Adipose Tissue: A Regulator for Obesity and Its Complications
Journal Title: International Journal of Biochemistry Research & Review - Year 2016, Vol 9, Issue 1
Abstract
Adipose tissue is a key player in whole body metabolism and excess adipose tissue poses a major risk factor for the development of metabolic disorders such as type 2 diabetes. In response to nutritional overload, de novo adipocyte differentiation can serve as an adaptive mechanism by increasing the storage capacity of adipose tissue and maintaining normal adipocyte function. This in turn prevents systemic lipid overload, which is a major cause for insulin resistance. Adipose tissue is of two types; the fat storing white adipose tissue and the thermogenic brown adipose tissue. While the former is implicated in obesity, insulin resistance and diabetes, the latter is a physiological anti-obesogenic and antidiabetic through adaptive thermogenesis by uncouplers proteins. Obesity results from the imbalanced energy intake for expenditure with excessive fat accumulation in adipose tissue. Obesity is associated with numerous metabolic disorders, including hyperlipidemia, diabetes mellitus, hypertension, stroke, osteoarthritis, infertility and certain types of cancer. Obesity is associated with chronic subclinical inflammation in which the metabolism of adipose tissue plays an important role. The adipose tissue is an endocrine organ which has a fundamental role in metabolic, inflammatory, cardiovascular homeostatic regulation through lipogenesis, lipolysis, steroidogeneis, and secretion of several biologically active adipokines and pro-inflammatory cytokines with diverse protein structures and functions. This review article will mainly focus on the pathophysiological changes of adipose tissue fat during obesity in relation to energy expenditure towards prevention or development of obesity and its complications.
Authors and Affiliations
Shaik Rahiman, Tarek H El-Metwally, Divya Shrivastava
Keywords
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- EP ID EP351118
- DOI 10.9734/IJBCRR/2016/18221
- Views 120
- Downloads 0
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