Serum chemerin levels are associated with the presence and extent of coronary artery disease.
ABSTRACT The aim of the study was to examine whether serum chemerin levels are associated with the presence and the extent of coronary artery disease (CAD).
A total of 132 patients with CAD and 56 patients without CAD who underwent coronary angiography for the evaluation of CAD were enrolled in this study. Serum levels of chemerin were measured using an enzyme-linked immunosorbent assay.
Serum chemerin levels were significantly elevated in CAD patients compared with those without CAD. Multivariate logistic regression analysis showed that serum chemerin levels were significantly associated with the presence of CAD. In CAD patients, chemerin was positively correlated with BMI (r=0.274, P=0.001) and triglycerides (r=0.190, P=0.029), and yet correlated with low-density lipoprotein-cholesterol (r=0.228, P=0.008); the association of chemerin with triglycerides and low-density lipoprotein-cholesterol remained significant after adjusting for BMI (P<0.05 and P<0.01). At multiple stepwise regression analysis, serum chemerin levels were an independent predictor of the stenosis score (β=0.193, P=0.034).
Our data suggest that increased chemerin levels are associated with the presence of CAD and that serum chemerin levels may reflect the extent of coronary atherosclerosis.
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ABSTRACT: Cytokines appear to be major regulators of adipose tissue metabolism. Therapeutic modulation of cytokine systems offers the possibility of major changes in adipose tissue behaviour. Cytokines within adipose tissue originate from adipocyte, preadipocyte and other cell types. mRNA expression studies show that adipocytes can synthesise both tumour necrosis factor alpha (TNF-alpha) and several interleukins (IL), notably IL-1beta and IL-6. Other adipocyte products with 'immunological' actions include complement system products and macrophage colony-stimulating factor. Cytokine secretion within adipocytes appears similar to that of other cells. There is general agreement that circulating TNF-alpha and IL-6 concentrations are mildly elevated in obesity. Most studies suggest increased TNF-alpha mRNA expression or secretion in vitro in adipose tissue from obese subjects. The factors regulating cytokine release within adipose tissue appear to include usual 'inflammatory' stimuli such as lipopolysaccaride, but also the size of the fat cells per se and catecholamines. There is conflicting data about whether insulin and cortisol regulate TNF-alpha. The effects of cytokines within adipose tissue include some actions that might be characterised as metabolic. TNF-alpha and IL-6 inhibit lipoprotein lipase, and TNF-alpha additionally stimulates hormone-sensitive lipase and induces uncoupling protein expression. TNF-alpha also down regulates insulin-stimulated glucose uptake via effects on glucose transporter 4, insulin receptor autophosphorylation and insulin receptor substrate-1. All these effects will tend to reduce lipid accumulation within adipose tissue. Other effects appear more 'trophic', and include the induction of apoptosis, regulation of cell size and induction of de-differentiation (the latter involving reduced peroxisome proliferator-activated receptor gamma). Cytokines are important stimulators and repressors of other cytokines. In addition, cytokines appear to modulate other regulatory systems. Examples of the latter include effects on leptin secretion (probably stimulation followed by inhibition) and reduction of beta3-adrenoceptor expression. There seems to be no clear agreement as to which cytokines derived from adipose tissue act as remote regulators, i.e. hormones. Leptin, which is structurally a cytokine, is also a hormone. IL-6 appears to be released systemically by adipose tissue, but TNF-alpha is probably not. Both leptin and IL-6 appear to act on the hypothalamus, IL-6 acts on the liver, while leptin may have actions on the pancreas. The importance of the immune system in whole-body energy balance provides a rationale for the links between cytokines and adipose tissue. It seems clear that TNF-alpha is a powerful autocrine and paracrine regulator of adipose tissue. Other cytokines, notably leptin, and possibly IL-6, have lesser actions on adipose tissue. These cytokines act as hormones, reporting the state of adipose tissue stores throughout the body.Proceedings of The Nutrition Society 09/2001; 60(3):349-56. · 3.67 Impact Factor
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ABSTRACT: The metabolic effects of obesity have made this highly prevalent disease one of the most common risk factors for diabetes, hypertension, and atherosclerosis, the leading causes of end-stage renal failure. However, obesity per se, as defined by body mass index, is less predictive of the development of these diseases than is the presence of a constellation of obesity-related abnormalities now known as the metabolic syndrome. Recognition of this syndrome, which can readily be identified in clinical settings using defined threshold values for waist circumference, BP, fasting glucose, and dyslipidemia, allows for earlier intervention in these high-risk patients. Systemic insulin resistance has been implicated as one possible factor that links visceral obesity to adverse metabolic consequences; however, the mechanism whereby adipose tissue causes alterations in insulin sensitivity remains unclear. Infection and inflammation are commonly associated with insulin resistance, and visceral obesity is associated with a chronic, low-grade inflammatory state, suggesting that inflammation may be a potential mechanism whereby obesity leads to insulin resistance. Moreover, adipose tissue is now recognized as an immune organ that secretes numerous immunomodulatory factors and seems to be a significant source of inflammatory signals known to cause insulin resistance. Therefore, inflammation within white adipose tissue may be a crucial step contributing to the emergence of many of the pathologic features that characterize the metabolic syndrome and result in diabetes and atherosclerosis. This review describes the role of proinflammatory cytokines and hormones released by adipose tissue in generating the chronic inflammatory profile associated with visceral obesity.Journal of the American Society of Nephrology 12/2004; 15(11):2792-800. · 8.99 Impact Factor
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ABSTRACT: Although assessment of traditional coronary heart disease risk factors can often stratify individuals into low- or high-risk categories, additional means are needed to more precisely classify people clinically defined as intermediate-risk, to guide the intensity of risk-reducing therapies. The recognition that inflammatory pathways are important in the progression of atherosclerosis and its complications has prompted investigation to identify circulating risk markers that may be useful in risk stratification. This article summarizes recent studies on the current use of an emerging group of inflammatory markers: soluble CD-40 ligand, interleukin-18, myeloperoxidase, B-type natriuretic peptides, secretory phospholipase A(2), lipoprotein-associated phospholipase A(2), and C-reactive protein. The demonstration that lowering C-reactive protein along with low-density lipoprotein cholesterol with statins reduces events beyond cholesterol lowering alone suggests that titration of therapies using other emerging inflammatory markers may further reduce the toll of atherosclerosis in adult populations.Current Cardiology Reports 11/2009; 11(6):452-9.