Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adipokines are peptides secreted by adipose tissue that affect whole-body energy metabolism. Their dysregulated production in obesity has implicated them as important mediators in the pathogenesis of obesity-related risk factors for diabetes and cardiovascular disease. PBEF/visfatin/Nampt has recently been described as a novel adipokine with insulin mimetic properties. However, whether it is an authentic adipokine relevant to the metabolic syndrome remains a matter of some debate.
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PMID:Is PBEF/visfatin/Nampt an authentic adipokine relevant to the metabolic syndrome? 1736 69

Statins exert anti-inflammatory, anti-atherogenic actions. The mechanisms responsible for these effects remain only partially elucidated. Diabetes and obesity are characterized by low-grade inflammation. Metabolic and endocrine adipocyte dysfunction is known to play a crucial role in the development of these disorders and the related cardiovascular complications. Thus, direct modulation of adipocyte function may represent a mechanism of pleiotropic statin actions. We investigated effects of atorvastatin on apoptosis, differentiation, endocrine, and metabolic functions in murine white and brown adipocyte lines. Direct exposure of differentiating preadipocytes to atorvastatin strongly reduced lipid accumulation and diminished protein expression of the differentiation marker CCAAT/enhancer binding protein-beta (CEBP-beta). In fully differentiated adipocytes, however, lipid accumulation remained unchanged after chronic atorvastatin treatment. Furthermore, cell viability was reduced in response to atorvastatin treatment in proliferating and differentiating preadipocytes, but not in differentiated cells. Moreover, atorvastatin induced apoptosis and inhibited protein kinase B (AKT) phosphorylation in proliferating and differentiating preadipocytes, but not in differentiated adipocytes. On the endocrine level, direct atorvastatin treatment of differentiated white adipocytes enhanced expression of the pro-inflammatory adipokine interleukin-6 (IL-6), and downregulated expression of the insulin-mimetic and anti-inflammatory adipokines visfatin and adiponectin. Finally, these direct adipotropic endocrine effects of atorvastatin were paralleled by the acute inhibition of insulin-induced glucose uptake in differentiated white adipocytes, while protein expression of the thermogenic uncoupling protein-1 (UCP-1) in brown adipocytes remained unchanged. Taken together, our data for the first time demonstrate direct differentiation state-dependent effects of atorvastatin including apoptosis, modulation of pro-inflammatory and glucostatic adipokine expression, and insulin resistance in adipose cells. These differential interactions may explain variable clinical observations.
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PMID:Direct adipotropic actions of atorvastatin: differentiation state-dependent induction of apoptosis, modulation of endocrine function, and inhibition of glucose uptake. 1737 28

To investigate the role of the novel adipokine visfatin in type 2 diabetes mellitus and obesity and to examine its association with visceral and subcutaneous fat in Asian Indians, who have increased susceptibility to type 2 diabetes mellitus and coronary artery disease, 150 subjects with type 2 diabetes mellitus (75 men, 75 women) and 150 age- and sex-matched subjects with normal glucose tolerance were recruited from the Chennai Urban Rural Epidemiology Study, a population-based study done in Chennai, southern India. Anthropometric and biochemical measurements were done by using standardized techniques. Fasting serum visfatin levels were measured by enzyme-linked immunosorbent assay. Visceral and subcutaneous fat were measured by computerized tomography in a subset of 130 individuals. Serum visfatin levels were significantly higher in diabetic subjects compared with nondiabetic subjects (11.4+/-5.9 vs 9.8+/-4.3 ng/mL, P=.008). However, this association was lost when adjusted for body mass index (odds ratio [OR], 1.048; 95% confidence interval [CI], 0.997-1.101; P=.067) or waist circumference (OR, 1.050; 95% CI, 0.999-1.104; P=.057). Serum visfatin showed a significant association with obesity even after adjusting for age, sex, and type 2 diabetes mellitus (OR, 1.060; 95% CI, 1.005-1.119; P=.033). Visceral fat, but not subcutaneous fat, was significantly associated with serum visfatin levels even after adjusting for age, sex, type 2 diabetes mellitus, and body mass index (P=.002). In Asian Indians, serum visfatin levels are associated with obesity and visceral fat but not with subcutaneous fat. Although visfatin levels are increased in type 2 diabetes mellitus, the association seems to be primarily through obesity.
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PMID:Serum visfatin in relation to visceral fat, obesity, and type 2 diabetes mellitus in Asian Indians. 1737 18

It has been recently reported that activation of PPAR-delta, by specific agonists or genetic manipulation, alleviates dyslipidemia, hyperglycemia, and insulin resistance in animal models of obesity and type 2 diabetes. The purpose of the present study was to determine whether the PPAR-delta agonist has a direct effect on adipokines in visceral adipose tissue of rats and in cultured adipocytes. We examined the expression of visfatin, adiponectin, and resistin mRNA in visceral adipose tissue of Wistar rats fed a high-fat diet and 3T3-L1 adipocytes treated with PPAR-delta agonist (L-165041). Body weight and biochemical measurements were performed. Rats fed a high-fat diet showed a greater increase in body weight than those fed a standard diet (P<0.05), and treatment with L-165041 (10 mg/kg/day) significantly decreased weight gain (P<0.05). The concentration of total cholesterol was lower, and HDL cholesterol was higher in L-165041-treated rats (P<0.05). In the visceral adipose tissue of L-165041-treated rats, visfatin and adiponectin mRNA levels significantly increased compared to those of the untreated rats (P<0.05). However, the expression of resistin decreased in the L-165041-treated rats. Furthermore, in cultured 3T3-L1 adipocytes, the level of visfatin and adiponectin mRNA was up-regulated in response to L-165041 treatment for nine days. By contrast, resistin mRNA levels were down-regulated by L-165041 treatment. The present study provides a novel evidence to suggest that the PPAR-delta agonist has regulatory effects on a variety of adipokines, and these effects might explain some of their metabolic function.
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PMID:Effect of PPAR-delta agonist on the expression of visfatin, adiponectin, and resistin in rat adipose tissue and 3T3-L1 adipocytes. 1741 7

Visfatin with the official gene name pre-B cell colony-enhancing factor 1 (PBEF) and the protein name nicotinamide phosphoribosyltransferase (NAMPT) is a recently discovered adipocyte-secreted protein that was shown by some to be associated with visceral fat and insulin resistance. To explore the link between PBEF/NAMPT/visfatin and lipid metabolism, we analyzed the relation of its plasma level with several parameters of adiposity, insulin resistance and the circulating blood lipid profile in a group of general population (n = 40) and a group of subjects who are genetically predisposed to insulin resistance and hyperlipidemia (n = 35). In both groups and pooled cohort, PBEF/NAMPT/visfatin lacked association with whole body adiposity, but correlated positively with HDL-cholesterol and negatively with triglycerides. The data suggested a negative correlation of the PBEF level with visceral fat and insulin resistance. But this negative correlation completely disappeared after adjustment for lipid profile. We concluded that circulating PBEF/NAMPT/visfatin level is an indicator of beneficial lipid profile in non-diabetic Caucasian subjects. The relation to lipid metabolism does not depend on visceral obesity and insulin resistance, but may be linked to its enzymatic function in NAD metabolism.
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PMID:The circulating PBEF/NAMPT/visfatin level is associated with a beneficial blood lipid profile. 1742 83

Adiponectin and visfatin are newly discovered adipokines that are strongly expressed in human visceral adipose tissue. To identify new regulatory mechanisms in fat, the effect of TNF-alpha (TNF) on adiponectin, on its two receptors, and on visfatin was investigated by incubating human visceral adipose tissue from patients without diabetes mellitus with TNF for 24, 48 and 72 hours. The mRNA expression of visfatin, adiponectin, and its two receptors, as well as the protein expression of adiponectin were determined. A decrease of adiponectin mRNA expression of 97% after incubation with TNF (5.75 nmol/l) for 24 hours, a decrease of 91% after 48 hours, and a decrease of 96% after 72 hours were measured. The reduction of protein expression was measured to be 42% after 24 hours, 28% after 48 hours, and 39% after 72 hours of incubation with TNF (5.75 nmol/l). The mRNA level of adiponectin receptor 1 (AdipoR1) was elevated about 72% after 48 hours of incubation and 67% after 72 hours of incubation, whereas the mRNA expression of adiponectin receptor 2 (AdipoR2) was not altered significantly. The visfatin mRNA level was found to be highly increased by 255% after 24 hours and 335% after 48 hours and 341% after 72 hours of incubation with TNF (5.75 nmol/l). Our results support the concept of visceral adipose tissue as an endocrine organ. We demonstrate that TNF has regulatory functions on adiponectin, AdipoR1 and on visfatin in human visceral adipose tissue. TNF levels are elevated in states of obesity and insulin resistance. Due to this fact TNF could be the reason that there is a decrease in the level of adiponectin, whereas there is an increase in the level of visfatin in states of obesity and insulin resistance.
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PMID:TNF-alpha alters visfatin and adiponectin levels in human fat. 1744 61

Interest in the biology of white adipose tissue (WAT) has increased dramatically since the discovery of leptin in 1994. The identification of the product of the gene obese (ob) threw light on the role of adipose tissue in the physiopathology of obesity-related diseases, and spurred the identification of numerous other adipokines, many of a pro-inflammatory nature. It has become increasingly evident that WAT-derived cytokines mediate between obesity-related exogenous factors (nutrition and lifestyle) and the molecular events that lead to metabolic syndrome and inflammatory and/or autoimmune conditions. Here, we review recent adipokine research, with particular attention to the roles of leptin, adiponectin, resistin, visfatin, apelin, vaspin and hepcidin in such conditions.
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PMID:The emerging role of adipokines as mediators of inflammation and immune responses. 1750 80

Visfatin is a peptide predominantly expressed in visceral adipose tissue and was hypothesized to be related to obesity and insulin resistance. In the present study, we investigated the effects of genetic variations in the visfatin gene (pre-B-cell colony-enhancing factor 1 [PBEF1]) on obesity, metabolic parameters, and blood pressure (BP) in 2 children cohorts. We genotyped 3 representative single nucleotide polymorphisms (rs9770242, -948G>T, rs4730153) in 731 schoolchildren and in an independent cohort of 167 obese children. There was no association of any of the 3 polymorphisms or their haplotypes with body mass index (BMI), waist-to-hip ratio, or parameters of glucose, insulin, or lipid metabolism in either cohort. However, the -948G variant was associated with significantly higher diastolic BP in obese children (P < .05 after adjusting for age, sex, pubertal stage, and height). Haplotype analyses confirmed the [T-G-A] haplotype to be significantly related to increased diastolic BP in both schoolchildren and obese children. In conclusion, genetic variants in PBEF1 may be associated with increased BP in children but are not likely to contribute significantly to the variation in body mass index and glucose, insulin, or lipid metabolism.
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PMID:Effects of genetic variation in the visfatin gene (PBEF1) on obesity, glucose metabolism, and blood pressure in children. 1751 9

The aim of the present study was to determine serum concentrations of visfatin in obese women in comparison to normal-weight controls. Study subjects were 21 obese women without additional disease (age, 29.0+/-4.9 years; body mass index, 37.1+/-6.1 kg/m2) and 16 healthy, normal-weight women (age, 29.9+/-5.4 years; body mass index, 22.5+/-1.7 kg/m2). Body composition was measured by bioimpedance. Serum concentrations of visfatin were assayed with an enzyme-linked immunosorbent assay kit (Phoenix Pharmaceuticals, Burlingame, CA). Insulin was determined by radioimmunoassay and glucose by colorimetric method. Serum concentration of visfatin was significantly higher in obese women when compared to controls. Positive correlations between serum concentrations of visfatin and insulin in the obese group were found. In the control group, we observed positive correlations between serum concentrations of visfatin and glucose. In conclusion, the observed increase of visfatin in obesity may be a counterregulation preventing further glucose increase.
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PMID:Serum concentration of visfatin in obese women. 1761 61

Adipose tissue has recently been identified as an endocrine organ. Visfatin is a novel adipocytokine predominantly secreted from visceral adipocytes. Visceral obesity is an important component of metabolic syndrome; however, the relationship between visfatin levels and metabolic syndrome is not clear. The purpose of this study was to explore the association between visfatin levels and anthropometry and parameters of metabolic syndrome. Anthropometric measurements included height, weight, body mass index, waist and hip circumferences, waist-to-hip ratio, and blood pressure. Metabolic parameters including fasting serum visfatin, fasting serum insulin and fasting plasma glucose, lipid profiles, and uric acid levels were measured. Data of 500 subjects (244 men and 256 women) were used for the analysis. There was no significant difference in serum visfatin levels between male and female subjects. Visfatin correlated negatively with body mass index (beta = -.011, P = .025) in male subjects; however, visfatin did not correlate with any other anthropometric or any metabolic parameters in male subjects. There was no correlation between visfatin levels and any anthropometric parameters in female subjects; however, it did correlate positively with high-density lipoprotein cholesterol levels (beta = .126, P = .006) and correlate negatively with low-density lipoprotein cholesterol levels (beta = -.039, P = .010) in female subjects. In conclusion, visfatin is not related to most anthropometric parameters and most parameters of metabolic syndrome. It may play a role in cholesterol homeostasis in women.
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PMID:The relationship between visfatin levels and anthropometric and metabolic parameters: association with cholesterol levels in women. 1769 64


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