Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Visfatin is highly expressed in adipose tissue (mainly by the stromal cells), but it is also ubiquitously present in most tissues. Visfatin, which plays a role in nicotinamide adenine dinucleotide (NAD) biosynthesis, has been implicated in inflammatory states. Controversial results exist about the expression, circulating levels and the role of visfatin in atherosclerosis-related diseases. Most studies showed increased levels of visfatin in diabetes mellitus, obesity, hypertension, renal and cardiovascular disease. However, other studies reported lower levels of visfatin in these diseases. The discrepancies in clinical studies may be attributed to the multifactorial regulation of visfatin. There is evidence that visfatin expression and circulating levels are influenced by fat area and distribution, inflammatory state, renal function, iron metabolism, hormones as well as several other factors. Furthermore, discrepancies and lack of correlation between commercially available visfatin assays have been reported. More research is needed to better understand the factors that control its synthesis/release and to evaluate the role of visfatin in atherosclerosis-related disease. Large studies with homogeneous populations will probably be needed to answer these questions. Whether visfatin will eventually become a therapeutic target remains to be established.
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PMID:Visfatin/PBEF and atherosclerosis-related diseases. 1948 30

We tested the hypothesis that concentrations of adipocytokines are altered in SLE and associated with coronary atherosclerosis, insulin resistance and inflammation. Concentrations of resistin, leptin, adiponectin and visfatin were measured in 109 patients with SLE and 78 control subjects. Coronary calcification was measured using electron beam-computed tomography, and insulin resistance was defined by the homeostasis model assessment index. Concentrations of adiponectin (28.7 +/- 17.9 vs 22.0 +/- 15.3 microg/mL, P = 0.003), leptin (41.1 +/- 49.9 vs 19.8 +/- 24.6 ng/mL, P < 0.001) and visfatin (7.5 +/- 10.5 vs 4.5 +/- 2.8 ng/mL, P < 0.001) were higher in patients with SLE than in controls. These differences remained significant after adjustment for age, race, sex and body mass index (BMI; all P values < 0.02). Concentrations of resistin (10.7 +/- 7.6 vs 9.1 +/- 5.1 ng/mL, P = 0.41) did not differ in patients and controls. In patients with SLE, leptin was positively associated with BMI (rho = 0.80, P < 0.001), insulin resistance (rho = 0.46, P < 0.001) and C-reactive protein (CRP) (rho = 0.30, P = 0.002), whereas adiponectin was negatively associated with the same factors (rho = -0.40, P < 0.001; rho = -0.38, P < 0.001; rho = -0.22, P = 0.02, respectively). None of the adipocytokines were associated with coronary atherosclerosis in SLE. In conclusion, patients with SLE have increased concentrations of adiponectin, leptin and visfatin. Lower concentrations of adiponectin and higher concentrations of leptin are associated with insulin resistance, BMI and CRP in patients with SLE.
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PMID:Adipocytokines in systemic lupus erythematosus: relationship to inflammation, insulin resistance and coronary atherosclerosis. 1957 4

White adipose tissue is an endocrine organ producing numerous proteins known as adipokines, which include leptin, adiponectin, resistin, visfatin, and other factors, which are involved in most metabolic disorders. In obesity, plasma leptin concentrations are high due to leptin resistance that may result from the attenuation of leptin signaling in the hypothalamus. Leptin acts to inhibit appetite, stimulate thermogenesis, enhance fatty acid oxidation, decrease glucose, and reduce body weight, and fat. A reduced adiponectin level has been associated with insulin resistance, dyslipidemia, and atherosclerosis, and its low level is a predictor of later development of type 2 diabetes. Resistin expression is low in adipose tissue and high in bone marrow and lungs, its role in glucose homeostasis remains controversial, it has been associated with insulin resistance and obesity. Visfatin is a secretory protein highly enriched in visceral adipocytes, liver, muscle, and lymphocytes. An increase of visfatin levels in obesity was related to preservation of insulin sensitivity, it enhances glucose uptake by adipocytes and inhibits hepatocyte glucose release, it induces tyrosine phosphorylation, and interacts with insulin receptors. Many studies are still being conducted to highlight the role of adipokines in metabolic disorders.
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PMID:Adipokines and etiopathology of metabolic disorders. 1975 Feb 55

Cardiovascular diseases are currently the most frequent cause of death in Poland and their incidence continually rises. This is related to the high incidence of obesity associated with insulin resistance, which is present in type 2 diabetes mellitus. Adipose tissue produces multiple cytokines(TNF-alpha, IL-6, PAI-1, CRP, angiotensinogen, leptin, adiponectin, visfatin, apelin, resistin)which decrease insulin sensitivity and induce inflammatory processes, endothelial dysfunction,and atherosclerosis. This article presents the link between obesity, insulin resistance, and type 2 diabetes mellitus according to studies conducted in vitro and in animal models. In human studies, the influence of resistin on the development of insulin resistance is controversial. The article underlines the role of resisitin in the development of inflammatory processes and endothelial dysfunction in humans. In clinical studies, resistin was shown to be a predictive factor of coronary artery disease and mortality connected with cardiovascular diseases.
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PMID:[Resistin: a pathogenic factor or a biomarker of metabolic disorders and inflammation?]. 1994 Mar 27

Visfatin is a proinflammatory and potentially insulin-mimetic adipokine contributing to whole body glucose and lipid metabolism, as well as atherosclerosis. Monocyte chemoattractant protein (MCP)-1 is an adipocyte-secreted protein which might play a crucial role in metabolic and vascular disease. MCP-1 expression and secretion after visfatin treatment were determined by quantitative real-time reverse transcription-PCR and enzyme-linked immunosorbent assay (ELISA) in fully differentiated human mesenchymal stem cell-derived adipocytes (hMSC-Ads) in vitro. In addition, circulating levels of MCP-1 and visfatin were quantified by ELISA in 60 patients (30 nondiabetic, 30 diabetic) and MCP-1 serum levels in mice were determined after visfatin treatment in vivo. Interestingly, protein secretion and mRNA production of MCP-1 were induced significantly in hMSC-Ads after visfatin stimulation. Visfatin-induced MCP-1 secretion 1.9-fold after 8 h and 2.5-fold after 24 h relative to untreated cells (P < 0.05). MCP-1 mRNA synthesis was significantly stimulated by visfatin with maximal upregulation detectable at 250 ng/ml visfatin and after 4 h of treatment. Signaling studies suggested that p44/42 mitogen-activated protein (MAP) kinase is involved in visfatin-induced MCP-1 mRNA expression in hMSC-Ads. Detectability of visfatin in serum predicted circulating MCP-1 independent of age and gender in humans in vivo. MCP-1 serum levels were significantly increased more than twofold after visfatin treatment in mice in vivo. Taken together, our results demonstrate that visfatin upregulates MCP-1 supporting a possible role of MCP-1 in mediating the proinflammatory effects of visfatin.
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PMID:Visfatin is a positive regulator of MCP-1 in human adipocytes in vitro and in mice in vivo. 2003 81

Low-grade inflammation is important in the development of obesity related pathologies such as insulin resistance and type 2 diabetes, and also cardiovascular disease. Visfatin/PBEF/Nampt and resistin are proinflammatory adipokines secreted from adipocytes, monocytes, and macrophages, and have been linked to atherosclerotic plaque formation, recently. The aim of the present study was to investigate if the expression of these molecules in circulating blood monocytes is altered in obese and/or type 2 diabetic human subjects. Monocytes were isolated by CD14-antibody based magnetic cell sorting from blood samples of 17 lean controls, 20 obese nondiabetic subjects, and 19 obese patients with type 2 diabetes. FACS analysis was performed to test purity of the cell preparations. Expression of the different adipokines was measured by multiplex real-time PCR on RNA-level. Visfatin/PBEF/Nampt was found to be very strongly expressed in monocytes, whereas resistin levels were significantly lower. Furthermore, visfatin/PBEF/Nampt expression was significantly upregulated in obese type 2 diabetic patients, whereas obese nondiabetics exhibited similar levels compared to lean controls, indicating that visfatin/PBEF/Nampt levels are related to type 2 diabetes rather than to obesity. In contrast, resistin expression displayed a different pattern being significantly increased in obese subjects compared to controls but not related to type 2 diabetes. These data suggest a differential role for these two proinflammatory adipokines in linking metabolic diseases to atherosclerosis with visfatin/PBEF/Nampt being more important in patients with type 2 diabetes and resistin in obese but nondiabetic human subjects.
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PMID:Visfatin/PBEF/Nampt and resistin expressions in circulating blood monocytes are differentially related to obesity and type 2 diabetes in humans. 2009 60

The adipose tissue is an endocrine organ producing substances called adipocytokines that have different effects on lipid metabolism, metabolic syndrome, and cardiovascular risk. Visfatin was recently described as an adipocytokine with potentially important effects on glucose metabolism and atherosclerosis. Visfatin has been linked to several inflammatory conditions, beta cell function, and cardiovascular disease. The growing number of publications on the subject shall bring further evidence about this adipocytokine. Its findings may contribute in the identification of higher risk individuals for diabetes and cardiovascular disease with a better comprehension about the complex intercorrelation between adiposity, glucose metabolism and vascular disease.
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PMID:Visfatin, glucose metabolism and vascular disease: a review of evidence. 2034 49

Adipose tissue is now considered an important endocrine organ that secretes a large number of physiologically active peptides affecting metabolic homeostasis of human body: they are collectively referred to as adipocytokines. Leptin is a key hormone in the regulation of food intake, energy expenditure, neuroendocrine and immune function. Leptin is related with obesity and its metabolic disorders; starvation-induced depletion of fat stores is accompanied by alterations of circulating adipocytokines that may have potential repercussions in the pathophysiology of anorexia nervosa. Adiponectin enhances insulin sensitivity, controls body weight, prevents atherosclerosis and negatively regulates immune functions. Plasma adiponectin relates inversely to adiposity and reflects the sequelae of accumulation of excess adiposity. Resistin is a protein hormone produced both by adipocytes and immunocompetent cells that affect fuel homeostasis and insulin action. Plasma resistin levels are decreased in anorectic patients, while plasma adiponectin levels are increased. Plasma ghrelin levels present opposite changes in obesity and anorexia nervosa, suggesting that ghrelin is a good marker of nutritional status. Visfatin shows to correlate with visceral fat mass in patients with obesity. Its possible role in patients with anorexia nervosa is unknown. In conclusion, obesity is defined as a state of low-grade inflammation, which is associated with increased leptin, resistin and ghrelin levels and decreased adiponectin levels; anorexia nervosa is characterized by opposite changes. Finally, plasma adipocytokines levels can represent a sensitive parameter of nutritional status that reflects changes in the level of body fat in children and adolescents with obesity and anorexia nervosa.
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PMID:[Adipocytokines: potential biomarkers for childhood obesity and anorexia nervosa]. 2044 Feb 37

Fat accumulation has been shown to play important roles in the development of obesity-related disorders such as atherosclerosis, diabetes mellitus and hypertension. Recent studies have shown that fat tissue is not a simple energy storage organ, but exerts important endocrine functions. These are achieved predominantly through release of adipocytokines, which include several novel molecules released by adipocytes like leptin, resistin, adiponectin or visfatin, as well as some more classical cytokines released possibly by inflammatory cells, like TNF-alpha and IL-6. Adipocytokines may affect cardiovascular, hepatic, muscular and metabolic function. In this review, the recent research work of adipocytokines will be discussed.
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PMID:[Adipocytokines: factors with various suggested functions]. 2048 43

Obesity leads to several chronic morbidities including type 2 diabetes, dyslipidaemia, atherosclerosis and hypertension, which are major components of the metabolic syndrome. White adipose tissue (WAT) metabolism and WAT-derived factors (fatty acids and adipokines) play an important role in the development of these metabolic disturbances. In fact, dysregulated adipokine secretion from the expanded WAT of obese individuals contributes to the development of systemic low-grade inflammation, insulin resistance and metabolic syndrome. The n-3 PUFA EPA and DHA have been widely reported to have protective effects in a range of chronic inflammatory conditions including obesity. In fact, n-3 PUFA have been shown to ameliorate low-grade inflammation in adipose tissue associated with obesity and up-regulate mitochondrial biogenesis and induce beta-oxidation in WAT in mice. Moreover, the ability of n-3 PUFA to regulate adipokine gene expression and secretion has been observed both in vitro and in vivo in rodents and human subjects. The present article reviews: (1) the physiological role of adiponectin, leptin and pre-B cell colony-enhancer factor/visfatin, three adipokines with immune-modulatory properties involved in the regulation of metabolism and insulin sensitivity and (2) the actions of n-3 PUFA on these adipokines focusing on the underlying mechanisms and the potential relationship with the beneficial effects of these fatty acids on obesity-associated metabolic disorders. It can be concluded that the ability of n-3 PUFA to improve obesity and insulin resistance conditions partially results from the modulation of WAT metabolism and the secretion of bioactive adipokines including leptin, adiponectin and visfatin.
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PMID:Regulation of adipokine secretion by n-3 fatty acids. 2054 Aug 25


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