Book Section #18403

Abstract

Over the past decade, adipose tissue has received much attention not only for its endocrine properties but equally also for its immunological activity. In consideration of this, it has become increasingly apparent that adipose-secreted factors such as leptin, tumor necrosis factor (TNF)-a, IL- 6, adiponectin and more recently, resistin appears implicated in some inflammatory and metabolic disease. Resistin, in particular, has received meticulous attention as a potential factor in obesity-mediated type 2 diabetes mellitus (T2DM), Metabolic Syndrome, and Cardiovascular. Serum levels of resistin, an adipose tissue-derived adipokine, are increased in human obesity and are positively correlated with atherosclerotic cardiovascular disease. As such, several notable questions remain to be answered within the field of resistin biology. For instance, what conclusion can be drawn with regards the physiological function of resistin? Do the studies over the past year evaluate a role for resistin in the pathogenesis of obesity-associated inflammation and T2DM, Metabolic Syndrome, and Cardiovascular, or merely add to the chaos and confusion in the existing literature? These chapter results reveal that resistin is a highly attractive therapeutic target in factors related to diseases humans. Because current evidence appears to suggest that resistin is a proinflammatory cytokine. Thus, like many other adipocytokines, resistin may possess a dual role in contributing to metabolic disease: first through its direct effects on substrate metabolism and second, through regulating inflammation within its target tissues. The chemistry of resistin has also been the subject of investigation and like adiponectin, the homo-oligomerization of this protein has a bearing on its function. This chapter reviewed to summarize data about structure and function resistin. Also, role and contribution of resistin in the initiation and progression of pathophysiology actions among human and other mammalians reviewed. Summarize data have obtained from clinical researches and animal studies. © 2018 by Nova Science Publishers, Inc.