Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0497406 (overweight)
 26,365 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the study was to investigate the effects of energy restriction with or without pegylated recombinant leptin (PEG-leptin) treatment on ghrelin, adiponectin, insulin and glucose concentrations. A randomized double-blind placebo-controlled trial was performed in 24 moderately overweight/obese men. PEG-leptin or placebo was administered weekly for 6 weeks, combined with a restricted energy intake of 2.1 MJ/d. At days 1, 25, and 46 a blood sample was taken and body-weight (BW) was measured. Days 1-25 was named phase 1, and days 25-46 phase 2. During phase 1 the rate of BW loss was significantly higher in the PEG-leptin compared to the placebo group (0.38+/-0.07 vs 0.32+/-0.06 kg/d, p<0.05). The rate of BW loss during phase 2 was 0.24+/-0.08 and 0.18+/-0.09 kg/d, respectively (p=0.07). In both groups the rate of BW loss during phase 1 was significantly higher than during phase 2 (p<0.001). Energy balance (EB) was significantly more negative during phase 1 than during phase 2 in both groups (p<0.0005). During phase 1 insulin, glucose and adiponectin decreased significantly in both groups. Adiponectin and ghrelin concentrations changed in the opposite direction between phase 1 and phase 2 (p<0.05). Initial BW loss due to a considerable negative EB induced decreased ghrelin, adiponectin, insulin and glucose levels. However, when EB became less negative and the rate of BW loss decreased, these changes were reversed for adiponectin and ghrelin. The PEG-leptin injections did not have an effect on the changes in insulin, glucose and adiponectin, but had an effect on the changes in ghrelin concentrations.
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PMID:Effects of very low calorie diet induced body weight loss with or without human pegylated recombinant leptin treatment on changes in ghrelin and adiponectin concentrations. 1743 47

Strategies used to counteract overweight include generally endurance exercise. Force-resistance exercise has not been tested yet with this objective. The aim of this study was to investigate the response of the main regulatory hormones of food intake (insulin, adiponectin, leptin, ghrelin) and corticosterone, to a short force resistance exercise. Two groups of 16 rats, 65 days old, weighing 330g, were constituted. A standard diet (containing glucid: 72.2, lipid: 7.7, protid: 20% calories) was given "ad libitum". One group served as control, the second group was submitted to exercise training during 5 weeks. Training reduced the rats body weight by 6.4% and the total food intake during the 5 weeks by 11%. Training lowered the insulin and ghrelin levels, while corticosterone level was increased. Insulin, ghrelin and corticosterone only reached the significant threshold p<0.05. Thus, it seems that exercise, even of low intensity and duration, induces changes on hormones that regulate food intake and limit overweight.
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PMID:Effect of a moderate exercise on the regulatory hormones of food intake in rats. 1746 89

Central adiposity plays an important role in the insulin resistance of the polycystic ovary syndrome (PCOS) through the dysregulated production of various adipokines. Polycystic ovary syndrome has also been described as a low-grade inflammation state characterized by elevated levels of C-reactive protein (CRP). Furthermore, CRP is a strong independent predictor of the metabolic syndrome and cardiovascular disease. Recently, the adiponectin-to-leptin (A/L) ratio has been proposed as a potential atherogenic index in obese type 2 diabetic patients. The aim of this study was to evaluate the potential role of the A/L ratio in the metabolic and proinflammatory phenotype of PCOS. We studied 74 Greek women with PCOS (38 normal-weight and 36 overweight-obese women). The A/L ratio was negatively correlated with BMI (r = -0.79 P < .001), homeostasis model assessment (r = -0.642, P < .001), triglycerides (r = -0.67, P < .001), and total cholesterol (r = -0.38, P < .01), and positively correlated with high-density lipoprotein cholesterol (r = 0.38, P < .01) and sex hormone-binding globulin (r = 0.39, P = .001). After controlling for BMI, the A/L ratio was independently associated with insulin resistance indexes and triglycerides. Furthermore, the A/L ratio was negatively correlated with CRP (r = -0.746, P < .0001). Multiple regression analysis revealed that BMI and the A/L ratio were the only independent significant determinants of CRP (beta = .436, P = .003 and beta = -.398, P = .007, respectively). Studying normal-weight and overweight-obese women separately, we found an independent association between the A/L ratio and CRP in both groups (beta = -.460, P = .009 in normal-weight women and beta = -.570, P = .001 in overweight-obese women). In conclusion, the A/L ratio may serve as a biomarker of both insulin resistance and low-grade inflammation, providing the link between these cardiovascular risk factors in women with PCOS.
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PMID:The adiponectin-to-leptin ratio in women with polycystic ovary syndrome: relation to insulin resistance and proinflammatory markers. 1751 8

The aim of the present study was to examine the effect of exercise training on adipokines, inflammatory markers, and oxidative stress in overweight children. Nineteen overweight children were randomly assigned to an aerobic exercise training or sedentary control group for 8 weeks. Measurements included peak oxygen uptake (V o(2)max), body weight and composition, adipokines (C-reactive protein, interleukin 6, tumor necrosis factor alpha, adiponectin, leptin, and resistin), and oxidative stress (8-isoprostane). There were no differences between groups for change in body weight or composition over the 8 weeks. Exercise training improved V o(2)max (exercise group, 1.64 +/- 0.13 to 1.85 +/- 0.17L/min vs control group, 1.83 +/- 0.12 to 1.60 +/- 0.13 L/min, P < .05) but did not change any of the measured adipokines or the marker of systemic oxidative stress, 8-isoprostane. These data suggest that in the absence of weight loss, exercise training alone does not improve the adipokine profile or levels of oxidative stress in overweight children.
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PMID:In the absence of weight loss, exercise training does not improve adipokines or oxidative stress in overweight children. 1757 Feb 65

We examined the relationships between plasma vitamin C, adiposity, and the collagen-like adipokine, adiponectin. Of 118 sedentary, nonsmoking adults participating in the cross-sectional trial (35 men and 83 women aged 38.7 +/- 1.0 y with BMI of 30.4 +/- 0.6 kg/m2, plasma vitamin C concentrations of 43.5 +/- 1.3 micromol/L, and plasma adiponectin concentrations of 8.9 +/- 0.3 mg/L), 54% were obese and 24% were overweight. Plasma vitamin C was inversely related to BMI, percentage of body fat, and waist circumference in both women and men (r = -0.383 to -0.497, P < 0.025). In women but not men, these associations remained significant after controlling for body mass. Plasma vitamin C was directly related to plasma adiponectin in the women after controlling for age and vitamin C supplement use (r = 0.222, P = 0.049) but not after controlling for body mass. Twenty obese men and women participated in an intervention trial and consumed an energy-restricted diet low in vitamin C (approximately 38 mg/d) for 8 wk. Subjects were stratified by age, gender, and BMI and randomly assigned to receive placebo or vitamin C (500 mg) capsules daily. At baseline, plasma adiponectin was directly related to plasma vitamin C (r = 0.609, P = 0.021) and inversely related to body mass (r = -0.785, P = 0.001). Body mass decreased significantly during the 8 wk study in both the vitamin C (n = 6, -5.9 +/- 0.9 kg) and placebo groups (n = 8, -6.5 +/- 0.7 kg). Plasma adiponectin increased 13% from baseline by wk 8 in both groups (P < 0.05). In summary, plasma vitamin C was inversely related to markers of adiposity, particularly in women, but vitamin C supplementation did not influence the circulating concentration of adiponectin.
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PMID:Plasma vitamin C is inversely related to body mass index and waist circumference but not to plasma adiponectin in nonsmoking adults. 1758 27

Current knowledge on gamma glutamyl transpeptidase (gammaGTP) was reviewed. This enzyme, which is mainly expresses on the cell surface, is thought to participate in catalyzing glutathione breakdown, resulting in the formation of cystein, a thiol compound exerting antioxidant effects. The most important role of this enzyme in vivo seems to recover cystein from extracellular glutathione to preserve intracellular homeostasis of oxidative stress. Increase in environmental oxidative stress may induce this enzyme via NFkB. However, its excessive induction may contrary raise oxidative stress and cause subsequent organ injuries since cysteinylglycine, an intermediate of the glutathione breakdown, affects the iron metabolism, resulting in the production of free radicals. Recently, there are multiple lines of evidence that the development of hypertension, hyperlipidemia, diabetes mellitus is associated with increased serum gammaGTP levels. The oxidative stress derived from gammaGTP may participate in the development of these morbid conditions and would account for these associations. However, since subjects associated with excessive drinking and overweight, two major factors increasing serum gammaGTP level are usually suffering from hypertension, hyperlipidemia, diabetes mellitus, it is most likely that the associations are attributed to excessive drinking and overweight. We recently demonstrated that level of serum gammaGTP is inversely associated with that of serum adiponectin, a sort of adipocytokines. In that abnormalities of adipocytokines including adiponectin cause hypertension, hyperlipidemia, diabetes mellitus as well as fatty liver that is associated with increased gammaGTP level, the status of adipocytokines may stand behind the associations among these factors in obese subjects. Moreover, we demonstrated that serum gammaGTP level is inversely associated with subjects' statuses of lifestyles evaluated by Breslow's lifestyle index, suggesting that serum gammaGTP activity could be a tool for screening of subjects with unhealthy lifestyles. In that unhealthy lifestyles cause various morbid conditions designated as lifestyle-related diseases that is thought to comprehend metabolic syndrome and/or alcohol-related diseases, such screening and intervention in their correction should be significant to prevent their development. The consensus currently reached is that increased serum gammaGTP activity is associated with increased mortality. In that excessive drinking, obesity, as well as improper lifestyle elevate serum gammaGTP activity meanwhile cause various morbid conditions that make lifespan shorter, the view is not surprising.
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PMID:[Gamma glutamyl transpeptidase (gammaGTP) in the era of metabolic syndrome]. 1766 41

Adiponectin circulates as trimer (LMW), hexamer (MMW) and high molecular weight multimer (HMW) but the distribution and effects of these isoforms have not been studied in detail. Monocytes were isolated from normal weight and overweight controls and patients with type 2 diabetes mellitus (T2D) and monocytic release of IL-6 positively correlated with the body mass index (BMI). HMW-adiponectin further enhanced and LMW-adiponectin reduced IL-6 release in monocytes. Systemic total adiponectin, and the HMW isoform were not different in these groups but MMW-adiponectin was lower in T2D, and LMW-adiponectin was reduced in the obese and T2D. Circulating LMW-adiponectin negatively correlated to monocytic IL-6 release. Systemic IL-6 was higher in the obese control group and T2D, respectively, but did not correlate with monocytic IL-6 secretion. Therefore, the current study indicates that HMW-adiponectin exerts pro- and LMW-adiponectin antiinflammatory effects and reduced LMW-adiponectin in obesity may partly contribute to elevated monocytic IL-6 release.
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PMID:Low molecular weight adiponectin negatively correlates with the waist circumference and monocytic IL-6 release. 1767 73

Thirty-four children were assessed for body composition, blood pressure, lipids, glucose tolerance, markers of insulin resistance, oxidative stress, and adipokines. Children were divided into 3 groups: (1) normal weight, (2) overweight but otherwise healthy, and (3) overweight with the metabolic syndrome. There were no differences among any of the groups for age or Tanner stage, and anthropometric variables were similar between the overweight and the overweight with the metabolic syndrome groups. Differences across groups were found for high-density lipoprotein cholesterol (P < .001), triglycerides (P < .01), fasting insulin (P < .001), homeostasis model assessment (P < .01), adiponectin (P < .05), leptin (P < .0001), C-reactive protein (P < .0001), interleukin 6 (P < .0001), and 8-isoprostane (P < .001). In children, oxidative stress and adipokine levels worsen throughout the continuum of obesity and especially in the presence of components of the metabolic syndrome. Overweight children with components of the metabolic syndrome may be at elevated risk for future cardiovascular disease.
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PMID:Oxidative stress and adverse adipokine profile characterize the metabolic syndrome in children. 1767 10

Our first aim was to determine whether an isocaloric intervention using alpha-linolenic acid (ALA) in the form of flaxseed oil would alter adiponectin levels among overweight, otherwise healthy, males and females, and our second aim was to test for any potential modification of this intervention by 2 single nucleotide polymorphisms (276 and 45) in the adiponectin gene. Subjects included healthy adult males and females (approximately 81% female; average age, 38 years) with increased waist circumference (mean, 99 cm) and body mass index (mean, 30 kg/m(2)) who were free of chronic disease, not taking medications, and sedentary. Subjects met weekly with a registered dietician for 8 weeks. The control subjects (n = 27) were instructed not to alter their habitual diet and the ALA group (n = 30) was instructed to follow an enriched ALA diet by using flaxseed oil capsules (increasing ALA to 5% of total energy intake) and to lower their dietary fat consumption by a commensurate amount. Diets were analyzed using the Food Intake and Analysis System (v. 3.0, University of Texas School of Public Health, 1998). Fasting blood samples were obtained before and after the 8-week intervention. We found significant decreases (P = .02) in adiponectin (10.12 microg/mL pre, 9.23 microg/mL post) in the ALA group as compared with the control group (7.93 microg/mL pre, 8.10 microg/mL post) after the intervention. We also saw a decline in adiponectin in all genotype groups with the greatest decline among those carrying the rare T allele of single nucleotide polymorphism 276. There were no significant changes in fasting insulin, glucose, or quantitative insulin sensitivity check index values as a result of this intervention. In conclusion, this study suggests that supplementing with ALA for 8 weeks may lower adiponectin levels among healthy individuals, and this effect appears to be independent of polymorphisms in the adiponectin gene. Although the change in adiponectin in response to the omega-3 fatty acids was not accompanied by any change in glucose, insulin, or quantitative insulin sensitivity check index, long-term implications of such a decrease should be considered in future studies.
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PMID:Adiponectin levels are reduced, independent of polymorphisms in the adiponectin gene, after supplementation with alpha-linolenic acid among healthy adults. 1769 63

Low serum adiponectin is a known cardiovascular risk in adult chronic kidney disease (CKD). However, adiponectin concentrations and their relation with other cardiovascular risks have not been studied in children with preterminal CKD. Forty-four children and adolescents who were aged 6 to 21 yr and had stages 2 to 4 CKD had serum adipocytes, lipoproteins, markers of inflammation, homocysteine, and insulin levels determined cross-sectionally. There were 29 lean (body mass index [BMI] <85th percentile) and 15 nonlean (BMI > or =85th percentile) patients. Mean serum adiponectin level was 30.6 +/- 14.1 microg/ml (range 7.1 to 67.8 microg/ml). A total of 83% of patients had elevated adiponectin level. Despite similar kidney function, lean patients had significantly higher adiponectin levels than nonlean patients (34.1 +/- 13.4 microg/ml versus 23.6 +/- 13.3 microg/ml; P = 0.02). In univariate analysis, serum adiponectin negatively correlated with age (r = -0.34, P = 0.02), BMI (r = -0.47, P = 0.001), leptin (r = -0.41, P = 0.006), GFR (r = -0.39, P = 0.02), and insulin (r = -0.36, P = 0.01) and positively correlated with ApoA2 (r = 0.30, P = 0.04); no significant associations were found with markers of inflammation or homocysteine. Multivariate stepwise analysis showed that GFR (beta = -0.008, P = 0.001), BMI (beta = -0.16, P = 0.015), and age (beta = -0.04, P = 0.018) independently predicted serum adiponectin levels. Separate analysis of lean patients showed no significant relations with age or BMI; only GFR independently predicted serum adiponectin level (beta = -0.01, P = 0.0008). It is concluded that serum adiponectin is elevated in children and adolescents with stages 2 to 4 CKD and that decreased kidney function is a major determinant of elevated adiponectin concentrations. Despite overall elevated adiponectin, overweight patients display lower serum adiponectin levels and might be at risk for future cardiovascular complications.
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PMID:Adiponectin in children with chronic kidney disease: role of adiposity and kidney dysfunction. 1769 86


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