Role of resistin in obesity, insulin resistance and Type II diabetes.
نویسندگان
چکیده
Resistin is a member of a class of cysteine-rich proteins collectively termed resistin-like molecules. Resistin has been implicated in the pathogenesis of obesity-mediated insulin resistance and T2DM (Type II diabetes mellitus), at least in rodent models. In addition, resistin also appears to be a pro-inflammatory cytokine. Taken together, resistin, like many other adipocytokines, may possess a dual role in contributing to disease risk. However, to date there has been considerable controversy surrounding this 12.5 kDa polypeptide in understanding its physiological relevance in both human and rodent systems. Furthermore, this has led some to question whether resistin represents an important pathogenic factor in the aetiology of T2DM and cardiovascular disease. Although researchers still remain divided as to the role of resistin, this review will place available data on resistin in the context of our current knowledge of the pathogenesis of obesity-mediated diabetes, and discuss key controversies and developments.
منابع مشابه
ارتباط سطح سرمی رزیستین با شاخص های مقاومت به انسولین در افراد چاق دیابتی و غیر دیابتی
Background: Resistin, an adipocyte secreted factor, has been suggested to link obesity with type 2 diabetes and insulin resistance in rodent models but its relevance to human diabetes remains uncertain. The aim of this study was to investigate the relationship between serum resistin concentrations with insulin resistance and obesity indices in type 2 diabetes and non-diabetic obese subjects.Met...
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OBJECTIVE Although adipocyte-derived murine resistin links insulin resistance to obesity, the role of human resistin, predominantly expressed in mononuclear cells and induced by inflammatory signals, remains unclear. Given the mounting evidence that obesity and type 2 diabetes are inflammatory diseases, we sought to determine the relationship between inflammatory increases in human resistin and...
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عنوان ژورنال:
- Clinical science
دوره 109 3 شماره
صفحات -
تاریخ انتشار 2005