VITAMIN D AND TISSULAR EXPRESSION OF VITAMIN D RECEPTOR IN OBESITY
Abstract
Vitamin D (VitD), a lipid-soluble hormone, is able to regulate the transcription of many genes through vitamin D receptor (vitD receptor - VDR). It has been shown that VitD deficiency is associated with obesity, characterized by a low degree inflammatory state, which contribute to the pathogeny of metabolic syndrome and type 2 diabetes mellitus. VitD deficiency is a public health problem, at the same time the global prevalence of obesity and cardiovascular diseases is continuously growing. Evidence from recent studies on animal models suggest that VitD or VDR deficiency promotes cardiomyocyte hypertrophy, which can be one of the mechanisms for increasing cardiovascular risk. The heart is one of the target organs of action for VitD, because VDR is expressed in cardiomyocytes. Also, previous in vitro studies have shown that VitD is able to inhibit the production of monocyte chemotactic factors (MCP-1) and other pro-inflammatory mediators in human preadipocytes and mature adipocytes. Inflammation is an important factor in the pathogenesis of atherosclerosis. In obesity there are not known data about correlations between plasma levels of VitD and VDR expression in the subcutaneous fat tissue, epicardial visceral adipose tissue, and in particular in myocardium. Also, there are still no studies to test VDR expression in myocardial cells and to investigate the results of dietary VitD supplementation on the expression of VDR in the epicardial adipose tissue and myocardium.
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