کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2196152 | 1550899 | 2013 | 6 صفحه PDF | دانلود رایگان |
ABSTRACTThe renin–angiotensin–aldosterone system (RAAS) is known to be closely linked to the pathogenesis of insulin resistance. The angiotensin (Ang) II type 1 (AT1) receptor mediates the major effects of Ang II in adipose tissue, and blockade of the AT1 receptor improves insulin sensitivity, with enhanced adipocyte differentiation. In contrast, the role of angiotensin type 2 (AT2) receptor activation in insulin sensitivity is still controversial, although AT2 receptor functions are thought to be mutually antagonistic against those of the AT1 receptor in the cardiovascular system. Aldosterone exerts its biological roles via the mineralocorticoid receptor (MR), and inhibition of MR signaling in adipose tissue ameliorates inflammation, with upregulation of insulin-mediated glucose transport and adipocyte differentiation. Clinical studies indicate that blockade of RAAS prevents the new onset of type 2 diabetes and improves the metabolic syndrome in diabetic patients. We here review the recent concepts of the roles of RAAS in adipose tissue.
► Role of renin–angiotensin aldosterone system (RAAS) in adipocyte tissue.
► Variation of angiotensin II receptors in adipocyte differentiation.
► Regulation of RAAS provides a new therapeutic approach to the metabolic syndrome.
Journal: Molecular and Cellular Endocrinology - Volume 378, Issues 1–2, 25 September 2013, Pages 23–28