor densities and dissociation constants. No statistically significant difference in any of these parameters was found between the normal subjects and nine of the 11 patients with orthostatic intolerance. The venous contractile response to norepinephrine was excessive in one patient and was virtually absent in another. Because supersensitivity of the hand veins to norepinephrine suggests up-regulation of alpha 2-receptors resulting from postganglionic autonomic insufficiency, this finding in one patient with sympathicotonic orthostatic hypotension might have been caused by venous denervation. The venous unresponsiveness to norepinephrine in the other patient presumably resulted from a defect in the venous receptors or smooth muscle function. It is evident that norepinephrine responsiveness and the innervation of the arterioles and hand veins was normal in the other nine patients, in whom the defect must have been mediated by some other mechanism. PMID:2160509

  15. Prevalence of intolerance to food additives among Danish school children.

    PubMed

    Fuglsang, G; Madsen, C; Saval, P; Osterballe, O

    1993-08-01

    The prevalence of intolerance to food additives was assessed in a group of unselected school children aged 5-16 years. A study group of 271 children was selected on the basis of the results of a questionnaire on atopic disease answered by 4,274 (86%) school children in the municipality of Viborg, Denmark. The children in the study group followed an elimination diet for two weeks before they were challenged with a mixture of food preservatives, colourings and flavours. The challenge was open and the additives were prepared as a fizzy lemonade. If the open challenge was positive, a double-blind placebo controlled challenge with gelatine capsules was performed. The study included 281 children, 10 were excluded, and the remaining 271 children were given the open challenge (98 healthy controls and 173 with atopic symptoms). The open challenge was negative in all 98 healthy control children who had not reported any atopic symptoms. Of the 173 children reporting present or previous atopic disease 17 had a positive open challenge. Of these 17 children 1 experienced gastrointestinal symptoms, 13 reacted with aggravation of atopic eczema, and 3 with urticaria. Twelve of these 17 children went through the double-blind challenge which was positive in 6 cases. Five of these 6 children had positive reactions to synthetic colourings and 1 to citric acid. No serious reactions were seen. Based upon calculations of the results from this study and an earlier multi-center study in children referred to hospital clinics, the prevalence of intolerance to food additives in school children is estimated to be 1-2%. PMID:8220800

  16. Resistant hypertension - an update.

    PubMed

    Pasha, K; Towhiduzzaman, M; Manwar, A; Jahan, M U

    2015-04-01

    Patients with hypertension are increasing in Bangladesh. Among these patients a growing number of patients are having resistant hypertension faced by both primary care physicians and specialists. There is no data regarding prevalence of resistant hypertension in Bangladesh, but clinical trials abroad suggests that it is not rare, involving perhaps 20% to 30% of study participants. Cardiovascular risk is undoubtedly increased in such patients and the condition is often complicated by multiple other cardiovascular risk factors such as obesity, sleep apnea, diabetes, and chronic kidney disease. Resistant hypertension is almost always multifactorial in etiology. Successful treatment requires identification and reversal of lifestyle factors contributing to treatment resistance; diagnosis and appropriate treatment of secondary causes of hypertension; and use of effective multi drug regimens. Studies of resistant hypertension are limited by the high cardiovascular risk of patients within this subgroup, which generally precludes safe withdrawal of medications; presence of multiple disease processes and their associated medical therapies, which confound interpretation of study results. Therefore we should concentrate on expanding our knowledge of the causes of resistant hypertension which will allow for more effective prevention and/or treatment which is essential to improve long-term clinical management of this condition. PMID:26007281

  17. Perioperative hypertension management

    PubMed Central

    Varon, Joseph; Marik, Paul E

    2008-01-01

    Perioperative hypertension is commonly encountered in patients that undergo surgery. While attempts have been made to standardize the method to characterize the intraoperative hemodynamics, these methods still vary widely. In addition, there is a lack of consensus concerning treatment thresholds and appropriate therapeutic targets, making absolute recommendations about treatment difficult. Nevertheless, perioperative hypertension requires careful management. When treatment is necessary, therapy should be individualized for the patient. This paper reviews the pharmacologic agents and strategies commonly used in the management of perioperative hypertension. PMID:18827911

  18. Sinistral portal hypertension

    PubMed Central

    Thompson, Richard J; Taylor, Mark A; McKie, Lloyd D; Diamond, Thomas

    2006-01-01

    Sinistral, or left-sided, portal hypertension is a rare cause of upper gastrointestinal haemorrhage. There are many causes of sinistral portal hypertension. The primary pathology usually arises in the pancreas and results in compression of the pancreatic vein. This compression causes backpressure in the left portal venous system and subsequent gastric varices. Management is usually surgical to treat the underlying pathology and splenectomy to decompress the left portal venous system. This paper presents four cases of sinistral portal hypertension followed by a literature review of the reported causes and management issues. PMID:16964806

  19. Lung Disease and Hypertension

    PubMed Central

    Imaizumi, Yuki; Eguchi, Kazuo; Kario, Kazuomi

    2014-01-01

    Chronic obstructive pulmonary disease (COPD) patients are at a high risk of developing cardiovascular diseases. Airflow limitation is a predictor of future risks of hypertension and cardiovascular events. COPD is now understood as a systemic inflammatory disease, with the focus on inflammation of the lungs. An association between inflammation and sympathetic overactivity has also been reported. In this article, we review the association between chronic lung disease and the risks of hypertension, cardiovascular morbidity, the underlying mechanisms, and the therapeutic approach to hypertension and cardiovascular diseases in patients with lung diseases. PMID:26587450

  20. Determination of fructose metabolic pathways in normal and fructose-intolerant children: a 13C NMR study using [U-13C]fructose.

    PubMed

    Gopher, A; Vaisman, N; Mandel, H; Lapidot, A

    1990-07-01

    An inborn deficiency in the ability of aldolase B to split fructose 1-phosphate is found in humans with hereditary fructose intolerance (HFI). A stable isotope procedure to elucidate the mechanism of conversion of fructose to glucose in normal children and in HFI children has been developed. A constant infusion of D-[U-13C]fructose was given nasogastrically to control and to HFI children. Hepatic fructose conversion to glucose was estimated by examination of 13C NMR spectra of plasma glucose. The conversion parameters in the control and HFI children were estimated on the basis of doublet/singlet values of the plasma beta-glucose C-1 splitting pattern as a function of the rate of fructose infusion (0.26-0.5 mg/kg per min). Significantly lower values (approximately 3-fold) for fructose conversion to glucose were obtained for the HFI patients as compared to the controls. A quantitative determination of the metabolic pathways of fructose conversion to glucose was derived from 13C NMR measurement of plasma [13C]glucose isotopomer populations. The finding of isotopomer populations of three adjacent 13C atoms at glucose C-4 (13C3-13C4-13C5) suggests that there is a direct pathway from fructose, by-passing fructose-1-phosphate aldolase, to fructose 1,6-bisphosphate. The metabolism of fructose by fructose-1-phosphate aldolase activity accounts for only approximately 50% of the total amount of hepatic fructose conversion to glucose. It is suggested that phosphorylation of fructose 1-phosphate to fructose 1,6-bisphosphate by 1-phosphofructokinase occurs in human liver (and intestine) when fructose is administered nasogastrically; 47% and 27% of the total fructose conversion to glucose in controls and in HFI children, respectively, takes place by way of this pathway. In view of the marked decline by 67% in synthesis of glucose from fructose in HFI subjects found in this study, the extent of [13C]glucose formation from a "trace" amount (approximately 20 mg/kg) of [U-13C]fructose infused into the patient can be used as a safe and noninvasive diagnostic test for inherent faulty fructose metabolism. PMID:2371280

  1. Determination of fructose metabolic pathways in normal and fructose-intolerant children: a 13C NMR study using [U-13C]fructose.

    PubMed Central

    Gopher, A; Vaisman, N; Mandel, H; Lapidot, A

    1990-01-01

    An inborn deficiency in the ability of aldolase B to split fructose 1-phosphate is found in humans with hereditary fructose intolerance (HFI). A stable isotope procedure to elucidate the mechanism of conversion of fructose to glucose in normal children and in HFI children has been developed. A constant infusion of D-[U-13C]fructose was given nasogastrically to control and to HFI children. Hepatic fructose conversion to glucose was estimated by examination of 13C NMR spectra of plasma glucose. The conversion parameters in the control and HFI children were estimated on the basis of doublet/singlet values of the plasma beta-glucose C-1 splitting pattern as a function of the rate of fructose infusion (0.26-0.5 mg/kg per min). Significantly lower values (approximately 3-fold) for fructose conversion to glucose were obtained for the HFI patients as compared to the controls. A quantitative determination of the metabolic pathways of fructose conversion to glucose was derived from 13C NMR measurement of plasma [13C]glucose isotopomer populations. The finding of isotopomer populations of three adjacent 13C atoms at glucose C-4 (13C3-13C4-13C5) suggests that there is a direct pathway from fructose, by-passing fructose-1-phosphate aldolase, to fructose 1,6-bisphosphate. The metabolism of fructose by fructose-1-phosphate aldolase activity accounts for only approximately 50% of the total amount of hepatic fructose conversion to glucose. It is suggested that phosphorylation of fructose 1-phosphate to fructose 1,6-bisphosphate by 1-phosphofructokinase occurs in human liver (and intestine) when fructose is administered nasogastrically; 47% and 27% of the total fructose conversion to glucose in controls and in HFI children, respectively, takes place by way of this pathway. In view of the marked decline by 67% in synthesis of glucose from fructose in HFI subjects found in this study, the extent of [13C]glucose formation from a "trace" amount (approximately 20 mg/kg) of [U-13C]fructose infused into the patient can be used as a safe and noninvasive diagnostic test for inherent faulty fructose metabolism. Images PMID:2371280

  2. Hypertension Risk Subsequent to Gestational Dysglycemia Is Modified by Race/Ethnicity

    PubMed Central

    Bentley-Lewis, Rhonda; Huynh, Jennifer; Li, Sylvia; Wenger, Julia; Thadhani, Ravi

    2016-01-01

    Gestational diabetes mellitus is associated with an increased risk of type 2 diabetes mellitus and hypertension. Additionally, gestational dysglycemia has been associated with an increased risk of type 2 diabetes mellitus but not yet associated with hypertension subsequent to pregnancy in long-term follow-up. Therefore, we set out to examine this relationship as well as the role of race/ethnicity in modifying this relationship. We analyzed a prospective observational cohort followed between 1998 and 2007. There were 17 655 women with self-reported race/ethnicity and full-term, live births. A 1-hour 50 g oral glucose-load test and a 3-hour 100 g oral glucose-tolerance test enabled third trimester stratification of women into 1 of 4 glucose-tolerance groups: (1) normal (n=15 056); (2) abnormal glucose-load test (n=1558); (3) abnormal glucose-load and -tolerance tests (n=520); and (4) gestational diabetes mellitus (n=521). Women were then followed for a mean±standard deviation of 4.1±2.9 years after delivery for the development of hypertension. Although gestational diabetes mellitus was associated with an increased risk of hypertension after pregnancy (odds ratio [95% confidence interval]: 1.58 [1.02, 2.45]; P=0.04), dysglycemia defined by an abnormal glucose-load test predicted hypertension only among black women (4.52 [1.24, 16.52]; P=0.02). The risk of hypertension after pregnancy among dysglycemia groups not meeting criteria for gestational diabetes mellitus varied based on the race/ethnicity of the population. Further research on the implications of the intersection of race/ethnicity and gestational dysglycemia on subsequent hypertension is warranted. PMID:26573715

  3. Hypertension Risk Subsequent to Gestational Dysglycemia Is Modified by Race/Ethnicity.

    PubMed

    Bentley-Lewis, Rhonda; Huynh, Jennifer; Li, Sylvia; Wenger, Julia; Thadhani, Ravi

    2016-01-01

    Gestational diabetes mellitus is associated with an increased risk of type 2 diabetes mellitus and hypertension. Additionally, gestational dysglycemia has been associated with an increased risk of type 2 diabetes mellitus but not yet associated with hypertension subsequent to pregnancy in long-term follow-up. Therefore, we set out to examine this relationship as well as the role of race/ethnicity in modifying this relationship. We analyzed a prospective observational cohort followed between 1998 and 2007. There were 17 655 women with self-reported race/ethnicity and full-term, live births. A 1-hour 50 g oral glucose-load test and a 3-hour 100 g oral glucose-tolerance test enabled third trimester stratification of women into 1 of 4 glucose-tolerance groups: (1) normal (n=15 056); (2) abnormal glucose-load test (n=1558); (3) abnormal glucose-load and -tolerance tests (n=520); and (4) gestational diabetes mellitus (n=521). Women were then followed for a mean±standard deviation of 4.1±2.9 years after delivery for the development of hypertension. Although gestational diabetes mellitus was associated with an increased risk of hypertension after pregnancy (odds ratio [95% confidence interval]: 1.58 [1.02, 2.45]; P=0.04), dysglycemia defined by an abnormal glucose-load test predicted hypertension only among black women (4.52 [1.24, 16.52]; P=0.02). The risk of hypertension after pregnancy among dysglycemia groups not meeting criteria for gestational diabetes mellitus varied based on the race/ethnicity of the population. Further research on the implications of the intersection of race/ethnicity and gestational dysglycemia on subsequent hypertension is warranted. PMID:26573715

  4. Lactose intolerance and African Americans: implications for the consumption of appropriate intake levels of key nutrients.

    PubMed

    2009-10-01

    Lactose intolerance is a complex condition that is complicated by cultural beliefs and perceptions about the consumption of dairy products. These attitudes about dairy may contribute to inadequate intake of key nutrients that may impact conditions that contribute to health disparities in African Americans. While a complex health problem, lactose intolerance is easy to treat. However, no treatment can improve the body's ability to produce lactase. Yet, symptoms can be controlled through dietary strategies. This position paper emphasizes the importance of using patient and provider-level strategies in order to reduce the risks to the health of African Americans that may accrue as a result of dairy nutrient deficiency. Evaluation and assessment of interventions tested is critical so that evidence-based approaches to addressing dairy nutrient deficiency and lactose Intolerance can be created. Lastly, it is essential for physicians to communicate key messages to their patients. Since dairy nutrients address important health concerns, the amelioration of lactose intolerance is an investment in health. Lactose intolerance is common, is easy to treat, and can be managed. It is possible to consume dairy even in the face of a history of maldigestion or lactose intolerant issues. Gradually increasing lactose in the diet--drinking small milk portions with food, eating yogurt, and consuming cheese--are effective strategies for managing lactose intolerance and meeting optimal dairy needs. PMID:19899495

  5. Lifelong Obesity in a Polygenic Mouse Model Prevents Age- and Diet-Induced Glucose Intolerance– Obesity Is No Road to Late-Onset Diabetes in Mice

    PubMed Central

    Brenmoehl, Julia; Walz, Christina; Zeissler, Anja; Tuchscherer, Armin; Piechotta, Marion; Wiesner, Rudolf J.; Bielohuby, Maximilian; Hoeflich, Andreas

    2013-01-01

    Aims/Hypothesis Visceral obesity holds a central position in the concept of the metabolic syndrome characterized by glucose intolerance in humans. However, until now it is unclear if obesity by itself is responsible for the development of glucose intolerance. Methods We have used a novel polygenic mouse model characterized by genetically fixed obesity (DU6) and addressed age- and high fat diet-dependent glucose tolerance. Results Phenotype selection over 146 generations increased body weight by about 2.7-fold in male 12-week DU6 mice (P<0.0001) if compared to unselected controls (Fzt:DU). Absolute epididymal fat mass was particularly responsive to weight selection and increased by more than 5-fold (P<0.0001) in male DU6 mice. At an age of 6 weeks DU6 mice consumed about twice as much food if compared to unselected controls (P<0.001). Absolute food consumption was higher at all time points measured in DU6 mice than in Fzt:DU mice. Between 6 and 12 weeks of age, absolute food intake was reduced by 15% in DU6 mice (P<0.001) but not in Fzt:DU mice. In both mouse lines feeding of the high fat diet elevated body mass if compared to the control diet (P<0.05). In contrast to controls, DU6 mice did not display high fat diet-induced increases of epididymal and renal fat. Control mice progressively developed glucose intolerance with advancing age and even more in response to the high fat diet. In contrast, obese DU6 mice did neither develop a glucose intolerant phenotype with progressive age nor when challenged with a high fat diet. Conclusions/Interpretation Our results from a polygenic mouse model demonstrate that genetically pre-determined and life-long obesity is no precondition of glucose intolerance later in life. PMID:24236159

  6. High Blood Pressure (Hypertension)

    MedlinePlus

    ... Foot Complications DKA (Ketoacidosis) & Ketones Kidney Disease (Nephropathy) Gastroparesis Mental Health Step On Up Treatment & Care Blood ... Pressure (Hypertension) Stroke Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNS) Gastroparesis Heart Disease Mental Health Pregnancy Related Conditions donate ...

  7. Winter Hypertension: Potential mechanisms

    PubMed Central

    Fares, Auda

    2013-01-01

    Hypertension exhibits a winter peak and summer trough in countries both north and south of the equator. A variety of explanations have been proposed to account for the seasonal nature of hypertension. It is likely that this reflects seasonal variations in risk factors. Seasonal variations have been demonstrated in a number of risk factors may play essential roles for seasonality of hypertension such as noradrenalin, catecholamine and vasopressin, vitamin D, and serum cholesterol. However, a number of studies have also suggested a direct effect of environmental temperature and physical activity on blood pressure. This paper was design to review the available evidence on seasonal variations in hypertension and possible explanations for them. PMID:24421749

  8. Pregnancy-Induced Hypertension

    MedlinePlus

    ... Pregnancy-induced hypertension (PIH), also called toxemia or preeclampsia: This condition can cause serious problems for both ... delivery for my baby? Source NHBPEP Report on High Blood Pressure in Pregnancy: A Summary for Family Physicians by MA Zamorski, ...

  9. Hypertension (High Blood Pressure)

    MedlinePlus

    ... pressure to live. Without it, blood can't flow through our bodies and carry oxygen to our vital organs. But when blood pressure gets too high — a condition called hypertension — it can lead to ...

  10. Hypertensive heart disease

    MedlinePlus

    ... failure: pathophysiology and diagnosis. In: Goldman L, Schafer AI, eds. Goldman's Cecil Medicine . 24th ed. Philadelphia, PA: ... Victor RG. Arterial hypertension. In: Goldman L, Schafer AI, eds. Goldman's Cecil Medicine . 24th ed. Philadelphia, PA: ...

  11. Pulmonary Hypertension Association

    MedlinePlus

    ... those affected by PH. Our vision is a world without PH, empowered by hope. PHA Names Next ... Pulmonary Hypertension Association (PHA), the nation's oldest and world's largest organization supporting patients, caregivers, medical professionals and ...

  12. Self-Reported Symptoms of Cold Intolerance in Workers with Injuries of the Hand

    PubMed Central

    Schofield, Michel

    2008-01-01

    Cold intolerance is a well-recognized complication of crushing injuries and amputations in the hand. These symptoms are usually thought to resolve within 2 years of injury. The objectives of our study were to determine the prevalence and course over time of self-reported symptoms of cold intolerance in workers with hand injuries. Files from a large worker’s compensation carrier were randomly selected from index years 2, 4, 6, and 10 after a claim was made. Cohorts comprising cases with diagnostic codes corresponding to traumatic hand injuries and codes referring to non-trauma diagnoses in the hand were assembled for each of the years under consideration. A questionnaire was mailed to a total of 7,088 asking questions related to the symptom of cold intolerance. Twenty-five percent of the surveys were returned. Over 90% of trauma patients from all 4 years reported symptoms of cold intolerance. The rate of cold intolerance in the non-trauma group was between 59% and 69%. Individuals reporting cold intolerance indicated worsening over time in 50% of cases and improvement in only 9%. The severity of injury did not appear to be a factor in the development of cold intolerance. Symptoms of cold intolerance are highly prevalent in workers with significant hand injuries. Workers with non-trauma hand conditions also report a substantial prevalence of this symptom. The development of cold intolerance is not related to injury severity. The symptoms remain either static or deteriorate slightly over time. Improvement is experienced by less than 10% of patients. PMID:18780096

  13. Vagal modulation of hypertension.

    PubMed

    Petkovich, Bradley W; Vega, Joshua; Thomas, Sabu

    2015-04-01

    Resistant hypertension despite compliance with pharmacologic therapies continues to hamper optimal blood pressure control. Vagal modulation via direct stimulation of the body's parasympathetic nervous system is proving a promising therapeutic modality to help patients achieve their blood pressure goals. In this article, we review some of the key concepts of different vagal modulations for resistant hypertension including baroreflex activation therapy, renal sympathetic denervation, and direct vagal nerve stimulation. PMID:25794951

  14. Portal hypertension in children.

    PubMed

    Grimaldi, Chiara; de Ville de Goyet, Jean; Nobili, Valerio

    2012-06-01

    The main causes of intrahepatic portal hypertension in children are cirrhosis and congenital hepatic fibrosis. Non cirrhotic portal hypertension in children is mostly due to extrahepatic portal vein obstruction. In half of cases, no underlying disorder is found. The meso-Rex bypass is the preferred treatment, when it is possible. The closest to the portal vein the obstruction, the highest the risk of esophagogastric varices. PMID:22521554

  15. Comparative uptake of calcium from milk and a calcium-rich mineral water in lactose intolerant adults: implications for treatment of osteoporosis.

    PubMed

    Halpern, G M; Van de Water, J; Delabroise, A M; Keen, C L; Gershwin, M E

    1991-01-01

    Despite the links between low calcium (Ca) intake and age-related bone loss, hypertension, and colon cancer, the majority of Western populations have average daily Ca intakes substantially below recommended daily allowances. Although dietary products are widely known as a rich and valuable source of Ca in the diet, consumption of diary products is low and has been decreasing because of perceptions of excess calories and fat in the diet, as well as taste aversions. During the last decade, a marked increase in the consumption of bottled waters has occurred. Since some of these waters are characterized by high concentrations of Ca, we have studied Ca bioavailability from a Ca-rich water, using 15 lactose intolerant male individuals as subjects, and compared such bioavailability to that from milk. We report herein that the bioavailability of Ca from the water was generally as good as or better than that from milk, a food product well known for its very high Ca bioavailability. Indeed, in eight of 15 subjects, there was a higher level of Ca absorption from mineral water than from milk; bioavailability was equal in five of 15 subjects; in contrast, in two of 15 subjects, the bioavailability of Ca absorption from milk was greater than that from the mineral water. The potential implications of this observation for the prevention and management of age-related bone loss are important for preventive medicine and indicate a new, important source of dietary Ca for lactose intolerant individuals. PMID:1790046

  16. Resistant Hypertension and Chronotherapy

    PubMed Central

    Prkacin, Ingrid; Balenovic, Diana; Djermanovic-Dobrota, Vesna; Lukac, Iva; Drazic, Petra; Pranjic, Iva-Klara

    2015-01-01

    Resistant hypertension is defined as blood pressure that remains above 140/90 mmHg in spite of the continuous use of three antihypertensive agents in optimal dose, including diuretic, and lifestyle changes. According to data from United States of America and Europe, the prevalence ranges from 10 up to 30% in patients with hypertension. Numerous biological and lifestyle factors can contribute to the development of resistant hypertension: medications, volume overload, obesity, diabetes mellitus, older age, renal parenchymal and renovascular disease, primary aldosteronism, obstructive sleep apnea, pheochormocytoma, Cushing’s syndrome, thyroid diseases, aortic coarctation. For diagnosing patient’s history is important, assessing compliance, regular blood pressure measurement, physical examination, biochemical evaluation and noninvasive imaging. The evaluation including 24h ambulatory monitoring of blood pressure (ABPM) in the identification of “non-dipper” hypertension. Non-dipper has particular importance and the prevalence of abnormally high sleep blood pressure is very often in chronic kidney patients. Therapeutic restoration of normal physiologic blood pressure reduction during night-time sleep (circadial variation) is the most significant independent predictor of decreased risk and the basis for the chronotherapy. The resistant hypertension treatment is achieved with nonpharmacological and pharmacological approach, treating secondary hypertension causes and invasive procedures. PMID:26005390

  17. [Management of arterial hypertension].

    PubMed

    Groha, P; Schunkert, H

    2015-09-01

    Arterial hypertension is one of the most frequent diseases in the western world and is one of the three most important risk factors for heart diseases. The 2013 guidelines of the European Societies of Hypertension and Cardiology (ESH/ESC) provide a clear action plan for evidence-based diagnostics and therapeutic measures in hypertensive subjects and simplify target blood pressures across various patient groups. Non-pharmacological options play a central role in the treatment of arterial hypertension. The indications for drug therapy arise from three criteria including the level of hypertension, risk profile of the patient, as well as response to non-pharmacological therapy. For the first choice monotherapy five substance groups are available: diuretics, beta blockers, angiotensin-converting enzyme (ACE) inhibitors, angiotensin (AT) 1 receptor antagonists and calcium antagonists. By combination therapy, the responder rate can be significantly increased with respect to a normalization of blood pressure. A true treatment resistance, in which the therapeutic goal is not reached in spite of a triple combination with maximum dosage, is extremely rare. Further treatment options are combinations of four drug classes and changes of medication. Hypertensive emergencies require a rapid intervention; nevertheless, the magnitude of blood pressure lowering can greatly vary depending on the individual clinical picture. PMID:26303172

  18. Hypertension: quo vadis?

    PubMed

    Borghi, Claudio

    2012-11-01

    High blood pressure (BP) along with smoking habit and lipid disorders are the most important and modifiable risk factors for cardiovascular diseases. However, the prevalence of high BP has grown progressively over time with a progressive increase not only in the absolute number of patients but in the proportion of those showing BP values out of control. The increasing world-wide prevalence of hypertension and the related increase in burden of the disease due to diagnosis, treatment and management of the complications mandates both Health Authorities and research institutions to find out new strategies to improve the BP control. So, one of the main questions is which are the possible perspectives for the future of high BP management, and in particular how can we face the problem of hypertension in the near future? Four main points will be shortly discussed: the genetic contribution to hypertension development and control, the availability of effective preventive strategies, the improvement of disease management, and the role of extensive control of concomitant risk factors. It is relatively easy to suppose that the integration of the best available knowledge with the more recent diagnostic and therapeutic achievements will improve the management of hypertension through a more effective detection of subjects at risk who will undergo an earlier diagnosis leading to a more tailored, tolerated and effective treatment of the hypertensive disease. This means that the future direction of the hypertension management is the simpler: the patient instead of the disease. PMID:23259570

  19. Improving hypertension self-management with community health coaches.

    PubMed

    Dye, Cheryl J; Williams, Joel E; Evatt, Janet Hoffman

    2015-03-01

    Approximately two thirds of those older than 60 years have a hypertension diagnosis. The aim of our program, Health Coaches for Hypertension Control, is to improve hypertension self-management among rural residents older than 60 years through education and support offered by trained community volunteers called Health Coaches. Participants received baseline and follow-up health risk appraisals with blood work, educational materials, and items such as blood pressure monitors and pedometers. Data were collected at baseline, 8 weeks, and 16 weeks on 146 participants who demonstrated statistically significant increases in hypertension-related knowledge from baseline to 8 weeks that persisted at 16 weeks, as well as significant improvements in stage of readiness to change behaviors and in actual behaviors. Furthermore, clinically significant decreases in all outcome measures were observed, with statistically significant changes in systolic blood pressure (-5.781 mmHg; p = .001), weight (-2.475 lb; p < .001), and glucose (-5.096 mg/dl; p = .004) after adjusting for multiple comparisons. Although 40.4% of participants met the Healthy People 2020 definition of controlled hypertension at baseline, the proportion of participants meeting this definition at 16 weeks postintervention increased to 51.0%. This article describes a university-community-hospital system model that effectively promotes hypertension self-management in a rural Appalachian community. PMID:24837989

  20. GLP-2 as Beneficial Factor in the Glucose Homeostasis in Mice Fed a High Fat Diet.

    PubMed

    Baldassano, Sara; Rappa, Francesca; Amato, Antonella; Cappello, Francesco; Mulè, Flavia

    2015-12-01

    Glucagon like peptide-2 (GLP-2) is a gastrointestinal hormone released in response to dietary nutrients, which acts through a specific receptor, the GLP-2 receptor (GLP-2R). The physiological effects of GLP-2 are multiple, involving also the intestinal adaptation to high fat diet (HFD). In consideration of the well-known relationship between chronic HFD and impaired glucose metabolism, in the present study we examined if the blocking of the GLP-2 signaling by chronic treatment with the GLP-2R antagonist, GLP-2 (3-33), leads to functional consequences in the regulation of glucose metabolism in HFD-fed mice. Compared with animals fed standard diet (STD), mice at the 10th week of HFD showed hyperglycaemia, glucose intolerance, high plasma insulin level after glucose load, increased pancreas weight and β cell expansion, but not insulin resistance. In HFD fed mice, GLP-2 (3-33) treatment for 4 weeks (from the 6th to the 10th week of diet) did not affect fasting glycaemia, but it significantly increased the glucose intolerance, both fasting and glucose-induced insulin levels, and reduced the sensitivity to insulin leading to insulin-resistance. In GLP-2 (3-33)-treated HFD mice pancreas was significantly heavier and displayed a significant increase in β-cell mass in comparison with vehicle-treated HFD mice. In STD mice, the GLP-2 (3-33) treatment did not affect fasted or glucose-stimulated glycemia, insulin, insulin sensitivity, pancreas weight and beta cell mass. The present study suggests that endogenous GLP-2 may act as a protective factor against the dysregulation of the glucose metabolism that occurs in HFD mice, because GLP-2 (3-33) worsens glucose metabolism disorders. PMID:25967277

  1. Nicotinamide nucleotide transhydrogenase: a link between insulin secretion, glucose metabolism and oxidative stress.

    PubMed

    Freeman, H; Shimomura, K; Cox, R D; Ashcroft, F M

    2006-11-01

    This paper reviews recent studies on the role of Nnt (nicotinamide nucleotide transhydrogenase) in insulin secretion and detoxification of ROS (reactive oxygen species). Glucose-stimulated insulin release from pancreatic beta-cells is mediated by increased metabolism. This elevates intracellular [ATP], thereby closing KATP channels (ATP-sensitive potassium channels) and producing membrane depolarization, activation of voltage-gated Ca2+ channels, Ca2+ influx and, consequently, insulin secretion. The C57BL/6J mouse displays glucose intolerance and reduced insulin secretion, which results from a naturally occurring deletion in the Nnt gene. Transgenic expression of the wild-type Nnt gene in C57BL/6J mice rescues the phenotype. Knockdown of Nnt in the insulin-secreting cell line MIN6 with small interfering RNA dramatically reduced Ca2+ influx and insulin secretion. Similarly, mice carrying ENU (N-ethyl-N-nitrosourea)-induced loss-of-function mutations in Nnt were glucose intolerant and secreted less insulin during a glucose tolerance test. Islets isolated from these mice showed impaired insulin secretion in response to glucose, but not to the KATP channel blocker tolbutamide. This is explained by the fact that glucose failed to elevate ATP in Nnt mutant islets. Nnt is a nuclear-encoded mitochondrial protein involved in detoxification of ROS. beta-Cells isolated from Nnt mutant mice showed increased ROS production on glucose stimulation. We hypothesize that Nnt mutations enhance glucose-dependent ROS production and thereby impair beta-cell mitochondrial metabolism, possibly via activation of uncoupling proteins. This reduces ATP production and lowers KATP channel activity. Consequently, glucose-dependent electrical activity and insulin secretion are impaired. PMID:17052203

  2. Continuous Glucose Monitoring

    MedlinePlus

    ... glucose levels. What are the prospects for an artificial pancreas? To overcome the limitations of current insu ... glucose monitoring and insulin delivery by developing an artificial pancreas. An artificial pancreas is a system that ...

  3. Blood Glucose Monitoring Devices

    MedlinePlus

    ... the Bar for Blood Glucose Meter Performance Recalls & Alerts Shasta Technologies GenStrip Blood Glucose Test Strips May ... Latest Recalls Report an Adverse Event MedWatch Safety Alerts News Releases Consumer Updates About FDA Contact FDA ...

  4. Pharmacological therapy of feed intolerance in the critically ills

    PubMed Central

    Nguyen, Nam Q

    2014-01-01

    Feed intolerance in the setting of critical illness is associated with higher morbidity and mortality, and thus requires promptly and effective treatment. Prokinetic agents are currently considered as the first-line therapy given issues relating to parenteral nutrition and post-pyloric placement. Currently, the agents of choice are erythromycin and metoclopramide, either alone or in combination, which are highly effective with relatively low incidence of cardiac, hemodynamic or neurological adverse effects. Diarrhea, however, can occur in up to 49% of patients who are treated with the dual prokinetic therapy, which is not associated with Clostridium difficile infection and settled soon after the cessation of the drugs. Hence, the use of prokinetic therapy over a long period or for prophylactic purpose must be avoided, and the indication for ongoing use of the drug(s) must be reviewed frequently. Second line therapy, such as total parenteral nutrition and post-pyloric feeding, must be considered once adverse effects relating the prokinetic therapy develop. PMID:25133043

  5. Mechanisms of microgravity induced orthostatic intolerance: implications for effective countermeasures

    NASA Technical Reports Server (NTRS)

    Convertino, Victor A.

    2002-01-01

    The development of orthostatic hypotension and instability immediately after return from spaceflight has been a significant operational problem to astronauts for more than four decades. Significant reductions in stroke volume and peripheral vascular resistance contribute to ineffective maintenance of systemic arterial blood pressure during standing after spaceflight despite compensatory elevations in heart rate. The primary mechanism underlying reduced stroke volume appears to be a reduction in preload associated with reduced circulating blood volume, although cardiac atrophy might also contribute. Space flight and ground based experiments have demonstrated that an inability to provide adequate peripheral vasoconstriction in astronauts that become presyncopal may be associated with several mechanisms including reduced sympathetic nerve activity, arterial smooth muscle atrophy and/or hyporeactivity, hypersensitivity of beta-adrenergic receptors, etc. In addition, an inability to provide adequate tachycardia in presyncopal subjects may be associated with reduced carotid-cardiac baroreflex sensitivity. Based on the current knowledge and understanding of cardiovascular mechanisms that are altered during exposure to microgravity, a major focus of future research should be directed to the systematic evaluation of potential countermeasures that specifically target and restore the function of these mechanisms. Based on a preliminary systematic evaluation presented in this review, acute physical exercise designed to elicit maximal effort, G-suit inflation, artificial gravity, and specific pharmacological interventions, alone or in combination, have shown promise as successful countermeasures that provide protection against post-flight orthostatic intolerance.

  6. Genes and exercise intolerance: insights from McArdle disease.

    PubMed

    Nogales-Gadea, Gisela; Godfrey, Richard; Santalla, Alfredo; Coll-Cantí, Jaume; Pintos-Morell, Guillem; Pinós, Tomàs; Arenas, Joaquín; Martín, Miguel Angel; Lucia, Alejandro

    2016-02-01

    McArdle disease (glycogen storage disease type V) is caused by inherited deficiency of a key enzyme in muscle metabolism, the skeletal muscle-specific isoform of glycogen phosphorylase, "myophosphorylase," which is encoded by the PYGM gene. Here we review the main pathophysiological, genotypic, and phenotypic features of McArdle disease and their interactions. To date, moderate-intensity exercise (together with pre-exercise carbohydrate ingestion) is the only treatment option that has proven useful for these patients. Furthermore, regular physical activity attenuates the clinical severity of McArdle disease. This is quite remarkable for a monogenic disorder that consistently leads to the same metabolic defect at the muscle tissue level, that is, complete inability to use muscle glycogen stores. Further knowledge of this disorder would help patients and enhance understanding of exercise metabolism as well as exercise genomics. Indeed, McArdle disease is a paradigm of human exercise intolerance and PYGM genotyping should be included in the genetic analyses that might be applied in the coming personalized exercise medicine as well as in future research on genetics and exercise-related phenotypes. PMID:26465709

  7. Novel Epoxy Activated Hydrogels for Solving Lactose Intolerance

    PubMed Central

    Elnashar, Magdy M. M.; Hassan, Mohamed E.

    2014-01-01

    Lactose intolerance is a medical problem for almost 70% of the world population. Milk and dairy products contain 510%?w/v lactose. Hydrolysis of lactose by immobilized lactase is an industrial solution. In this work, we succeeded to increase the lactase loading capacity to more than 3-fold to 36.3?U/g gel using epoxy activated hydrogels compared to 11?U/g gel using aldehyde activated carrageenan. The hydrogel's mode of interaction was proven by FTIR, DSC, and TGA. The high activity of the epoxy group was regarded to its ability to attach to the enzyme's SH, NH, and OH groups, whereas the aldehyde group could only bind to the enzyme's NH2 group. The optimum conditions for immobilization such as epoxy chain length and enzyme concentration have been studied. Furthermore, the optimum enzyme conditions were also deliberated and showed better stability for the immobilized enzyme and the Michaelis constants, Km and Vmax, were doubled. Results revealed also that both free and immobilized enzymes reached their maximum rate of lactose conversion after 2?h, albeit, the aldehyde activated hydrogel could only reach 63% of the free enzyme. In brief, the epoxy activated hydrogels are more efficient in immobilizing more enzymes than the aldehyde activated hydrogel. PMID:25013804

  8. Novel epoxy activated hydrogels for solving lactose intolerance.

    PubMed

    Elnashar, Magdy M M; Hassan, Mohamed E

    2014-01-01

    "Lactose intolerance" is a medical problem for almost 70% of the world population. Milk and dairy products contain 5-10% w/v lactose. Hydrolysis of lactose by immobilized lactase is an industrial solution. In this work, we succeeded to increase the lactase loading capacity to more than 3-fold to 36.3 U/g gel using epoxy activated hydrogels compared to 11 U/g gel using aldehyde activated carrageenan. The hydrogel's mode of interaction was proven by FTIR, DSC, and TGA. The high activity of the epoxy group was regarded to its ability to attach to the enzyme's -SH, -NH, and -OH groups, whereas the aldehyde group could only bind to the enzyme's -NH2 group. The optimum conditions for immobilization such as epoxy chain length and enzyme concentration have been studied. Furthermore, the optimum enzyme conditions were also deliberated and showed better stability for the immobilized enzyme and the Michaelis constants, K m and V max, were doubled. Results revealed also that both free and immobilized enzymes reached their maximum rate of lactose conversion after 2 h, albeit, the aldehyde activated hydrogel could only reach 63% of the free enzyme. In brief, the epoxy activated hydrogels are more efficient in immobilizing more enzymes than the aldehyde activated hydrogel. PMID:25013804

  9. Wheat Allergy and Intolerence; Recent Updates and Perspectives.

    PubMed

    Pasha, Imran; Saeed, Farhan; Sultan, Muhammad Tauseef; Batool, Rizwana; Aziz, Mahwash; Ahmed, Waqas

    2016-01-01

    The current review paper highlights the complicacies associated with communities relying on wheat as their dietary staple. Although, wheat is an important source of nutrients but is also linked with allergenic responses in genetically susceptible subjects. The wheat proteins especially α-amylase inhibitors, ω-5 gliadins, prolamins, nonprolamin, glucoprotein, and profilins are of significance importance. The allergenic responses are further categorized into IgE-mediated and non-IgE-mediated reactions. Conjugation and degranulation of the IgEs with the allergens results in release of several mediators. In contrary, non-IgE-mediated wheat allergy depends on immune complexes formed by food and food antibodies and cell-mediated immunity. As results, different diseases tend to occur on the completion of these reactions, i.e., celiac disease, baker's asthma, diarrhea, atopic dermatitis, and urticaria. This instant paper highlighted the concept of food allergy with special reference to wheat. The models are developed that are included in this paper showing the wheat allergen, their possible routes, impact on human health, and indeed possible remedies. The paper would provide the basic information for the researchers, common man, and allied stakeholders to cater the issue in details. However, the issue needs the attention of the researchers as there is a need to clarify the issues of wheat allergy and wheat intolerance. PMID:24915366

  10. The Relationship Between Intolerance of Uncertainty, Sensory Sensitivities, and Anxiety in Autistic and Typically Developing Children.

    PubMed

    Neil, Louise; Olsson, Nora Choque; Pellicano, Elizabeth

    2016-06-01

    Guided by a recent theory that proposes fundamental differences in how autistic individuals deal with uncertainty, we investigated the extent to which the cognitive construct 'intolerance of uncertainty' and anxiety were related to parental reports of sensory sensitivities in 64 autistic and 85 typically developing children aged 6-14 years. Intolerance of uncertainty and anxiety explained approximately half the variance in autistic children's sensory sensitivities, but only around a fifth of the variance in typical children's sensory sensitivities. In children with autism only, intolerance of uncertainty remained a significant predictor of children's sensory sensitivities once the effects of anxiety were adjusted for. Our results suggest intolerance of uncertainty is a relevant construct to sensory sensitivities in children with and without autism. PMID:26864157

  11. Fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAPs) and nonallergic food intolerance: FODMAPs or food chemicals?

    PubMed Central

    Gibson, Peter R.

    2012-01-01

    Food intolerance in irritable bowel syndrome (IBS) is increasingly being recognized, with patients convinced that diet plays a role in symptom induction. Evidence is building to implicate fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAPs) in the onset of abdominal pain, bloating, wind and altered bowel habit through their fermentation and osmotic effects. Hypersensitivity to normal levels of luminal distension is known to occur in patients with IBS, with consideration of food chemical intolerance likely to answer many questions about this physiological process. This paper summarizes the evidence and application of the most common approaches to managing food intolerance in IBS: the low-FODMAP diet, the elimination diet for food chemical sensitivity and others including possible noncoeliac gluten intolerance. PMID:22778791

  12. [Blood glucose self monitoring].

    PubMed

    Wascher, Thomas C; Stechemesser, Lars

    2016-04-01

    Self monitoring of blood glucose contributes to the integrated management of diabetes mellitus. It, thus, should be available for all patients with diabetes mellitus type-1 and type-2. Self monitoring of blood glucose improves patients safety, quality of life and glucose control. The current article represents the recommendations of the Austrian Diabetes Association for the use of blood glucose self monitoring according to current scientific evidence. PMID:27052233

  13. Glucose Metabolism and Pancreatic Defects in Spinal Muscular Atrophy

    PubMed Central

    Bowerman, Melissa; Swoboda, Kathryn J.; Michalski, John-Paul; Wang, Gen-Sheng; Reeks, Courtney; Beauvais, Ariane; Murphy, Kelley; Woulfe, John; Screaton, Robert A.; Scott, Fraser W.; Kothary, Rashmi

    2014-01-01

    Objective Spinal muscular atrophy (SMA) is the number 1 genetic killer of young children. It is caused by mutation or deletion of the survival motor neuron 1 (SMN1) gene. Although SMA is primarily a motor neuron disease, metabolism abnormalities such as metabolic acidosis, abnormal fatty acid metabolism, hyperlipidemia, and hyperglycemia have been reported in SMA patients. We thus initiated an in-depth analysis of glucose metabolism in SMA. Methods Glucose metabolism and pancreas development were investigated in the Smn2B/− intermediate SMA mouse model and type I SMA patients. Results Here, we demonstrate in an SMA mouse model a dramatic cell fate imbalance within pancreatic islets, with a predominance of glucagon-producing α cells at the expense of insulin-producing β cells. These SMA mice display fasting hyperglycemia, hyperglucagonemia, and glucose resistance. We demonstrate similar abnormalities in pancreatic islets from deceased children with the severe infantile form of SMA in association with supportive evidence of glucose intolerance in at least a subset of such children. Interpretation Our results indicate that defects in glucose metabolism may play an important contributory role in SMA pathogenesis. PMID:22926856

  14. Fructose and lactose intolerance and malabsorption testing: the relationship with symptoms in functional gastrointestinal disorders

    PubMed Central

    Wilder-Smith, C H; Materna, A; Wermelinger, C; Schuler, J

    2013-01-01

    Background The association of fructose and lactose intolerance and malabsorption with the symptoms of different functional gastrointestinal disorders (FGID) remains unclear. Aim To investigate the prevalence of fructose and lactose intolerance (symptom induction) and malabsorption and their association with clinical gastrointestinal (GI) as well as non-GI symptoms in FGID and the outcome of dietary intervention. Methods Fructose and lactose intolerance (defined by positive symptom index) and malabsorption (defined by increased hydrogen/methane) were determined in 1372 FGID patients in a single centre using breath testing. Results were correlated with clinical symptoms in different FGID Rome III subgroups. The effectiveness of a targeted saccharide-reduced diet was assessed after 6–8 weeks. Results Intolerance prevalence across all FGIDs was 60% to fructose, 51% to lactose and 33% to both. Malabsorption occurred in 45%, 32% and 16% respectively. There were no differences in intolerance or malabsorption prevalence between FGID subgroups. FGID symptoms correlated with symptoms evoked during testing (r = 0.35–0.61. P < 0.0001), but not with malabsorption. Non-GI symptoms occurred more commonly in patients with intolerances. Methane breath levels were not associated with constipation using several cut-off thresholds. Adequate symptom relief was achieved in >80% of intolerant patients, irrespective of malabsorption. Conclusions Fructose and lactose intolerances are common in FGID and associated with increased non-GI symptoms, but not with specific FGID subtypes. Symptoms experienced during breath testing, but not malabsorption, correlate with FGID symptoms. Effective symptom relief with dietary adaptation is not associated with malabsorption. Mechanisms relating to the generation of GI and non-GI symptoms due to lactose and fructose in FGID need to be explored further. PMID:23574302

  15. Overview of glucose regulation.

    PubMed

    Tirone, T A; Brunicardi, F C

    2001-04-01

    Glucose homeokinesis is a remarkable process that provides glucose to the body for energy and a constant source of glucose to the brain while preventing hyperglycemia. The latter leads to excessive glycosylation of proteins, changing their structure and function and eventually affecting every organ system in the body. Despite a variable diet of feast and famine throughout the day, the body maintains strict blood glucose levels through a remarkable network between the pancreas, liver, adipose tissue, muscle, and brain. These interactions and both glucose production and utilization are discussed. Glucose production is governed by the liver, which can generate free glucose from hepatic glycogen stores and de novo through gluconeogenesis. Specific glucose transporters found on every cell of the body administer glucose utilization. Each transporter works with a different serum glucose level. The mechanism of these transporters and the specific glucose cycles are discussed. The purpose of this article is to review glucose regulation; it serves as a reference for the other presentations of this symposium. PMID:11344399

  16. Pregnancy with Portal Hypertension

    PubMed Central

    Aggarwal, Neelam; Negi, Neha; Aggarwal, Aakash; Bodh, Vijay; Dhiman, Radha K.

    2014-01-01

    Even though pregnancy is rare with cirrhosis and advanced liver disease, but it may co-exist in the setting of non-cirrhotic portal hypertension as liver function is preserved but whenever encountered together is a complex clinical dilemma. Pregnancy in a patient with portal hypertension presents a special challenge to the obstetrician as so-called physiological hemodynamic changes associated with pregnancy, needed for meeting demands of the growing fetus, worsen the portal hypertension thereby putting mother at risk of potentially life-threatening complications like variceal hemorrhage. Risks of variceal bleed and hepatic decompensation increase many fold during pregnancy. Optimal management revolves round managing the portal hypertension and its complications. Thus management of such cases requires multi-speciality approach involving obstetricians experienced in dealing with high risk cases, hepatologists, anesthetists and neonatologists. With advancement in medical field, pregnancy is not contra-indicated in these women, as was previously believed. This article focuses on the different aspects of pregnancy with portal hypertension with special emphasis on specific cause wise treatment options to decrease the variceal bleed and hepatic decompensation. Based on extensive review of literature, management from pre-conceptional period to postpartum is outlined in order to have optimal maternal and perinatal outcomes. PMID:25755552

  17. Sleep and Hypertension

    PubMed Central

    Harding, Susan M.

    2010-01-01

    Ambulatory BP studies indicate that even small increases in BP, particularly nighttime BP levels, are associated with significant increases in cardiovascular morbidity and mortality. Accordingly, sleep-related diseases that induce increases in BP would be anticipated to substantially affect cardiovascular risk. Both sleep deprivation and insomnia have been linked to increases in incidence and prevalence of hypertension. Likewise, sleep disruption attributable to restless legs syndrome increases the likelihood of having hypertension. Observational studies demonstrate a strong correlation between the severity of obstructive sleep apnea (OSA) and the risk and severity of hypertension, whereas prospective studies of patients with OSA demonstrate a positive relationship between OSA and risk of incident hypertension. Intervention trials with continuous positive airway pressure (CPAP) indicate a modest, but inconsistent effect on BP in patients with severe OSA and a greater likelihood of benefit in patients with most CPAP adherence. Additional prospective studies are needed to reconcile observational studies suggesting that OSA is a strong risk factor for hypertension with the modest antihypertensive effects of CPAP observed in intervention studies. PMID:20682533

  18. Hypertension in Women—Part II

    PubMed Central

    Pemu, Priscilla Igho; Ofili, Elizabeth

    2010-01-01

    In Part I, we reviewed the pathophysiology of hypertension in women This section focuses on the treatment of hypertension in special circumstances and special populations: pregnancy, preeclampsia, and lactation; hypertension in black women; and hypertension in the elderly. PMID:18550941

  19. [Urticaria and "aspirin intolerance"--part of an interdisciplinary pathogenetic principle? (author's transl)].

    PubMed

    Illig, L

    1981-03-15

    Like the so-called "aspirin asthma", the aspirin-induced provocation of chronic urticaria is a symptom of the intolerance syndrome. This may also be induced by various other drugs, particularly by indomethacin and food additives. The intolerance syndromes of the "Aspirin type", however, must be assigned to the "anaphylactoid reactions" in man which also include the non-immunologic reactions to radiographic contrast media and colloids in blood substitutes. It has not yet been investigated in how far the mechanisms of these three clinical types of anaphylactoid reactions are similar or identical; however, this appears to be the case at least with aspirin intolerance and anaphylactoid reactions to contrast media. According to our observations in 150 urticaria patients, the non-immunologic aspirin-induced urticaria (and probably also the "aspirin asthma") should furthermore be divided into real provocation within the meaning of a chemical Koebner phenomenon, and "aspirin urticaria" as a symptom of the intolerance syndrome as such. A rel provocation of pre-existent urticaria is much less frequent than superimposed urticaria as a mere symptom of the intolerance syndrome. An exact differentiation is only possible in patients without any clinical symptoms after additive-free diet as well as on the basis of the phenomenon of "figuration". The most important substance as mediator for intolerance urticaria is histamine. In contrast to the usual urticaria, H2-antagonists are an important adjuvant to the traditional H1-antagonists in the symptomatic therapy. PMID:7222893

  20. Relationships among perceived racial stress, intolerance of uncertainty, and worry in a black sample.

    PubMed

    Rucker, LaTanya S; West, Lindsey M; Roemer, Lizabeth

    2010-06-01

    The purpose of this study was to explore the relationships among chronic worry, perceived racial stress, and intolerance of uncertainty in a sample of adults who racially identify as Black. Intolerance of uncertainty has been associated with worry and generalized anxiety disorder in predominantly White samples. Given that racial stress is likely to increase worry, perhaps through the mechanism of intolerance of uncertainty, intolerance of uncertainty was hypothesized to mediate the relationship between perceived racial stress and chronic worry. A nonclinical sample of 77 Black undergraduate students at an urban university completed a series of questionnaires assessing the constructs of interest. Both perceived racial stress and intolerance of uncertainty were significantly correlated with chronic worry in this sample. Moreover, intolerance of uncertainty fully mediated the relationship between perceived racial stress and worry for these Black individuals. These findings are discussed in terms of directions for future research and implications for clinical interventions for Black individuals who are both exposed to racial stress and suffer from chronic worry. PMID:20412889

  1. Predictors of Beta-Blocker Intolerance and Mortality in Patients After Acute Coronary Syndrome

    PubMed Central

    De Stefano, Laercio Martins; Ferraz, Alex Lombardi Barbosa; Ferreira, Ana Lúcia dos Anjos; Gut, Ana Lúcia; Cogni, Ana Lúcia; Farah, Elaine; Matsubara, Beatriz Bojikian

    2013-01-01

    Purpose To investigate the predictors of intolerance to beta-blockers treatment and the 6-month mortality in hospitalized patients with acute coronary syndrome (ACS). Methods This was a single-center, prospective, and longitudinal study including 370 consecutive ACS patients in Killip class I or II. BBs were prescribed according to international guidelines and withdrawn if intolerance occurred. The study was approved by the institutional ethics committee of our university. Statistics: the clinical parameters evaluated at admission, and the related intolerance to BBs and death at 6 months were analyzed using logistic regression (p<0.05)in PATIENTS. Results BB intolerance was observed in 84 patients and was associated with no prior use of statins (OR: 2.16, 95%CI: 1.26–3.69, p= 0.005) and Killip class II (OR: 2.5, 95%CI: 1.30-4.75, p=0.004) in the model adjusted for age, sex, blood pressure, and renal function. There was no association with ST-segment alteration or left anterior descending coronary artery plaque. Intolerance to BB was associated with the greatest risk of death (OR: 4.5, 95%CI: 2.15–9.40, p<0.001). Conclusions After ACS, intolerance to BBs in the first 48 h of admission was associated to non previous use of statin and Killip class II and had a high risk of death within 6 months. PMID:24167581

  2. The negative influence of high-glucose ambience on neurogenesis in developing quail embryos.

    PubMed

    Chen, Yao; Fan, Jian-xia; Zhang, Zhao-long; Wang, Guang; Cheng, Xin; Chuai, Manli; Lee, Kenneth Ka Ho; Yang, Xuesong

    2013-01-01

    Gestational diabetes is defined as glucose intolerance during pregnancy and it is presented as high blood glucose levels during the onset pregnancy. This condition has an adverse impact on fetal development but the mechanism involved is still not fully understood. In this study, we investigated the effects of high glucose on the developing quail embryo, especially its impact on the development of the nervous system. We established that high glucose altered the central nervous system mophologically, such that neural tube defects (NTDs) developed. In addition, we found that high glucose impaired nerve differentiation at dorsal root ganglia and in the developing limb buds, as revealed by neurofilament (NF) immunofluorescent staining. The dorsal root ganglia are normally derived from neural crest cells (NCCs), so we examine the delamination of NCCs from dorsal side of the neural tube. We established that high glucose was detrimental to the NCCs, in vivo and in vitro. High glucose also negatively affected neural differentiation by reducing the number and length of neurites emanating from neurons in culture. We established that high glucose exposure caused an increase in reactive oxidative species (ROS) generation by primary cultured neurons. We hypothesized that excess ROS was the factor responsible for impairing neuron development and differentiation. We provided evidence for our hypothesis by showing that the addition of vitamin C (a powerful antioxidant) could rescue the damaging effects of high glucose on cultured neurons. PMID:23818954

  3. The Negative Influence of High-Glucose Ambience on Neurogenesis in Developing Quail Embryos

    PubMed Central

    Wang, Guang; Cheng, Xin; Chuai, Manli; Lee, Kenneth Ka Ho; Yang, Xuesong

    2013-01-01

    Gestational diabetes is defined as glucose intolerance during pregnancy and it is presented as high blood glucose levels during the onset pregnancy. This condition has an adverse impact on fetal development but the mechanism involved is still not fully understood. In this study, we investigated the effects of high glucose on the developing quail embryo, especially its impact on the development of the nervous system. We established that high glucose altered the central nervous system mophologically, such that neural tube defects (NTDs) developed. In addition, we found that high glucose impaired nerve differentiation at dorsal root ganglia and in the developing limb buds, as revealed by neurofilament (NF) immunofluorescent staining. The dorsal root ganglia are normally derived from neural crest cells (NCCs), so we examine the delamination of NCCs from dorsal side of the neural tube. We established that high glucose was detrimental to the NCCs, in vivo and in vitro. High glucose also negatively affected neural differentiation by reducing the number and length of neurites emanating from neurons in culture. We established that high glucose exposure caused an increase in reactive oxidative species (ROS) generation by primary cultured neurons. We hypothesized that excess ROS was the factor responsible for impairing neuron development and differentiation. We provided evidence for our hypothesis by showing that the addition of vitamin C (a powerful antioxidant) could rescue the damaging effects of high glucose on cultured neurons. PMID:23818954

  4. Apolipoprotein E Genotype and Sex Influence Glucose Tolerance in Older Adults: A Cross-Sectional Study

    PubMed Central

    Hanson, Angela J.; Banks, William A.; Hernandez Saucedo, Hector; Craft, Suzanne

    2016-01-01

    Background Glucose intolerance and apolipoprotein ε4 allele (E4+) are risk factors for Alzheimer's disease (AD). Insulin sensitizers show promise for treating AD, but are less effective in E4+ individuals. Little is known about how the APOE genotype influences glucose metabolism. Methods Cross-sectional analysis of 319 older adults who underwent oral glucose tolerance tests; a subset had insulin, amyloid beta (Aβ42), and Mini Mental Status Examination. Glucose and insulin patterns with respect to cognitive diagnosis, E4 status, and sex were examined with analysis of covariance and Pearson correlation. Results People with cognitive impairment had higher fasting insulin levels. E4 status did not affect fasting glucose values, whereas men had higher fasting glucose levels than women. E4+ men had the lowest and E4+ women had the highest glucose levels, compared to E4- groups; insulin did not differ by sex or E4 group. E4 status and sex moderated correlations between metabolic measures and AD risk factors including age and Aβ. Conclusions Insulin resistance was associated with cognitive impairment, and sex, E4 status, and glucose values are interrelated in older adults at risk of AD. Understanding glucose metabolism for different APOE and sex groups may help elucidate differences in therapeutic responses. PMID:27065114

  5. Renal specific secondary hypertension.

    PubMed

    Kalra, P A

    2007-01-01

    Chronic kidney disease (CKD) is now understood to affect over 5% of all adult patients and it conveys a risk of reduced survival in those affected. At least 80% of those patients with stages 3-5 CKD (i.e. GFR <60 ml/min) suffer with hypertension, and in most the major cause is due to pertubation of an important renal endocrine system, the renin-angiotensin-aldosterone (RAA) axis. In this article the epidemiology of renal-related hypertension and its importance in pre-disposing to the increased cardiovascular risk in renal disease are discussed. Hypertension is known to be a major cause of progressive loss of renal function in CKD, particularly because of activation of the RAA, and hence the case for blockade of this system with ACE inhibitors and Angiotensin receptor blockers is highlighted. PMID:17695554

  6. Stress and hypertension.

    PubMed Central

    Mustacchi, P.

    1990-01-01

    In susceptible persons emotional stress results in immediate sympathetic stimulation, with a vasomotor response that results in a high-output state and elevated blood pressure; the vasopressor response seems to be transient. There seems to be no longitudinal epidemiologic validation of the attractive hypothesis that transiently elevated blood pressures are the prelude to fixed hypertension, however. The acquisition of hypertension by populations abandoning their traditional mode of living has been attributed to the sociocultural stress inherent in westernization, but these studies usually have not taken into account concomitants of this type of acculturation, such as dietary changes and increased body weight. The inverse relationship of blood pressure levels to education could explain the development of hypertension when aspiration to upward mobility is thwarted. The severity of perceived occupational stress relates inversely to blood pressure, suggesting that familiarity with a job renders the demands made by the work environment more predictable and less threatening in terms of vasopressor response. PMID:2219875

  7. Valsartan use in pediatric hypertension.

    PubMed

    Meyers, Kevin E C; Behar, Brittany

    2011-03-01

    Hypertension affects up to 5% of school-aged children and is defined by an average systolic or diastolic blood pressure greater than the 95th percentile for age, sex and height. In prepubertal children a secondary cause for hypertension including renal disease, coarctation of the aorta or endocrine disease should be excluded by appropriate evaluation. The incidence and prevalence of essential hypertension in adolescents has increased together with the increase in obesity and now accounts for at least 50% of hypertension in this age group. Many children with primary hypertension and most children with secondary causes for hypertension require drug therapy. There are numerous drug classes that are presently used to treat hypertensive pediatric patients, which include β-blockers, peripheral α-blockers, direct vasodilators, ACE inhibitors, calcium channel blockers, diuretics and ARBs. This article will review the pharmacology of the ARB valsartan with respect to its efficacy, tolerability and safe use in hypertensive pediatric patients. PMID:21453020

  8. How Is Pulmonary Hypertension Diagnosed?

    MedlinePlus

    ... Hypertension Diagnosed? Your doctor will diagnose pulmonary hypertension (PH) based on your medical and family histories, a ... exam, and the results from tests and procedures. PH can develop slowly. In fact, you may have ...

  9. Chronic thromboembolic pulmonary hypertension.

    PubMed

    O'Connell, Caroline; Montani, David; Savale, Laurent; Sitbon, Olivier; Parent, Florence; Seferian, Andrei; Bulifon, Sophie; Fadel, Elie; Mercier, Olaf; Mussot, Sacha; Fabre, Dominique; Dartevelle, Philippe; Humbert, Marc; Simonneau, Grald; Jas, Xavier

    2015-12-01

    Chronic thromboembolic pulmonary hypertension (CTEPH) is a form of pulmonary hypertension (PH) characterized by the persistence of thromboembolic obstructing the pulmonary arteries as an organized tissue and the presence of a variable small vessel arteriopathy. The consequence is an increase in pulmonary vascular resistance resulting in progressive right heart failure. CTEPH is classified as group IV pulmonary hypertension according to the WHO classification of pulmonary hypertension. CTEPH is defined as precapillary pulmonary hypertension (mean pulmonary artery pressure?25mmHg with a pulmonary capillary wedge pressure?15mmHg) associated with mismatched perfusion defects on ventilation-perfusion lung scan and signs of chronic thromboembolic disease on computed tomography pulmonary angiogram and/or conventional pulmonary angiography, in a patient who received at least 3 months of therapeutic anticoagulation. CTEPH as a direct consequence of symptomatic pulmonary embolism (PE) is rare, and a significant number of CTEPH cases develop in the absence of history of PE. Thus, CTEPH should be considered in any patient with unexplained PH. Splenectomy, chronic inflammatory conditions such as inflammatory bowel disease, indwelling catheters and cardiac pacemakers have been identified as associated conditions increasing the risk of CTEPH. Ventilation-perfusion scan (V/Q) is the best test available for establishing the thromboembolic nature of PH. When CTEPH is suspected, patients should be referred to expert centres where pulmonary angiography, right heart catheterization and high-resolution CT scan will be performed to confirm the diagnosis and to assess the operability. Pulmonary endarterectomy (PEA) remains the gold standard treatment for CTEPH when organized thrombi involve the main, lobar or segmental arteries. This operation should only be performed by experienced surgeons in specialized centres. For inoperable patients, current ESC/ERS guidelines for the diagnosis and treatment of pulmonary hypertension recommend the use of riociguat and say that off-label use of drugs approved for PAH and pulmonary angioplasty may be considered in expert centres. PMID:26585271

  10. The prevention of hypertension.

    PubMed

    Tibblin, G; Eriksson, C G

    1977-01-01

    Our way to prevention is to find a list of traits known to be predictors of elevated blood pressure. This list of predictors offers means for the early identification of susceptibile persons. Years of experience in preventive work indicate that such identification is always useful for developing preventive programmes, since it gives a focus for action (5). Most of the predictors show possible ways in which action could be directed towards prevention of hypertension and reduction of elevated blood pressure. We will focus on salt, control of obesity, physical exercise, and meditation. We would like to discuss preventive aspects of hypertension and the possibility of treating with other methods than drugs. PMID:268928

  11. Cerebral vasoconstriction precedes orthostatic intolerance after parabolic flight

    NASA Technical Reports Server (NTRS)

    Serrador, J. M.; Shoemaker, J. K.; Brown, T. E.; Kassam, M. S.; Bondar, R. L.; Schlegel, T. T.

    2000-01-01

    The effects of brief but repeated bouts of micro- and hypergravity on cerebrovascular responses to head-up tilt (HUT) were examined in 13 individuals after (compared to before) parabolic flight. Middle cerebral artery mean flow velocity (MCA MFV; transcranial Doppler ultrasound), eye level blood pressure (BP) and end tidal CO(2) (P(ET)CO(2)) were measured while supine and during 80 degrees HUT for 30 min or until presyncope. In the postflight tests subjects were classified as being orthostatically tolerant (OT) (n = 7) or intolerant (OI) (n = 6). BP was diminished with HUT in the OT group in both tests (p < 0.05) whereas postflight BP was not different from supine in the OI group. Postflight compared to preflight, the reduction in P(ET)CO(2) with HUT (p < 0.05) increased in both groups, although significantly so only in the OI group (p < 0.05). The OI group also had a significant decrease in supine MCA MFV postflight (p < 0.05) that was unaccompanied by a change in supine P(ET)CO(2). The decrease in MCA MFV that occurred during HUT in both groups preflight (p < 0.05) was accentuated only in the OI group postflight, particularly during the final 30 s of HUT (p < 0.05). However, this accentuated decrease in MCA MFV was not correlated to the greater decrease in P(ET)CO(2) during the same period (R = 0.20, p = 0.42). Although cerebral vascular resistance (CVR) also increased in the OI group during the last 30 s of HUT postflight (p < 0.05), the dynamic autoregulatory gain was not simultaneously changed. Therefore, we conclude that in the OI individuals, parabolic flight was associated with cerebral hypoperfusion following a paradoxical augmentation of CVR by a mechanism that was not related to changes in autoregulation nor strictly to changes in P(ET)CO(2).

  12. Visual height intolerance and acrophobia: clinical characteristics and comorbidity patterns.

    PubMed

    Kapfhammer, Hans-Peter; Huppert, Doreen; Grill, Eva; Fitz, Werner; Brandt, Thomas

    2015-08-01

    The purpose of this study was to estimate the general population lifetime and point prevalence of visual height intolerance and acrophobia, to define their clinical characteristics, and to determine their anxious and depressive comorbidities. A case-control study was conducted within a German population-based cross-sectional telephone survey. A representative sample of 2,012 individuals aged 14 and above was selected. Defined neurological conditions (migraine, Menière's disease, motion sickness), symptom pattern, age of first manifestation, precipitating height stimuli, course of illness, psychosocial impairment, and comorbidity patterns (anxiety conditions, depressive disorders according to DSM-IV-TR) for vHI and acrophobia were assessed. The lifetime prevalence of vHI was 28.5% (women 32.4%, men 24.5%). Initial attacks occurred predominantly (36%) in the second decade. A rapid generalization to other height stimuli and a chronic course of illness with at least moderate impairment were observed. A total of 22.5% of individuals with vHI experienced the intensity of panic attacks. The lifetime prevalence of acrophobia was 6.4% (women 8.6%, men 4.1%), and point prevalence was 2.0% (women 2.8%; men 1.1%). VHI and even more acrophobia were associated with high rates of comorbid anxious and depressive conditions. Migraine was both a significant predictor of later acrophobia and a significant consequence of previous acrophobia. VHI affects nearly a third of the general population; in more than 20% of these persons, vHI occasionally develops into panic attacks and in 6.4%, it escalates to acrophobia. Symptoms and degree of social impairment form a continuum of mild to seriously distressing conditions in susceptible subjects. PMID:25262317

  13. Gluten intolerance: Sex-and age-related features

    PubMed Central

    Llorente-Alonso, MJ; Fernández-Aceñero, MJ; Sebastián, M

    2006-01-01

    OBJECTIVE: Gluten intolerance is an immune-mediated enteropathy associated with gluten-containing foods in genetically susceptible patients. The typical form mainly affecting children shows failure to thrive and/or gastrointestinal symptoms. The adult form is less typical, presenting vague gastrointestinal symptoms, iron deficiency (with or without anemia) or nonspecific serum chemistry abnormalities. The present study aims to analyze clinical and biochemical differences of celiac disease (CD) according to sex and age. PATIENTS AND METHODS: The present study reviewed clinical and biochemical features of patients with suspected CD admitted to the Hospital General of Móstoles (Madrid, Spain) between July 2001 and June 2005. Two hundred fifty-two patients were analyzed, in whom intestinal biopsy was performed due to clinical and/or biochemical abnormalities suggestive of CD. One hundred seventy-eight asymptomatic relatives of the affected patients were also included. Overall, 125 patients showed diagnostic features of CD in the intestinal biopsy. RESULTS: The results confirmed higher prevalence of typical forms of CD in children (67% in children compared with only 14.3% in adults). CD seemed to be more frequent in adult women than in men (ratio of women to men 4:1), but it is worth noting that men diagnosed were most often referred with a typical clinical picture, so atypical forms of the disease in men may have been underdiagnosed. CONCLUSIONS: CD shows atypical features in adults, and physicians must include this disorder in the differential diagnosis of adults with iron deficiency or slight hypertransaminasemia. Increased awareness of the disease and extensive availability of accurate serological tests will lead to improved diagnosis of this disorder, both in children and adults. PMID:17111054

  14. Pulmonary hypertension caused by pulmonary venous hypertension.

    PubMed

    Kulik, Thomas J

    2014-12-01

    The effect of pulmonary venous hypertension (PVH) on the pulmonary circulation is extraordinarily variable, ranging from no impact on pulmonary vascular resistance (PVR) to a marked increase. The reasons for this are unknown. Both acutely reversible pulmonary vasoconstriction and pathological remodeling (especially medial hypertrophy and intimal hyperplasia) account for increased PVR when present. The mechanisms involved in vasoconstriction and remodeling are not clearly defined, but increased wall stress, especially in small pulmonary arteries, presumably plays an important role. Myogenic contraction may account for increased vascular tone and also indirectly stimulate remodeling of the vessel wall. Increased wall stress may also directly cause smooth muscle growth, migration, and intimal hyperplasia. Even long-standing and severe pulmonary hypertension (PH) usually abates with elimination of PVH, but PVH-PH is an important clinical problem, especially because PVH due to left ventricular noncompliance lacks definitive therapy. The role of targeted PH therapy in patients with PVH-PH is unclear at this time. Most prospective studies indicate that these medications are not helpful or worse, but there is ample reason to think that a subset of patients with PVH-PH may benefit from phosphodiesterase inhibitors or other agents. A different approach to evaluating possible pharmacologic therapy for PVH-PH may be required to better define its possible utility. PMID:25610595

  15. Pulmonary hypertension caused by pulmonary venous hypertension

    PubMed Central

    2014-01-01

    Abstract The effect of pulmonary venous hypertension (PVH) on the pulmonary circulation is extraordinarily variable, ranging from no impact on pulmonary vascular resistance (PVR) to a marked increase. The reasons for this are unknown. Both acutely reversible pulmonary vasoconstriction and pathological remodeling (especially medial hypertrophy and intimal hyperplasia) account for increased PVR when present. The mechanisms involved in vasoconstriction and remodeling are not clearly defined, but increased wall stress, especially in small pulmonary arteries, presumably plays an important role. Myogenic contraction may account for increased vascular tone and also indirectly stimulate remodeling of the vessel wall. Increased wall stress may also directly cause smooth muscle growth, migration, and intimal hyperplasia. Even long-standing and severe pulmonary hypertension (PH) usually abates with elimination of PVH, but PVH-PH is an important clinical problem, especially because PVH due to left ventricular noncompliance lacks definitive therapy. The role of targeted PH therapy in patients with PVH-PH is unclear at this time. Most prospective studies indicate that these medications are not helpful or worse, but there is ample reason to think that a subset of patients with PVH-PH may benefit from phosphodiesterase inhibitors or other agents. A different approach to evaluating possible pharmacologic therapy for PVH-PH may be required to better define its possible utility. PMID:25610595

  16. 48-h Glucose infusion in humans: effect on hormonal responses, hunger and food intake

    PubMed Central

    Teff, Karen L.; Petrova, Maja; Havel, Peter J.; Townsend, Raymond R.

    2009-01-01

    Experimentally-induced hyperglycemia by prolonged glucose infusion allows investigation of the effects of sustained stimulation of the pancreatic ?-cell on insulin secretion and sensitivity. Hormonal responses to a meal following prolonged glucose infusions have not been investigated. To determine if a 48-h glucose infusion alters hormonal responses to a test meal as well as food intake and hunger in normal weight individuals, 16 subjects (8 men, 8 women, age 1830 y, mean BMI=21.71.6 kg/m2) were infused for 48-h with either saline (50 ml/h) or 15% glucose (200 mg/m2/min). Subjects ingested a 600 kcal mixed nutrient meal 3-h after infusion termination. Blood samples were taken during the 48-h and for 4 hours following food ingestion. The 48-h glucose infusion elicited a metabolic profile of a glucose intolerant obese subjects, with increased plasma glucose, insulin and leptin (all P<0.01) and increased HOMA-IR (P<0.001). During meal ingestion, early insulin secretion was increased (P<0.05) but postprandial glucose (P<0.01) and insulin (P<0.01) excursions were lower following the glucose infusion. Postprandial plasma triglyceride concentrations were increased after glucose compared with saline. Food intake and hunger ratings were not different between the two conditions. Plasma leptin levels were inversely correlated with hunger (P<0.03) in both conditions and with food intake (P<0.003) during the glucose condition only. Thus, a 48-h glucose infusion does not impair postprandial hormonal responses, alter food intake or hunger in normal weight subjects. The glucose-induced increases in plasma leptin result in a stronger inverse relationship between plasma leptin and hunger as well as food intake. These data are the first to demonstrate a relationship between leptin and hunger in normal weight, non-calorically restricted human subjects. PMID:17275862

  17. CNC-bZIP Protein Nrf1-Dependent Regulation of Glucose-Stimulated Insulin Secretion

    PubMed Central

    Zheng, Hongzhi; Fu, Jingqi; Xue, Peng; Zhao, Rui; Dong, Jian; Liu, Dianxin; Yamamoto, Masayuki; Tong, Qingchun; Qu, Weidong; Zhang, Qiang; Andersen, Melvin E.

    2015-01-01

    Abstract Aims: The inability of pancreatic β-cells to secrete sufficient insulin in response to glucose stimulation is a major contributing factor to the development of type 2 diabetes (T2D). We investigated both the in vitro and in vivo effects of deficiency of nuclear factor-erythroid 2-related factor 1 (Nrf1) in β-cells on β-cell function and glucose homeostasis. Results: Silencing of Nrf1 in β-cells leads to a pre-T2D phenotype with disrupted glucose metabolism and impaired insulin secretion. Specifically, MIN6 β-cells with stable knockdown of Nrf1 (Nrf1-KD) and isolated islets from β-cell-specific Nrf1-knockout [Nrf1(b)-KO] mice displayed impaired glucose responsiveness, including elevated basal insulin release and decreased glucose-stimulated insulin secretion (GSIS). Nrf1(b)-KO mice exhibited severe fasting hyperinsulinemia, reduced GSIS, and glucose intolerance. Silencing of Nrf1 in MIN6 cells resulted in oxidative stress and altered glucose metabolism, with increases in both glucose uptake and aerobic glycolysis, which is associated with the elevated basal insulin release and reduced glucose responsiveness. The elevated glycolysis and reduced glucose responsiveness due to Nrf1 silencing likely result from altered expression of glucose metabolic enzymes, with induction of high-affinity hexokinase 1 and suppression of low-affinity glucokinase. Innovation: Our study demonstrated a novel role of Nrf1 in regulating glucose metabolism and insulin secretion in β-cells and characterized Nrf1 as a key transcription factor that regulates the coupling of glycolysis and mitochondrial metabolism and GSIS. Conclusion: Nrf1 plays critical roles in regulating glucose metabolism, mitochondrial function, and insulin secretion, suggesting that Nrf1 may be a novel target to improve the function of insulin-secreting β-cells. Antioxid. Redox Signal. 22, 819–831. PMID:25556857

  18. Impaired glucose metabolism and exercise capacity with muscle-specific glycogen synthase 1 (gys1) deletion in adult mice

    PubMed Central

    Xirouchaki, Chrysovalantou E.; Mangiafico, Salvatore P.; Bate, Katherine; Ruan, Zheng; Huang, Amy M.; Tedjosiswoyo, Bing Wilari; Lamont, Benjamin; Pong, Wynne; Favaloro, Jenny; Blair, Amy R.; Zajac, Jeffrey D.; Proietto, Joseph; Andrikopoulos, Sofianos

    2016-01-01

    Objective Muscle glucose storage and muscle glycogen synthase (gys1) defects have been associated with insulin resistance. As there are multiple mechanisms for insulin resistance, the specific role of glucose storage defects is not clear. The aim of this study was to examine the effects of muscle-specific gys1 deletion on glucose metabolism and exercise capacity. Methods Tamoxifen inducible and muscle specific gys-1 KO mice were generated using the Cre/loxP system. Mice were subjected to glucose tolerance tests, euglycemic/hyperinsulinemic clamps and exercise tests. Results gys1-KO mice showed ≥85% reduction in muscle gys1 mRNA and protein concentrations, 70% reduction in muscle glycogen levels, postprandial hyperglycaemia and hyperinsulinaemia and impaired glucose tolerance. Under insulin-stimulated conditions, gys1-KO mice displayed reduced glucose turnover and muscle glucose uptake, indicative of peripheral insulin resistance, as well as increased plasma and muscle lactate levels and reductions in muscle hexokinase II levels. gys1-KO mice also exhibited markedly reduced exercise and endurance capacity. Conclusions Thus, muscle-specific gys1 deletion in adult mice results in glucose intolerance due to insulin resistance and reduced muscle glucose uptake as well as impaired exercise and endurance capacity. In brief This study demonstrates why the body prioritises muscle glycogen storage over liver glycogen storage despite the critical role of the liver in supplying glucose to the brain in the fasting state and shows that glycogen deficiency results in impaired glucose metabolism and reduced exercise capacity. PMID:26977394

  19. Inverse Association of Serum Docosahexaenoic Acid With Newly Diagnosed Hypertension

    PubMed Central

    Yang, Bo; Ding, Fang; Wang, Feng-Lei; Yu, Wei; Li, Duo

    2016-01-01

    Abstract Observational studies on circulating fatty acid (FA) and primary prevention of hypertension have yielded inconsistent results, and the association among the Chinese population is not fully clear. The aim of the study was to discern important FAs that can discriminate hypertensive patients from normotensive persons, and investigate associations between the important FAs and risk of hypertension. We conducted a case-control study nested within a community-based cohort of 2447 Chinese participants aged 35 to 79 years who completed a baseline assessment between October 2012 and April 2013. In all, 480 patients with newly diagnosed hypertension were identified at baseline and 480 normotensive individuals were randomly selected as matched normotensive controls. Controls were individually matched to cases by age (±2 y), sex, and recruitment center, with a 1:1 case-to-control ratio. Serum FA profile was compared between cases and controls by orthogonal partial least squares-discriminant analyses. Odds ratio (OR) with 95% confidence interval (CI) for newly diagnosed hypertension was estimated by a conditional logistical analysis. After adjustment for body mass index, education, profession, family history of hypertension, salt intake, heart rate, blood lipids, and fasting glucose levels, serum FA profile in hypertensive patients was typically characterized by higher 16:0 and 16:1n-7, and lower 18:2n-6 and 22:6n-3, compared with normotensive controls. Docosahexaenoic acid (22:6n-3) and palmitoleic acid (16:1n-7) were identified as the important FA contributing most to the intergroup separations. When comparing the highest and lowest quartile of FA composition, newly diagnosed hypertension was negatively associated with 22:6n-3 (OR 0.65; 95% CI, 0.45–0.93; P for trend = 0.02), but positively associated with 16:1n-7 (OR 2.14; 95% CI, 1.46–3.12; P for trend < 0.001). The associations remained pronounced after multiple adjustments and in further stratified analyses. In distinguishing hypertensive patients and normotensive persons, 22:6n-3 was considered as an important n-3 FA. Increased serum proportion of 22:6n-3 was associated with decreased odds of newly diagnosed hypertension, which suggests that high levels of 22:6n-3 in serum or perhaps in diet may be beneficial for prevention of hypertension in the Chinese population. PMID:26844451

  20. Oxidative stress and hypertension: Possibility of hypertension therapy with antioxidants

    PubMed Central

    Baradaran, Azar; Nasri, Hamid; Rafieian-Kopaei, Mahmoud

    2014-01-01

    Hypertension is a major risk factor for myocardial infarction, heart failure, stroke, peripheral arterial disease, and aortic aneurysm, and is a cause of chronic kidney disease. Hypertension is often associated with metabolic abnormalities such as diabetes and dyslipidemia, and the rate of these diseases is increasing nowadays. Recently it has been hypothesized that oxidative stress is a key player in the pathogenesis of hypertension. A reduction in superoxide dismutase and glutathione peroxidase activity has been observed in newly diagnosed and untreated hypertensive subjects, which are inversely correlated with blood pressure. Hydrogen peroxide production is also higher in hypertensive subjects. Furthermore, hypertensive patients have higher lipid hydroperoxide production. Oxidative stress is also markedly increased in hypertensive patients with renovascular disease. If oxidative stress is indeed a cause of hypertension, then, antioxidants should have beneficial effects on hypertension control and reduction of oxidative damage should result in a reduction in blood pressure. Although dietary antioxidants may have beneficial effects on hypertension and cardiovascular risk factors, however, antioxidant supplementation has not been shown consistently to be effective and improvement is not usually seen in blood pressure after treatment with single or combination antioxidant therapy in subjects thought to be at high risk of cardiovascular disease. This matter is the main focus of this paper. A list of medicinal plants that have been reported to be effective in hypertension is also presented. PMID:25097610

  1. Do patients with lactose intolerance exhibit more frequent comorbidities than patients without lactose intolerance? An analysis of routine data from German medical practices

    PubMed Central

    Schiffner, Rebecca; Kostev, Karel; Gothe, Holger

    2016-01-01

    Background The increase in food intolerances poses a burgeoning problem in our society. Food intolerances not only lead to physical impairment of the individual patient but also result in a high socio-economic burden due to factors such as the treatment required as well as absenteeism. The present study aimed to explore whether lactose intolerant (LI) patients exhibit more frequent comorbidities than non-LI patients. Methods The study was conducted on a case-control basis and the results were determined using routine data analysis. Routine data from the IMS Disease Analyzer database were used for this purpose. A total of 6,758 data records were processed and analyzed. Results There were significant correlations between LI and the incidence of osteoporosis, changes in mental status, and the presence of additional food intolerances. Comparing 3,379 LI vs. 3,379 non-LI patients, 34.5% vs. 17.7% (P<0.0001) suffered from abdominal pain; 30.6% vs. 17.2% (P<0.0001) from gastrointestinal infections; and 20.9% vs. 16.0% (P=0.0053) from depression. Adjusted odds ratios (OR) were the highest for fructose intolerance (n=229 LI vs. n=7 non-LI; OR 31.06; P<0.0001), irritable bowel syndrome (n=247 LI vs. n=44 non-LI; OR 5.23; P<0.0001), and bloating (n=351 LI vs. n=68 non-LI; OR 4.94; P<0.0001). Conclusion The study confirms that LI should not be regarded as an isolated illness but considered a possible trigger for further diseases. Additional research is necessary to assert more precise statements. PMID:27065730

  2. Frequency and determinants of white coat hypertension in mild to moderate hypertension: a primary care-based study. Monitorización Ambulatoria de la Presión Arterial (MAPA)-Area 5 Working Group.

    PubMed

    Martínez, M A; García-Puig, J; Martín, J C; Guallar-Castillón, P; Aguirre de Cárcer, A; Torre, A; Armada, E; Nevado, A; Madero, R S

    1999-03-01

    Most of the previous studies on white coat hypertension were performed in hypertension clinics or academic settings and included relatively small series of patients. Consequently, the prevalence of white coat hypertension in primary care settings and the clinical and epidemiologic characteristics of this subgroup of patients are not well known. We performed this study to estimate the frequency of white coat hypertension in a population of mildly to moderately hypertensive subjects attended in a primary care setting and to examine possible epidemiologic and clinical factors that may identify these patients. Patients included in the study underwent clinical interview, measurement of clinic blood pressure (BP) on three visits, determination of serum lipids, glucose, uric acid, and urinary albumin excretion, 24-h ambulatory BP monitoring, and M-mode and Doppler echocardiography. Patients were classified as white coat hypertensives if their daytime ambulatory BP were < 135/85 mm Hg. We studied 345 patients, 136 (39%) of whom were diagnosed with white coat hypertension. The frequency of white coat hypertension was inversely proportional to the severity of clinic BP values. The diagnosis of white coat hypertension was independently associated with female gender and low educational level. Left ventricular mass index and urinary albumin excretion were lower in the white-coat hypertensive group compared with the group with sustained hypertension. Our results show that a high proportion of patients with mild to moderate hypertension attended in a primary care setting have white coat hypertension. Some clinical characteristics may be helpful in the identification of this group of subjects. White coat hypertensives show less target-organ damage than sustained hypertensive patients. PMID:10192226

  3. Orthostatic intolerance in 6 degrees head-down tilt and lower body negative pressure loading

    NASA Astrophysics Data System (ADS)

    Yajima, Kazuyoshi; Miyamoto, Akira; Ito, Masao; Mano, Takaichi; Nakayama, Kiyoshi

    6 degrees head-down tilt bed rest experiment for 6 days was conducted at Nihon University Itabashi Hospital for 10 male athletes. In order to observe the orthostatic intolerance due to six days head-down tilt bed rest, 70 degrees head up tilt tests were performed before and after the head-down tilt. Two types of orthostatic intolerance were distinguished by the time course of their cardiovascular responses. One was vagotonia type and the other was brain anemia type. The latter type was commonly seen among astronauts after space flight due to the lack of plasma volume. As this volume change is considered to be initiated by some fluid loss from the lower extremities, analysis was made to clarify the relation between the leg volume change and the types of orthostatic intolerance. Nakayama proposed a Heart Rate Controllability Index, which is calculated from the initiate leg volume change and heart rate increase in head up tilt, for an indicator of the orthostatic intolerability. The index was applied to the subjects of six days head-down tilt above mentioned. For the subjects who showed a sign of presyncopy, the index values were higher or lower than that of the rest subjects who showed no sign of presyncopy. In order to evaluate the validity of the index, another experiment was conducted to induce an orthostatic intolerance by a different way of loading. The same types of orthostatic intolerance were observed and the index value hit high in the brain anemia type of orthostatic intolerance, while the vagotonia type showed relatively lower values than the normal group.

  4. Resistant hypertension in the elderly-second line treatments: aldosterone antagonists, central alpha-agonist agents, alpha-adrenergic receptor blockers, direct vasodilators, and exogenous nitric oxide donors.

    PubMed

    Musso, Carlos G; Alfie, Jose

    2015-01-01

    Resistant hypertension (RH) is a prevalent medical problem across all ages but is more frequent in elderly patients. This entity has to be distinguished from clinical settings which may simulate it such as apparent hypertension (pseudohypertension) or apparently resistant hypertension (pseudoresistant hypertension) [1]. An appropriate therapy for RH can be achieved by the addition of second line antihypertensive drugs: antialdosteronic diuretics, central agents, alpha blockers, direct vasodilating agents, and exogenous nitric oxide donors. These antihypertensive drugs are considered as second line drugs since they are less effective as monotherapy to reduce blood pressure (they induce counte regulatory responses that limit their antihypertensive effect such as volume expansion or reflex tachycardia) and prevent cardiovascular events, or due to significant adverse effects (postural hypotension, sedation, hyperkalemia). Second line drugs are also used when there is allergy or intolerance to the first line ones [2, 3]. PMID:25761104

  5. Management of hypertension.

    PubMed

    Kaplan, N M

    1992-11-01

    To provide maximal protection against the cardiovascular complications that accompany hypertension, the disease must be managed in ways to minimize the total cardiovascular risk burden. These involve five major steps: (1) careful monitoring of the blood pressure in response to appropriate therapy; (2) assessment of concomitant cardiovascular risk factors; (3) institution of life-style modifications needed to control both hypertension and other risk factors; (4) use of antihypertensive drugs, chosen to best manage the individual patient's overall risk burden and provided in a manner that will lower the pressure gently while avoiding adverse reactions; and (5) identifying and reaching the goal of therapy: levels of blood pressure that are neither too high to avoid increased risks for cerebral and renal damage nor too low to avoid increased risks for coronary ischemia. This monograph builds on the 30-year experience of one of the leading clinical investigators in the field to translate the multiple advances made in the management of hypertension into practical guidelines for improved care of the many millions of patients with this disease. Particular emphasis is directed toward certain therapeutic challenges, including the elderly, diabetic patients, and resistant hypertensive patients. PMID:1468345

  6. High Blood Pressure (Hypertension)

    MedlinePlus

    ... For Consumers Consumer Information by Audience For Women High Blood Pressure (Hypertension) Share Tweet Linkedin Pin it More sharing options ... En Español Who is at risk? How is high blood pressure treated? Understanding your blood pressure: What do the ...

  7. Carvedilol in hypertension treatment

    PubMed Central

    Stafylas, Panagiotis C; Sarafidis, Pantelis A

    2008-01-01

    Although β-blockers have been previously shown to effectively reduce blood pressure (BP) and have been used for hypertension treatment for over 40 years, their effect on cardiovascular morbidity and mortality in hypertensive patients remains controversial and its use in uncomplicated hypertension is currently under debate. However, data on the above field derive mainly from studies which were conducted with older agents, such as atenolol and metoprolol, while considerable pharamacokinetic and pharmacodynamic heterogeneity is present within the class of β-blockers. Carvedilol, a vasodilating non-cardioselective β-blocker, is a compound that seems to give the opportunity to the clinician to use a cardioprotective agent without the concerning hemodynamic and metabolic actions of traditional β-blocker therapy. In contrast with conventional β-blockers, carvedilol maintains cardiac output, has a less extended effect on heart rate and reduces BP by decreasing vascular resistance. Further, several studies has shown that carvedilol has a beneficial or at least neutral effect on metabolic parameters, such as glycemic control, insulin sensitivity, and lipid metabolism, suggesting that they could be used in subjects with the metabolic syndrome or diabetes without negative consequences. This article summarizes the distinct pharmacologic, hemodynamic, and metabolic properties of carvedilol in relation to conventional β-blockers, attempting to examine the potential use of this agent for hypertension treatment. PMID:18629377

  8. Pulmonary Hypertension and Pulmonary Vasodilators.

    PubMed

    Keller, Roberta L

    2016-03-01

    Pulmonary hypertension in the perinatal period can present acutely (persistent pulmonary hypertension of the newborn) or chronically. Clinical and echocardiographic diagnosis of acute pulmonary hypertension is well accepted but there are no broadly validated criteria for echocardiographic diagnosis of pulmonary hypertension later in the clinical course, although there are significant populations of infants with lung disease at risk for this diagnosis. Contributing cardiovascular comorbidities are common in infants with pulmonary hypertension and lung disease. It is not clear who should be treated without confirmation of pulmonary vascular disease by cardiac catheterization, with concurrent evaluation of any contributing cardiovascular comorbidities. PMID:26876130

  9. Hypertension, a health economics perspective.

    PubMed

    Alcocer, Luis; Cueto, Liliana

    2008-06-01

    The economic aspects of hypertension are critical to modern medicine. The medical, economic, and human costs of untreated and inadequately controlled hypertension are enormous. Hypertension is distributed unequally and with iniquity in different countries and regions of the world. Treatment of hypertension requires an investment over many years to prolong disease-free quality years of life. The high prevalence and high cost of the disease impacts on the microeconomics and macroeconomics of countries and regions. The criteria used for inclusion in clinical guidelines for hypertension impact on the cost and cost/utility of diagnosis or treatment. PMID:19124418

  10. Pharmacologic Management of Pediatric Hypertension.

    PubMed

    Misurac, Jason; Nichols, Kristen R; Wilson, Amy C

    2016-02-01

    Hypertension in children is common, and the prevalence of primary hypertension is increasing with the obesity epidemic and changing dietary choices. Careful measurement of blood pressure is important to correctly diagnose hypertension, as many factors can lead to inaccurate blood pressure measurement. Hypertension is diagnosed based on comparison of age-, sex-, and height-based norms with the average systolic and diastolic blood pressures on three separate occasions. In the absence of hypertensive target organ damage (TOD), stage I hypertension is managed first by diet and exercise, with the addition of drug therapy if this fails. First-line treatment of stage I hypertension with TOD and stage II hypertension includes both lifestyle changes and medications. First-line agents include angiotensin-converting enzyme (ACE) inhibitors, thiazide diuretics, and calcium-channel blockers. Hypertensive emergency with end-organ effects requires immediate modest blood pressure reduction to alleviate symptoms. This is usually accomplished with IV medications. Long-term reduction in blood pressure to normal levels is accomplished gradually. Specific medication choice for outpatient hypertension management is determined by the underlying cause of hypertension and the comparative adverse effect profiles, along with practical considerations such as cost and frequency of administration. Antihypertensive medication is initiated at a starting dose and can be gradually increased to effect. If ineffective at the recommended maximum dose, an additional medication with a complementary mechanism of action can be added. PMID:26597490

  11. The Improvement of Hypertension by Probiotics: Effects on Cholesterol, Diabetes, Renin, and Phytoestrogens

    PubMed Central

    Lye, Huey-Shi; Kuan, Chiu-Yin; Ewe, Joo-Ann; Fung, Wai-Yee; Liong, Min-Tze

    2009-01-01

    Probiotics are live organisms that are primarily used to improve gastrointestinal disorders such as diarrhea, irritable bowel syndrome, constipation, lactose intolerance, and to inhibit the excessive proliferation of pathogenic intestinal bacteria. However, recent studies have suggested that probiotics could have beneficial effects beyond gastrointestinal health, as they were found to improve certain metabolic disorders such as hypertension. Hypertension is caused by various factors and the predominant causes include an increase in cholesterol levels, incidence of diabetes, inconsistent modulation of renin and imbalanced sexual hormones. This review discusses the antihypertensive roles of probiotics via the improvement and/or treatment of lipid profiles, modulation of insulin resistance and sensitivity, the modulation of renin levels and also the conversion of bioactive phytoestrogens as an alternative replacement of sexual hormones such as estrogen and progesterone. PMID:19865517

  12. The Dietary Approaches to Stop Hypertension (DASH) eating pattern in special populations.

    PubMed

    Tyson, Crystal C; Nwankwo, Chinazo; Lin, Pao-Hwa; Svetkey, Laura P

    2012-10-01

    The Dietary Approaches to Stop Hypertension (DASH) trial showed that a diet rich in fruits, vegetables, low-fat dairy products with reduced total and saturated fat, cholesterol, and sugar-sweetened products effectively lowers blood pressure in individuals with prehypertension and stage I hypertension. Limited evidence is available on the safety and efficacy of the DASH eating pattern in special patient populations that were excluded from the trial. Caution should be exercised before initiating the DASH diet in patients with chronic kidney disease, chronic liver disease, and those who are prescribed renin-angiotensin-aldosterone system antagonist, but these conditions are not strict contraindications to DASH. Modifications to the DASH diet may be necessary to facilitate its use in patients with chronic heart failure, uncontrolled diabetes mellitus type II, lactose intolerance, and celiac disease. In general, the DASH diet can be adopted by most patient populations and initiated simultaneously with medication therapy and other lifestyle interventions. PMID:22846984

  13. Pulmonary hypertension in patient with elevated homocystein level and blast injuries.

    PubMed

    Zuljević, Ervin; Redzepi, Gzim; Plestina, Sanja; Vidjak, Vinko; Loncarić, Vlasta; Jakopović, Marko; Samarzija, Miroslav

    2009-03-01

    38-year-old man had chronic deep venous thrombosis (DVT) as a result of multiple injuries caused by an explosion of grenade 12 years ago, with recurrent pulmonary thromboembolisms and pulmonary hypertension which was unrecognized for a decade. Patient was admitted with a progressive dyspnea and exercise intolerance (NYHA II). The diagnosis was established according to clinical symptoms, transthoracic echocardiography, phlebography, lung scintigraphy and pulmonary angiography. Oral anticoagulant therapy was introduced and cava filter indicated to implant. During phlebography a floating thrombus was found in the inferior cava vein underneath renal vein. Implantation was delayed and patient received systemic fibrinolytic therapy with streptokinase (7500 000 UI within 4 days), followed by heparin infusion and warfarin. Post-fibrinolytic phlebography showed clear lumen of inferior vena cava. Fibrinolysis had also affected pulmonary hypertension-systolic pressure in the right ventricle measured by Doppler echocardiography decreased from 90 to 65 mmHg. Permanent intravenous cava filter was implanted. PMID:19408648

  14. The Dietary Approaches to Stop Hypertension (DASH) Eating Pattern in Special Populations

    PubMed Central

    Tyson, Crystal C.; Nwankwo, Chinazo; Lin, Pao-Hwa; Svetkey, Laura P.

    2015-01-01

    The Dietary Approaches to Stop Hypertension (DASH) trial showed that a diet rich in fruits, vegetables, low-fat dairy products with reduced total and saturated fat, cholesterol, and sugar-sweetened products effectively lowers blood pressure in individuals with prehypertension and stage I hypertension. Limited evidence is available on the safety and efficacy of the DASH eating pattern in special patient populations that were excluded from the trial. Caution should be exercised before initiating the DASH diet in patients with chronic kidney disease, chronic liver disease, and those who are prescribed renin-angiotensin-aldosterone system antagonist, but these conditions are not strict contraindications to DASH. Modifications to the DASH diet may be necessary to facilitate its use in patients with chronic heart failure, uncontrolled diabetes mellitus type II, lactose intolerance, and celiac disease. In general, the DASH diet can be adopted by most patient populations and initiated simultaneously with medication therapy and other lifestyle interventions. PMID:22846984

  15. γ-Oryzanol Enhances Adipocyte Differentiation and Glucose Uptake

    PubMed Central

    Jung, Chang Hwa; Lee, Da-Hye; Ahn, Jiyun; Lee, Hyunjung; Choi, Won Hee; Jang, Young Jin; Ha, Tae-Youl

    2015-01-01

    Recent studies show that brown rice improves glucose intolerance and potentially the risk of diabetes, although the underlying molecular mechanisms remain unclear. One of the phytochemicals found in high concentration in brown rice is γ-oryzanol (Orz), a group of ferulic acid esters of phytosterols and triterpene alcohols. Here, we found that Orz stimulated differentiation of 3T3-L1 preadipocytes and increased the protein expression of adipogenic marker genes such as peroxisome proliferator-activated receptor gamma (PPAR-γ) and CCAAT/enhanced binding protein alpha (C/EBPα). Moreover, Orz significantly increased the glucose uptake in insulin-resistant cells and translocation of glucose transporter type 4 (GLUT4) from the cytosol to the cell surface. To investigate the mechanism by which Orz stimulated cell differentiation, we examined its effects on cellular signaling of the mammalian target of rapamycin complex 1 (mTORC1), a central mediator of cellular growth and proliferation. The Orz treatment increased mTORC1 kinase activity based on phosphorylation of 70-kDa ribosomal S6 kinase 1 (S6K1). The effect of Orz on adipocyte differentiation was dependent on mTORC1 activity because rapamycin blocks cell differentiation in Orz-treated cells. Collectively, our results indicate that Orz stimulates adipocyte differentiation, enhances glucose uptake, and may be associated with cellular signaling mediated by PPAR-γ and mTORC1. PMID:26083118

  16. A role of the adaptive immune system in glucose homeostasis

    PubMed Central

    Bronsart, Laura L; Contag, Christopher H

    2016-01-01

    Objective The immune system, including the adaptive immune response, has recently been recognized as having a significant role in diet-induced insulin resistance. In this study, we aimed to determine if the adaptive immune system also functions in maintaining physiological glucose homeostasis in the absence of diet-induced disease. Research design and methods SCID mice and immunocompetent control animals were phenotypically assessed for variations in metabolic parameters and cytokine profiles. Additionally, the glucose tolerance of SCID and immunocompetent control animals was assessed following introduction of a high-fat diet. Results SCID mice on a normal chow diet were significantly insulin resistant relative to control animals despite having less fat mass. This was associated with a significant increase in the innate immunity-stimulating cytokines granulocyte colony-stimulating factor, monocyte chemoattractant protein 1 (MCP1), and MCP3. Additionally, the SCID mouse phenotype was exacerbated in response to a high-fat diet as evidenced by the further significant progression of glucose intolerance. Conclusions These results support the notion that the adaptive immune system plays a fundamental biological role in glucose homeostasis, and that the absence of functional B and T cells results in disruption in the concentrations of various cytokines associated with macrophage proliferation and recruitment. Additionally, the absence of functional B and T cells is not protective against diet-induced pathology. PMID:27026807

  17. Sources and severity of self-reported food intolerance after ileal pouch-anal anastomosis.

    PubMed

    Steenhagen, Elles; de Roos, Nicole M; Bouwman, Carolien A; van Laarhoven, Cees J H M; van Staveren, Wija A

    2006-09-01

    Data on food intolerance after ileal pouch-anal anastomosis are scarce. The aim of this study was to identify foods causing intolerance and to determine the nature and severity of reported symptoms. Patients from the Dutch Crohn's and Ulcerative Colitis Association were mailed a survey on food intolerance; 105 (31% men) of 137 patients took part. They all reported intolerance to one or more foods. Common symptoms (scored from 0=absent to 10=severe), included diarrhea (mean score=5.8), fatigue (mean score=5.5), and thirst (mean score=4.6). Spicy foods, cabbage, and citrus fruits (or juice) were most likely to decrease stool consistency, increase stool frequency, or cause perianal irritation. Onions, cabbage, or leeks were reported by 28% of the patients to cause flatulence. The urge to defecate was stronger after a cooked meal (45% within (1/2) hour) than after sandwiches (15% within (1/2) hour). Foods reported to increase stool consistency were potato products, bread, and bananas. This study demonstrates that food intolerance is a common, albeit mild, problem after ileal pouch-anal anastomosis. Food and nutrition professionals should encourage patients to base their food choices on individual tolerance as long as no (patho-) physiological-based evidence to the contrary is available. PMID:16963353

  18. Statin intolerance - an attempt at a unified definition. Position paper from an International Lipid Expert Panel.

    PubMed

    Banach, Maciej; Rizzo, Manfredi; Toth, Peter P; Farnier, Michel; Davidson, Michael H; Al-Rasadi, Khalid; Aronow, Wilbert S; Athyros, Vasilis; Djuric, Dragan M; Ezhov, Marat V; Greenfield, Robert S; Hovingh, G Kees; Kostner, Karam; Serban, Corina; Lighezan, Daniel; Fras, Zlatko; Moriarty, Patrick M; Muntner, Paul; Goudev, Assen; Ceska, Richard; Nicholls, Stephen J; Broncel, Marlena; Nikolic, Dragana; Pella, Daniel; Puri, Raman; Rysz, Jacek; Wong, Nathan D; Bajnok, Laszlo; Jones, Steven R; Ray, Kausik K; Mikhailidis, Dimitri P

    2015-03-16

    Statins are one of the most commonly prescribed drugs in clinical practice. They are usually well tolerated and effectively prevent cardiovascular events. Most adverse effects associated with statin therapy are muscle-related. The recent statement of the European Atherosclerosis Society (EAS) has focused on statin associated muscle symptoms (SAMS), and avoided the use of the term 'statin intolerance'. Although muscle syndromes are the most common adverse effects observed after statin therapy, excluding other side effects might underestimate the number of patients with statin intolerance, which might be observed in 10-15% of patients. In clinical practice, statin intolerance limits effective treatment of patients at risk of, or with, cardiovascular disease. Knowledge of the most common adverse effects of statin therapy that might cause statin intolerance and the clear definition of this phenomenon is crucial to effectively treat patients with lipid disorders. Therefore, the aim of this position paper was to suggest a unified definition of statin intolerance, and to complement the recent EAS statement on SAMS, where the pathophysiology, diagnosis and the management were comprehensively presented. PMID:25861286

  19. Lactose malabsorption and intolerance: What should be the best clinical management?

    PubMed

    Usai-Satta, Paolo; Scarpa, Mariella; Oppia, Francesco; Cabras, Francesco

    2012-06-01

    Lactose malabsorption (LM) is the incomplete hydrolysis of lactose due to lactase deficiency, which may occur as a primary disorder or secondary to other intestinal diseases. Primary adult-type hypolactasia is an autosomal recessive condition resulting from the physiological decline of lactase activity. Different methods have been used to diagnose LM. Lactose breath test represents the most reliable technique. A recent consensus conference has proposed the more physiological dosage of 25 g of lactose and a standardized procedure for breath testing. Recently a new genetic test, based on C/T13910 polymorphism, has been proposed for the diagnosis of adult-type hypolactasia, complementing the role of breath testing. LM represents a well-known cause of abdominal symptoms although only some lactose malabsorbers are also intolerants. Diagnosing lactose intolerance is not straightforward. Many non-malabsorber subjects diagnose themselves as being lactose intolerant. Blind lactose challenge studies should be recommended to obtain objective results. Besides several studies indicate that subjects with lactose intolerance can ingest up to 15 g of lactose with no or minor symptoms. Therefore a therapeutic strategy consists of a lactose restricted diet avoiding the nutritional disadvantages of reduced calcium and vitamin intake.Various pharmacological options are also available. Unfortunately there is insufficient evidence that these therapies are effective. Further double-blind studies are needed to demonstrate treatment effectiveness in lactose intolerance. PMID:22966480

  20. FOOD INTOLERANCES AND ASSOCIATED SYMPTOMS IN PATIENTS UNDERGOING FOBI-CAPELLA TECHNIQUE WITHOUT GASTRIC RING

    PubMed Central

    MOREIRA, Marcella de Arruda; ESPÍNOLA, Patrícia Ramos Maciel; de AZEVEDO, Camila Wanderley

    2015-01-01

    Background Bariatric surgery is considered the only effective method to treat refractory obesity, and especially for those in which clinical treatment was not successful. However, the appearance of food intolerances and clinical manifestations are quite common. Aim To identify food intolerances and associated them to symptoms in patients undergoing Fobi-Capella technique without gastric ring. Methods This was a cross-sectional study of adult patients who had more than one year after surgery. Demographic, anthropometric, weight and preoperative height data were investigated. Nutritional status was classified according to the criteria established by the World Health Organization. It was considered food intolerance the presence of nausea, vomiting, diarrhea or bloating after eating a particular food. Results The sample consisted of 61 patients who attended the nutritional consultation of which 26 (42.6%) had food intolerance, mostly related to red meat (n=12; 34.3%) during the first six months of operation; there was a significant difference between the periods between 0 and 6 months, and 7 to 12 (p=0.02). Among the symptoms reported by patients, nausea was the most recurrent until the 6th month, but without significant differences between the two periods (p=0.06). Conclusions The Fobi-Capella procedure without gastric ring promoted high frequency of intolerance to meat in general, especially for the red, chicken and fish, on this sequence; nausea was the most frequent symptom. These data suggest the need for adequate nutritional monitoring throughout the postoperative period. PMID:25861067

  1. Lactose malabsorption and intolerance: What should be the best clinical management?

    PubMed Central

    Usai-Satta, Paolo; Scarpa, Mariella; Oppia, Francesco; Cabras, Francesco

    2012-01-01

    Lactose malabsorption (LM) is the incomplete hydrolysis of lactose due to lactase deficiency, which may occur as a primary disorder or secondary to other intestinal diseases. Primary adult-type hypolactasia is an autosomal recessive condition resulting from the physiological decline of lactase activity. Different methods have been used to diagnose LM. Lactose breath test represents the most reliable technique. A recent consensus conference has proposed the more physiological dosage of 25 g of lactose and a standardized procedure for breath testing. Recently a new genetic test, based on C/T13910 polymorphism, has been proposed for the diagnosis of adult-type hypolactasia, complementing the role of breath testing. LM represents a well-known cause of abdominal symptoms although only some lactose malabsorbers are also intolerants. Diagnosing lactose intolerance is not straightforward. Many non-malabsorber subjects diagnose themselves as being lactose intolerant. Blind lactose challenge studies should be recommended to obtain objective results. Besides several studies indicate that subjects with lactose intolerance can ingest up to 15 g of lactose with no or minor symptoms. Therefore a therapeutic strategy consists of a lactose restricted diet avoiding the nutritional disadvantages of reduced calcium and vitamin intake.Various pharmacological options are also available. Unfortunately there is insufficient evidence that these therapies are effective. Further double-blind studies are needed to demonstrate treatment effectiveness in lactose intolerance. PMID:22966480

  2. Glucose /Oxygen Sensor

    NASA Astrophysics Data System (ADS)

    Parker, J. W.; Cox, M. E.

    1987-04-01

    Oxygen concentration has been measured using fluorescence quenching in solid polymer hosts. The feasibility of generalizing these oxygen transducers to a wider class of chemical sensors through coupling to other chemistries is proposed. An example of such coupling is given in a glucose/oxygen transducer. The glucose transducer is produced by entrapping an enzyme, glucose oxidase, in' the composite matrix of a hydrophilic oxygen transducer. Glucose oxidase catalyzes a reaction between glucose and oxygen, thereby lowering the local oxygen concentration. This transducer yields a glucose modified optical oxygen signal. The specific focus of this research is the development of a theoretical model that describes the coupling of glucose concentration to relative fluorescence intensity, the experimental measurement of the key parameters in this model, and the evaluation of the sensitivity of the variation in relative fluorescence intensity with changes in glucose concentration. The experimental parameters include the diffusivity of oxygen in PHEMA (1.36 x 10-7 cm2/s), the solubility ofoglucose in PHEMA (0.24 g in PHEMA/g in buffer), and the diffusivity of glucose in PHEMA (8.25 x 10-8 cm2/s). When these experimental parameters are incorporated, the model developed predicts critical design requirements of the transducer.

  3. Gut microbe-derived extracellular vesicles induce insulin resistance, thereby impairing glucose metabolism in skeletal muscle

    PubMed Central

    Choi, Youngwoo; Kwon, Yonghoon; Kim, Dae-Kyum; Jeon, Jinseong; Jang, Su Chul; Wang, Taejun; Ban, Minjee; Kim, Min-Hye; Jeon, Seong Gyu; Kim, Min-Sun; Choi, Cheol Soo; Jee, Young-Koo; Gho, Yong Song; Ryu, Sung Ho; Kim, Yoon-Keun

    2015-01-01

    Gut microbes might influence host metabolic homeostasis and contribute to the pathogenesis of type 2 diabetes (T2D), which is characterized by insulin resistance. Bacteria-derived extracellular vesicles (EVs) have been suggested to be important in the pathogenesis of diseases once believed to be non-infectious. Here, we hypothesize that gut microbe-derived EVs are important in the pathogenesis of T2D. In vivo administration of stool EVs from high fat diet (HFD)-fed mice induced insulin resistance and glucose intolerance compared to regular diet (RD)-fed mice. Metagenomic profiling of stool EVs by 16S ribosomal DNA sequencing revealed an increased amount of EVs derived from Pseudomonas panacis (phylum Proteobacteria) in HFD mice compared to RD mice. Interestingly, P. panacis EVs blocked the insulin signaling pathway in both skeletal muscle and adipose tissue. Moreover, isolated P. panacis EVs induced typical diabetic phenotypes, such as glucose intolerance after glucose administration or systemic insulin injection. Thus, gut microbe-derived EVs might be key players in the development of insulin resistance and impairment of glucose metabolism promoted by HFD. PMID:26510393

  4. Relationship between serum sex hormones and glucose, insulin and lipid abnormalities in men with myocardial infarction.

    PubMed Central

    Phillips, G B

    1977-01-01

    Fifteen patients who had had a myocardial infarction before the age of 43 were compared with thirteen age-matched normal subjects. Twelve of the patients and three of the controls had a delayed glucose and insulin peak in the glucose and insulin areas than normal curves. When the measurements of the four patients with the largest areas under the glucose tolerance curve were separated, significant correlations were observed in the remaining patients and controls. The ratio in serum of the concentrations of estradiol-17beta to testosterone (E/T) correlated with serum glucose area (r equals + 0.69, P is less than 0.001), insulin area (r equals + 0.80, P is less than 0.001), and the ratio of insulin area to glucose area (I/G) (r equals + 0.64, P is less than 0.005) in the glucose tolerance test. Serum cholesterol concentration correlated with E/T, insulin area, and I/G, and serum triglyceride concentration correlated with glucose area, I/G, and serum cholesterol concentration. The hypothesis is presented (i) that in men who have had a myocardial infarction, an abnormality in glucose tolerance and insulin response and elevation in serum cholesterol and triglyceride concentrations are all part of the same defect (glucose-insulin-lipid defect), (ii) that this glucose-insulin-lipid defect when glucose intolerance is present is the "mild diabetes" commonly associated with myocardial infarction but is based on a mechanism different from that of classical diabetes, (iii) that this glucose-insulin-lipid defect is secondary to an elevation in E/T, and (iv) that an alteration in the sex hormone milieu is the major predisposing factor for myocardial infarction. PMID:193114

  5. The glucose oxidase-peroxidase assay for glucose

    Technology Transfer Automated Retrieval System (TEKTRAN)

    The glucose oxidase-peroxidase assay for glucose has served as a very specific, sensitive, and repeatable assay for detection of glucose in biological samples. It has been used successfully for analysis of glucose in samples from blood and urine, to analysis of glucose released from starch or glycog...

  6. Increased waist/hip ratio, metabolic disturbances, and family history of hypertension.

    PubMed

    Widgren, B R; Herlitz, H; Wikstrand, J; Sjstrm, L; Berglund, G; Andersson, O K

    1992-10-01

    To test whether nonhypertensive subjects with a two-generation positive family history of hypertension (PFH) are characterized by disturbed glucose metabolism, 16 men (38 +/- 6 years old) with PFH and 25 subjects matched for age and with negative family histories of hypertension (NFH) were recruited. Blood pressure; serum lipids; erythrocyte transmembrane sodium transport; and the glucose, plasma insulin, and C-peptide responses to an oral glucose tolerance test were investigated. Subjects with PFH had higher blood pressure, body weight, body mass index (BMI), waist/hip ratio (WHR), and abdominal sagittal diameter than subjects with NFH. Baseline blood glucose, plasma insulin, serum lipids, and transmembrane sodium transport did not differ between the two groups. Blood glucose levels at 90 and 120 minutes after oral glucose were significantly higher in subjects with PFH than in controls. Blood glucose adjusted for BMI and WHR at 90 minutes was significantly related to a PFH. Plasma insulin level at 90 minutes during the glucose load was significantly higher in subjects with PFH. In multivariate analysis, WHR was significantly related to baseline blood pressure, insulin, and cholesterol, whereas BMI was significantly associated with the insulin response to the oral glucose tolerance test. Transmembrane sodium transport was significantly related to blood pressure only. In conclusion, subjects with PFH are characterized by increased body weight and BMI, increased visceral fat accumulation, and an altered blood glucose response to an oral glucose load. It was also shown that WHR was related to blood pressure and that BMI was more related to cholesterol and response to glucose loading than a PFH was. PMID:1398891

  7. GLUT2, glucose sensing and glucose homeostasis.

    PubMed

    Thorens, Bernard

    2015-02-01

    The glucose transporter isoform GLUT2 is expressed in liver, intestine, kidney and pancreatic islet beta cells, as well as in the central nervous system, in neurons, astrocytes and tanycytes. Physiological studies of genetically modified mice have revealed a role for GLUT2 in several regulatory mechanisms. In pancreatic beta cells, GLUT2 is required for glucose-stimulated insulin secretion. In hepatocytes, suppression of GLUT2 expression revealed the existence of an unsuspected glucose output pathway that may depend on a membrane traffic-dependent mechanism. GLUT2 expression is nevertheless required for the physiological control of glucose-sensitive genes, and its inactivation in the liver leads to impaired glucose-stimulated insulin secretion, revealing a liver-beta cell axis, which is likely to be dependent on bile acids controlling beta cell secretion capacity. In the nervous system, GLUT2-dependent glucose sensing controls feeding, thermoregulation and pancreatic islet cell mass and function, as well as sympathetic and parasympathetic activities. Electrophysiological and optogenetic techniques established that Glut2 (also known as Slc2a2)-expressing neurons of the nucleus tractus solitarius can be activated by hypoglycaemia to stimulate glucagon secretion. In humans, inactivating mutations in GLUT2 cause Fanconi-Bickel syndrome, which is characterised by hepatomegaly and kidney disease; defects in insulin secretion are rare in adult patients, but GLUT2 mutations cause transient neonatal diabetes. Genome-wide association studies have reported that GLUT2 variants increase the risks of fasting hyperglycaemia, transition to type 2 diabetes, hypercholesterolaemia and cardiovascular diseases. Individuals with a missense mutation in GLUT2 show preference for sugar-containing foods. We will discuss how studies in mice help interpret the role of GLUT2 in human physiology. PMID:25421524

  8. The Comparative Efficacy and Safety of the Angiotensin Receptor Blockers in the Management of Hypertension and Other Cardiovascular Diseases

    PubMed Central

    Abraham, Hazel Mae A.; White, C. Michael; White, William B.

    2014-01-01

    All national guidelines for the management of hypertension recommend angiotensin receptor blockers (ARBs) as an initial or add-on antihypertensive therapy. The 8 available ARBs have variable clinical efficacy when used for control of hypertension. Additive blood pressure (BP) lowering effects have been demonstrated when ARBs are combined with thiazide diuretics or dihydropyridine calcium channel blockers, augmenting hypertension control. Furthermore, therapeutic use of ARBs goes beyond their antihypertensive effects with evidence-based benefits in heart failure and diabetic renal disease particularly among ACE inhibitor intolerant patients. On the other hand, combining renin-angiotensin system blocking agents, a formerly common practice among medical subspecialists focusing on the management of hypertension, have ceased to do so as there is not only evidence of cardiovascular benefit, but modest evidence of harm, particularly with regard to renal dysfunction. The ARBs are very well tolerated as monotherapy as well as in combination with other anti-hypertensive medications that improve adherence to therapy and have become a mainstay in the treatment of stage 1 and 2 hypertension. PMID:25416320

  9. Blood pressure and plasma renin activity as predictors of orthostatic intolerance

    NASA Technical Reports Server (NTRS)

    Harrison, M. H.; Kravik, S. E.; Geelen, G.; Keil, L.; Greenleaf, J. E.

    1985-01-01

    The effect of 3 h standing, followed by a period of head-up tilt (HUT) on physiological response (orthostatic tolerance, blood pressure and heart rate), as well as on plasma vasopressin (PVP) and renin activity (PRA) were studied in 13 dehydrated (to 2.4 pct loss of body weight) subjects. Seven subjects showed signs of orthostatic intolerance (INT), manifested by sweating, pallor, nausea and dizziness. Prior to these symptoms, the INT subjects exhibited lower systolic (SP) and pulse (PP) pressures, and an elevated PRA, compared to the tolerant (TOL) subjects. HUT has aggravated increases of RPA in the INT subjects and caused an increase, higher than in TOL subjects, in PVP, while rehydration has greatly attenuated the PVP response to the HUT and decreased the PRA response. It is concluded that dehydration, together with measurements of SP, PP and PRA, may serve as a means of predicting orthostatic intolerance and may provide a physiological model for studying the causes of intolerance.

  10. (51Cr)EDTA intestinal permeability in children with cow's milk intolerance

    SciTech Connect

    Schrander, J.J.; Unsalan-Hooyen, R.W.; Forget, P.P.; Jansen, J. )

    1990-02-01

    Making use of ({sup 51}Cr)EDTA as a permeability marker, we measured intestinal permeability in a group of 20 children with proven cow's milk intolerance (CMI), a group of 17 children with similar complaints where CMI was excluded (sick controls), and a group of 12 control children. ({sup 51}Cr)EDTA test results (mean +/- SD) were 6.85 +/- 3.64%, 3.42 +/- 0.94%, and 2.61 +/- 0.67% in the group with CMI, the sick control, and the control group, respectively. When compared to both control groups, patients with cow's milk intolerance (CMI) showed a significantly increased small bowel permeability. We conclude that the ({sup 51}Cr)EDTA test can be helpful for the diagnosis of cow's milk intolerance.

  11. Genetic difference in HLA-DR phenotypes between coeliac disease and transitory gluten intolerance.

    PubMed Central

    Meuli, R; Pichler, W J; Gaze, H; Lentze, M J

    1995-01-01

    Genetic differences in HLA phenotypes were studied in coeliac disease to investigate why some patients do not react with mucosal damage after gluten challenge. Forty five children with coeliac disease and 16 with transitory gluten intolerance were typed; 76 subjects served as controls. HLA phenotypes in children with coeliac disease had significantly higher proportions of DR3/X and DR5/7 than controls (48.8% v 11.8% and 26.7% v 5.3%). Children with transitory gluten intolerance had lower DR3/X (43.8%) than children with coeliac disease and there were no DR5/7 phenotypes. Further analysis of similarly well defined cases might show whether genetic differences in the DR3/X and DR5/7 phenotypes can serve as a marker for the permanence of gluten intolerance. PMID:7717732

  12. Use of Mycophenolate Mofetil in Patients with Severe Localized Scleroderma Resistant or Intolerant to Methotrexate.

    PubMed

    Mertens, Jorre S; Marsman, Diane; van de Kerkhof, Peter C M; Hoppenreijs, Esther P A H; Knaapen, Hanneke K A; Radstake, Timothy R D; de Jong, Elke M G J; Seyger, Marieke M B

    2016-04-12

    To assess the efficacy and safety of mycophenolate mofetil (MMF) in patients with localized scleroderma (LoS) resistant or intolerant to previous treatment with methotrexate (MTX). A case series of patients with LoS treated with MMF. Outcome was assessed through clinical examination. Adverse events were documented. Seven patients with LoS were treated with MMF. Median age at MMF initiation was 15 years (range 7-74 years). Three patients received MMF due to MTX ineffectiveness and 4 due to MTX intolerance. Disease remission was achieved in 4 patients and maintained in one patient. One patient showed a favourable response, but had to discontinue treatment due to elevated liver enzymes. The remaining patient experienced disease progression. MMF was shown to improve the clinical condition of patients with refractory LoS and may be a relatively safe alternative in patients who are intolerant to MTX. PMID:26582717

  13. Odor and Noise Intolerance in Persons with Self-Reported Electromagnetic Hypersensitivity

    PubMed Central

    Nordin, Steven; Neely, Gregory; Olsson, David; Sandström, Monica

    2014-01-01

    Lack of confirmation of symptoms attributed to electromagnetic fields (EMF) and triggered by EMF exposure has highlighted the role of individual factors. Prior observations indicate intolerance to other types of environmental exposures among persons with electromagnetic hypersensitivity (EHS). This study assessed differences in odor and noise intolerance between persons with EHS and healthy controls by use of subscales and global measures of the Chemical Sensitivity Scale (CSS) and the Noise Sensitivity Scale (NSS). The EHS group scored significantly higher than the controls on all CSS and NSS scales. Correlation coefficients between CSS and NSS scores ranged from 0.60 to 0.65 across measures. The findings suggest an association between EHS and odor and noise intolerance, encouraging further investigation of individual factors for understanding EMF-related symptoms. PMID:25166918

  14. Orthostatic intolerance and the postural tachycardia syndrome: genetic and environment pathophysiologies. Neurolab Autonomic Team

    NASA Technical Reports Server (NTRS)

    Robertson, D.; Shannon, J. R.; Biaggioni, I.; Ertl, A. C.; Diedrich, A.; Carson, R.; Furlan, R.; Jacob, G.; Jordan, J.

    2000-01-01

    Orthostatic intolerance is a common problem for inbound space travelers. There is usually tachycardia on standing but blood pressure may be normal, low or, rarely, elevated. This condition is analogous to the orthostatic intolerance that occurs on Earth in individuals with orthostatic tachycardia, palpitations, mitral valve prolapse, and light-headedness. Our studies during the Neurolab mission indicated that sympathetic nerve traffic is raised in microgravity and that plasma norepinephrine is higher than baseline supine levels but lower than baseline upright levels. A subgroup of patients with familial orthostatic intolerance differ from inbound space travelers in that they have an alanine-to-to-proline mutation at amino acid position 457 in their norepinephrine transporter gene. This leads to poor clearance of norepinephrine from synapses, with consequent raised heart rate. Clinical features of these syndromes are presented.

  15. Hypertension in perspective

    PubMed Central

    Terpstra, W.F.; Zijlstra, F.

    2005-01-01

    Decisions about the management of hypertensive patients should not be based on the level of blood pressure alone, but also on the presence of other risk factors, target organ damage and cardiovascular and renal disease. The results of echocardiography and carotid ultrasonography aids in the stratification of absolute cardiovascular risk as recently advocated by the guidelines of the European Society of Hypertension 2003. Therefore, the detection of target organ damage by ultrasound techniques allows an accurate identification of high-risk patients. Cardiovascular risk stratification only based on a simple routine work-up can often underestimate overall risk, thus leading to a potentially inadequate therapeutic management especially of low-medium risk patients. PMID:25696486

  16. The Misdiagnosis of Hypertension

    PubMed Central

    Ogedegbe, Gbenga; Pickering, Thomas G.; Clemow, Lynn; Chaplin, William; Spruill, Tanya M.; Albanese, Gabrielle M.; Eguchi, Kazuo; Burg, Matthew; Gerin, William

    2016-01-01

    Background The white coat effect (defined as the difference between blood pressure [BP] measurements taken at the physician’s office and those taken outside the office) is an important determinant of misdiagnosis of hypertension, but little is known about the mechanisms underlying this phenomenon. We tested the hypothesis that the white coat effect may be a conditioned response as opposed to a manifestation of general anxiety. Methods A total of 238 patients in a hypertension clinic wore ambulatory blood pressure monitors on 3 separate days 1 month apart. At each clinic visit, BP readings were manually triggered in the waiting area and the examination room (in the presence and absence of the physician) and were compared with the mercury sphygmomanometer readings taken by the physician in the examination room. Patients completed trait and state anxiety measures before and after each BP assessment. Results A total of 35% of the sample was normotensive, and 9%, 37%, and 19% had white coat, sustained, and masked hypertension, respectively. The diagnostic category was associated with the state anxiety measure (F3,237 = 6.4, P < .001) but not with the trait anxiety measure. Patients with white coat hypertension had significantly higher state anxiety scores (t = 2.67, P < .01), with the greatest difference reported during the physician measurement. The same pattern was observed for BP changes, which generally paralleled the changes in state anxiety (t = 4.86, P < .002 for systolic BP; t = 3.51, P < .002 for diastolic BP). Conclusions These findings support our hypothesis that the white coat effect is a conditioned response. The BP measurements taken by physicians appear to exacerbate the white coat effect more than other means. This problem could be addressed with uniform use of automated BP devices in office settings. PMID:19064830

  17. Intestinal glucose metabolism revisited.

    PubMed

    Mithieux, Gilles; Gautier-Stein, Amandine

    2014-09-01

    It is long known that the gut can contribute to the control of glucose homeostasis via its high glucose utilization capacity. Recently, a novel function in intestinal glucose metabolism (gluconeogenesis) was described. The intestine notably contributes to about 20-25% of total endogenous glucose production during fasting. More importantly, intestinal gluconeogenesis is capable of regulating energy homeostasis through a communication with the brain. The periportal neural system senses glucose (produced by intestinal gluconeogenesis) in the portal vein walls, which sends a signal to the brain to modulate hunger sensations and whole body glucose homeostasis. Relating to the mechanism of glucose sensing, the role of the glucose receptor SGLT3 has been strongly suggested. Moreover, dietary proteins mobilize intestinal gluconeogenesis as a mandatory link between their detection in the portal vein and their effect of satiety. In the same manner, dietary soluble fibers exert their anti-obesity and anti-diabetic effects via the induction of intestinal gluconeogenesis. FFAR3 is a key neural receptor involved in the specific sensing of propionate to activate a gut-brain reflex arc triggering the induction of the gut gluconeogenic function. Lastly, intestinal gluconeogenesis might also be involved in the rapid metabolic improvements induced by gastric bypass surgeries of obesity. PMID:24969963

  18. Glucose monitoring during Ramadan.

    PubMed

    Jabbar, Abdul

    2015-05-01

    In patients with diabetes who intend to fast during Ramadan, self-monitoring of blood glucose (SMBG) is an important tool. During this month, a long established treatment regimen, including medications, physical activity and diet plan, is changed to achieve concordance with the rules of fasting. Without proper glucose monitoring, it is not possible to achieve good glycaemic control. PMID:26013788

  19. Glucose: detection and analysis

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Glucose is an aldosic monosaccharide that is centrally entrenched in the processes of photosynthesis and respiration, serving as an energy reserve and metabolic fuel in most organisms. As both a monomer and as part of more complex structures such as polysaccharides and glucosides, glucose also pla...

  20. Assessment and treatment of cardiovascular risk in prediabetes: impaired glucose tolerance and impaired fasting glucose.

    PubMed

    DeFronzo, Ralph A; Abdul-Ghani, Muhammad

    2011-08-01

    Individuals with impaired glucose tolerance (IGT) and/or impaired fasting glucose (IFG) are at high risk, not only to develop diabetes mellitus, but also to experience an adverse cardiovascular (CV) event (myocardial infarction, stroke, CV death) later in life. The underlying pathophysiologic disturbances (insulin resistance and impaired β-cell function) responsible for the development of type 2 diabetes are maximally/near maximally expressed in subjects with IGT/IFG. These individuals with so-called prediabetes manifest all of the same CV risk factors (dysglycemia, dyslipidemia, hypertension, obesity, physical inactivity, insulin resistance, procoagulant state, endothelial dysfunction, inflammation) that place patients with type 2 diabetes at high risk for macrovascular complications. The treatment of these CV risk factors should follow the same guidelines established for patients with type 2 diabetes, and should be aggressively followed to reduce future CV events. PMID:21802577

  1. Portal hypertensive enteropathy

    PubMed Central

    Mekaroonkamol, Parit; Cohen, Robert; Chawla, Saurabh

    2015-01-01

    Portal hypertensive enteropathy (PHE) is a condition that describes the pathologic changes and mucosal abnormalities observed in the small intestine of patients with portal hypertension. This entity is being increasingly recognized and better understood over the past decade due to increased accessibility of the small intestine made possible by the introduction of video capsule endoscopy and deep enteroscopy. Though challenged by its diverse endoscopic appearance, multiple scoring systems have been proposed to classify the endoscopic presentation and grade its severity. Endoscopic findings can be broadly categorized into vascular and non-vascular lesions with many subtypes of both categories. Clinical manifestations of PHE can range from asymptomatic incidental findings to fatal gastrointestinal hemorrhage. Classic endoscopic findings in the setting of portal hypertension may lead to a prompt diagnosis. Occasionally histopathology and cross sectional imaging like computed tomography or magnetic resonance imaging may be helpful in establishing a diagnosis. Management of overt bleeding requires multidisciplinary approach involving hepatologists, endoscopists, surgeons, and interventional radiologists. Adequate resuscitation, reduction of portal pressure, and endoscopic therapeutic intervention remain the main principles of the initial treatment. This article reviews the existing evidence on PHE with emphasis on its classification, diagnosis, clinical manifestations, endoscopic appearance, pathological findings, and clinical management. A new schematic management of ectopic variceal bleed is also proposed. PMID:25729469

  2. Mortality patterns in hypertension.

    PubMed

    Arima, Hisatomi; Barzi, Federica; Chalmers, John

    2011-12-01

    Raised blood pressure (BP) is responsible for 7.6 million deaths per annum worldwide (13.5% of the total), more than any other risk factors. Around 54% of stroke and 47% of coronary heart disease are attributable to high BP. Over 80% of this burden occurs in low and middle income countries (LMIC). BP and cardiovascular mortality are rising rapidly in LMIC. Although age-specific BP and cardiovascular mortality are falling in developed nations, the overall number of cardiovascular death continues to rise in accord with the rapid aging of societies. Because of the continuous relationship between BP and cardiovascular deaths down to 115/75 mmHg, BP-related disease also contributes to cardiovascular death among people below the hypertensive threshold of 140/90 mmHg. Hypertension remains "the silent killer". Reductions in the burden of BP-related death require the parallel application of the population strategy at community level and the clinical strategy focusing on new and improved treatments for people with hypertension. PMID:22157565

  3. Hypertension in Chronic Glomerulonephritis

    PubMed Central

    2015-01-01

    Chronic glomerulonephritis (GN), which includes focal segmental glomerulosclerosis and proliferative forms of GN such as IgA nephropathy, increases the risk of hypertension. Hypertension in chronic GN is primarily volume dependent, and this increase in blood volume is not related to the deterioration of renal function. Patients with chronic GN become salt sensitive as renal damage including arteriolosclerosis progresses and the consequent renal ischemia causes the stimulation of the intrarenal renin-angiotensin-aldosterone system(RAAS). Overactivity of the sympathetic nervous system also contributes to hypertension in chronic GN. According to the KDIGO guideline, the available evidence indicates that the target BP should be ≤140mmHg systolic and ≤90mmHg diastolic in chronic kidney disease patients without albuminuria. In most patients with an albumin excretion rate of ≥30mg/24 h (i.e., those with both micro-and macroalbuminuria), a lower target of ≤130mmHg systolic and ≤80mmHg diastolic is suggested. The use of agents that block the RAAS system is recommended or suggested in all patients with an albumin excretion rate of ≥30mg/ 24 h. The combination of a RAAS blockade with a calcium channel blocker and a diuretic may be effective in attaining the target BP, and in reducing the amount of urinary protein excretion in patients with chronic GN. PMID:26848302

  4. Hypertension in Chronic Glomerulonephritis.

    PubMed

    Ihm, Chun-Gyoo

    2015-12-01

    Chronic glomerulonephritis (GN), which includes focal segmental glomerulosclerosis and proliferative forms of GN such as IgA nephropathy, increases the risk of hypertension. Hypertension in chronic GN is primarily volume dependent, and this increase in blood volume is not related to the deterioration of renal function. Patients with chronic GN become salt sensitive as renal damage including arteriolosclerosis progresses and the consequent renal ischemia causes the stimulation of the intrarenal renin-angiotensin-aldosterone system(RAAS). Overactivity of the sympathetic nervous system also contributes to hypertension in chronic GN. According to the KDIGO guideline, the available evidence indicates that the target BP should be ≤140mmHg systolic and ≤90mmHg diastolic in chronic kidney disease patients without albuminuria. In most patients with an albumin excretion rate of ≥30mg/24 h (i.e., those with both micro-and macroalbuminuria), a lower target of ≤130mmHg systolic and ≤80mmHg diastolic is suggested. The use of agents that block the RAAS system is recommended or suggested in all patients with an albumin excretion rate of ≥30mg/ 24 h. The combination of a RAAS blockade with a calcium channel blocker and a diuretic may be effective in attaining the target BP, and in reducing the amount of urinary protein excretion in patients with chronic GN. PMID:26848302

  5. Hypertension in the elderly.

    PubMed

    Robles, Nicolas R; Macias, Juan F

    2015-01-01

    Data collected over a 30-year period have demonstrated the increasing prevalence of hypertension with age. Aging is an inevitable part of life and brings along two inconvenient events: physiologic decline and disease state. High blood pressure (HBP) is an important risk factor for cardiovascular morbidity and mortality, particularly in the elderly. It is a significant and often asymptomatic chronic disease, which requires optimal control and persistent adherence to prescribed medication to reduce the risks of cardiovascular, cerebrovascular and renal disease. Hypertension in the elderly patients represents a management dilemma to geriatric and cardiovascular specialists and other practitioners. Furthermore, with the wide adoption of multiple drug strategies targeting subgroups of hypertensive patients with specific risk conditions to lower blood pressure (BP), difficult questions arise about how aggressive treatment of elderly patients should be. The purpose of the following chapter article is to review the pathophysiology of aging as well as the epidemiology and the clinical assessment of high blood pressure (HBP) in older people. PMID:25761101

  6. Managing hypertension by polyphenols.

    PubMed

    Fernández-Arroyo, Salvador; Camps, Jordi; Menendez, Javier A; Joven, Jorge

    2015-06-01

    Some polyphenols, obtained from plants of broad use, induce a favorable endothelial response in hypertension and beneficial effects in the management of other metabolic cardiovascular risks. Previous studies in our laboratories using the calyces of Hibiscus sabdariffa as a source of polyphenols show that significant effects on hypertension are noticeable in humans only when provided in high amounts. Available data are suggestive in animal models and ex vivo experiments, but data in humans are difficult to acquire. Additionally, and despite the low bioavailability of polyphenols, intervention studies provide evidence for the protective effects of secondary plant metabolites. Assumptions on public health benefits are limited by the lack of scientific knowledge, robust data derived from large randomized clinical trials, and an accurate assessment of the bioactive components provided by common foodstuff. Because it is likely that clinical effects are the result of multiple interactions among different polyphenols rather than the isolated action of unique compounds, to provide polyphenol-rich botanical extracts as dietary supplements is a suggestive option. Unfortunately, the lack of patent perspectives for the pharmaceutical industries and the high cost of production and release for alimentary industries will hamper the performance of the necessary clinical trials. Here we briefly discuss whether and how such limitations may complicate the extensive use of plant-derived products in the management of hypertension and which steps are the necessary to deal with the predictable complexity in a possible clinical practice. PMID:25714729

  7. Insulin resistance in young, lean male subjects with essential hypertension.

    PubMed

    Penesova, A; Cizmarova, E; Belan, V; Blazicek, P; Imrich, R; Vlcek, M; Vigas, M; Selko, D; Koska, J; Radikova, Z

    2011-06-01

    Impaired insulin action, frequently found in essential hypertension (HT), is modified by other factors, such as higher age, accumulation of body fat, dyslipidaemia, impaired glucose metabolism and endothelial dysfunction. In addition, antihypertensive and insulin-sensitizing medication itself may significantly affect cardiovascular and metabolic milieu. The aim of this study was to assess insulin sensitivity, acute insulin response, lipidaemic status and the adipokines' concentrations with regard to abdominal fat distribution in young, lean male subjects with treatment-naïve essential HT and in matched healthy normotensive (NT) subjects. We studied 27 HT patients (age: 19.9±0.6 years; body mass index (BMI): 22.9±0.5 kg m(-2)) and 15 NT controls (age: 22.3±1.0 years; BMI: 23.7±0.6 kg m(-2)). The subjects underwent an oral and an intravenous glucose tolerance test (OGTT, IVGTT) on separate days in random order. Higher fasting insulin (P<0.001), non-esterified fatty acids (P<0.05) and plasminogen activator inhibitor factor 1 concentrations (P<0.05) were found in HT patients when compared with NT patients. Despite comparable anthropometric parameters and body fat distribution assessed by magnetic resonance imaging in both groups, newly diagnosed untreated young hypertensive male subjects showed decreased insulin sensitivity, augmented insulin response to both oral and intravenous glucose load (P<0.01; P<0.05 respectively) and 'higher still normal' 2-h plasma glucose levels during OGTT. Untreated, young, lean hypertensive male subjects, with distribution of abdominal adipose tissue and lipid profile comparable with their healthy NT matched counterparts, showed considerable signs of insulin resistance and hyperinsulinaemia. We hypothesize that insulin resistance is the initial feature, which is influenced by several environmental factors, and HT is one of their common consequences. PMID:20631738

  8. Glucagon chronically impairs hepatic and muscle glucose disposal.

    PubMed

    Chen, Sheng-Song; Zhang, Yiqun; Santomango, Tammy S; Williams, Phillip E; Lacy, D Brooks; McGuinness, Owen P

    2007-03-01

    Defects in insulin secretion and/or action contribute to the hyperglycemia of stressed and diabetic patients, and we hypothesize that failure to suppress glucagon also plays a role. We examined the chronic impact of glucagon on glucose uptake in chronically catheterized conscious depancreatized dogs placed on 5 days of nutritional support (NS). For 3 days of NS, a variable intraportal infusion of insulin was given to maintain isoglycemia (approximately 120 mg/dl). On day 3 of NS, animals received a constant low infusion of insulin (0.4 mU.kg-1.min-1) and either no glucagon (CONT), basal glucagon (0.7 ng.kg-1.min-1; BasG), or elevated glucagon (2.4 ng.kg-1.min-1; HiG) for the remaining 2 days. Glucose in NS was varied to maintain isoglycemia. An additional group (HiG+I) received elevated insulin (1 mU.kg-1.min-1) to maintain glucose requirements in the presence of elevated glucagon. On day 5 of NS, hepatic substrate balance was assessed. Insulin and glucagon levels were 10+/-2, 9+/-1, 7+/-1, and 24+/-4 microU/ml, and 24+/-5, 39+/-3, 80+/-11, and 79+/-5 pg/ml, CONT, BasG, HiG, and HiG+I, respectively. Glucagon infusion decreased the glucose requirements (9.3+/-0.1, 4.6+/-1.2, 0.9+/-0.4, and 11.3+/-1.0 mg.kg-1.min-1). Glucose uptake by both hepatic (5.1+/-0.4, 1.7+/-0.9, -1.0+/-0.4, and 1.2+/-0.4 mg.kg-1.min-1) and nonhepatic (4.2+/-0.3, 2.9+/-0.7, 1.9+/-0.3, and 10.2+/-1.0 mg.kg-1.min-1) tissues decreased. Additional insulin augmented nonhepatic glucose uptake and only partially improved hepatic glucose uptake. Thus, glucagon impaired glucose uptake by hepatic and nonhepatic tissues. Compensatory hyperinsulinemia restored nonhepatic glucose uptake and partially corrected hepatic metabolism. Thus, persistent inappropriate secretion of glucagon likely contributes to the insulin resistance and glucose intolerance observed in obese and diabetic individuals. PMID:17132827

  9. Prevalence of Hypertension in Boloor Diabetes Study (BDS-II) and its Risk Factors

    PubMed Central

    Adhikari, Prabha; Pathak, Rahul; Kotian, Mangalore Shashidhar; Ullal, Sheetal

    2015-01-01

    Introduction Hypertension is a major public health problem in India and worldwide. Since hypertension is often asymptomatic, it commonly remains undetected, leading to serious complications if untreated. Hypertension is one of the leading causes of end stage renal disease. It doubles the risk of developing coronary artery disease, increases the risk of congestive heart failure by four folds and that of cerebrovascular disease and stroke by seven folds. Hypertension is directly responsible for 57% of all stroke deaths and 42% of coronary heart disease deaths in India. Aim To identify prevalence and risk factors for hypertension in a semi urban population of Mangalore, who participated in Boloor Diabetes Study (BDS-II). Materials and Methods This cross-sectional study was conducted on 551 subjects aged ≥ 20 years who were randomly selected. Hypertension was diagnosed and classified according to Joint National Committee 7 (JNC) criteria. Blood pressure was measured by a doctor using calibrated sphygmomanometer. Anthropometric measurements, lipid and glucose estimations were done for all subjects. Statistical analysis was done using Chi-square test and student’s t-test (unpaired). Multivariate logistic regression analysis was done using hypertension as dependent variable and the various risk factors as independent variables. Results Overall prevalence of hypertension in the community was 41% (227/551) (40.9% in men, 41.3% in women). Prehypertension was found in 40% (223/551) (45.4% in men, 38.1% in women), and only 18.3% (101/551) had normal blood pressure. Stage I hypertension was seen in 29.7% (164/551) (28.9% in men, 30.1% in women). Stage II hypertension was seen in 11.4% (63/551) (12% in men, 11% in women). Age, obesity, diabetes, serum cholesterol and serum triglycerides were strongly associated with hypertension. Only 46% (254/551) of the hypertensive subjects were aware that they were hypertensive. Conclusion Prevalence of hypertension was high in this population. Nearly 54% were unaware of their hypertensive status. Prevalence increased with age, obesity, diabetic status and dyslipidemia. Nearly half of subjects were prehypertensives. This study highlights the need for regular screening coupled with educational programmes to detect, improve awareness and optimally treat hypertension in the community to reduce cardiovascular and renal complications. PMID:26674015

  10. [Management of pregnancy induced hypertension].

    PubMed

    Suzuki, Yoshikatsu; Matsuura, Ayano; Yamamoto, Tamao

    2015-11-01

    Pregnancy induced hypertension (PIH) is classified according to the severity of hypertension. The Japan Society of Hypertension made practice guidelines in 2014, and the Japan Society for the Study of Hypertension in Pregnancy made guidelines subsequently in 2015, too. Both guidelines state that the basic treatment for PIH is the interruption of pregnancy, and antihypertensive therapy should be given for protection in mother complicated by severe hypertension. The fetal heart rates should be monitored enough due to worsening fetal circulation. It recommends that methyldopa, hydralazine, labetalol, and long-acting nifedipine (only after 20 weeks of gestation) should be used as the first-choice antihypertensive oral drugs. Intravenous administration should be selected when a hypertensive emergency occurs. PMID:26619665

  11. Glucose metabolism ontogenesis in rainbow trout (Oncorhynchus mykiss) in the light of the recently sequenced genome: new tools for intermediary metabolism programming.

    PubMed

    Marandel, Lucie; Véron, Vincent; Surget, Anne; Plagnes-Juan, Élisabeth; Panserat, Stéphane

    2016-03-01

    The rainbow trout (Oncorhynchus mykiss), a carnivorous fish species, displays a 'glucose-intolerant' phenotype when fed a high-carbohydrate diet. The importance of carbohydrate metabolism during embryogenesis and the timing of establishing this later phenotype are currently unclear. In addition, the mechanisms underlying the poor ability of carnivorous fish to use dietary carbohydrates as a major energy substrate are not well understood. It has recently been shown in trout that duplicated genes involved in glucose metabolism may participate in establishing the glucose-intolerant phenotype. The aim of this study was therefore to provide new understanding of glucose metabolism during ontogenesis and nutritional transition, taking into consideration the complexity of the trout genome. Trout were sampled at several stages of development from fertilization to hatching, and alevins were then fed a non-carbohydrate or a high-carbohydrate diet during first feeding. mRNA levels of all glucose metabolism-related genes increased in embryos during the setting up of the primitive liver. After the first meal, genes rapidly displayed expression patterns equivalent to those observed in the livers of juveniles. g6pcb2.a (a glucose 6-phosphatase-encoding gene) was up-regulated in alevins fed a high-carbohydrate diet, mimicking the expression pattern of gck genes. The g6pcb2.a gene may contribute to the non-inhibition of the last step of gluconeogenesis and thus to establishing the glucose-intolerant phenotype in trout fed a high-carbohydrate diet as early as first feeding. This information is crucial for nutritional programming investigations as it suggests that first feeding would be too late to programme glucose metabolism in the long term. PMID:26747908

  12. Saturated- and n-6 polyunsaturated-fat diets each induce ceramide accumulation in mouse skeletal muscle: reversal and improvement of glucose tolerance by lipid metabolism inhibitors.

    PubMed

    Frangioudakis, G; Garrard, J; Raddatz, K; Nadler, J L; Mitchell, T W; Schmitz-Peiffer, C

    2010-09-01

    Lipid-induced insulin resistance is associated with intracellular accumulation of inhibitory intermediates depending on the prevalent fatty acid (FA) species. In cultured myotubes, ceramide and phosphatidic acid (PA) mediate the effects of the saturated FA palmitate and the unsaturated FA linoleate, respectively. We hypothesized that myriocin (MYR), an inhibitor of de novo ceramide synthesis, would protect against glucose intolerance in saturated fat-fed mice, while lisofylline (LSF), a functional inhibitor of PA synthesis, would protect unsaturated fat-fed mice. Mice were fed diets enriched in saturated fat, n-6 polyunsaturated fat, or chow for 6 wk. Saline, LSF (25 mg/kg x d), or MYR (0.3 mg/kg x d) were administered by mini-pumps in the final 4 wk. Glucose homeostasis was examined by glucose tolerance test. Muscle ceramide and PA were analyzed by mass spectrometry. Expression of LASS isoforms (ceramide synthases) was evaluated by immunoblotting. Both saturated and polyunsaturated fat diets increased muscle ceramide and induced glucose intolerance. MYR and LSF reduced ceramide levels in saturated and unsaturated fat-fed mice. Both inhibitors also improved glucose tolerance in unsaturated fat-fed mice, but only LSF was effective in saturated fat-fed mice. The discrepancy between ceramide and glucose tolerance suggests these improvements may not be related directly to changes in muscle ceramide and may involve other insulin-responsive tissues. Changes in