ER stress in adipocytes and insulin resistance: Mechanisms and significance (Review)

Abstract

Adipose tissue (AT) has numerous important functions within the body. Of particular importance is its role as an endocrine organ in the control of whole body glucose and lipid metabolism, which is achieved by the secretion of various proteins. Among these proteins are adipokines, such as adiponectin, leptin, resistin, interleukin 6 and tumor necrosis factor a. An imbalance in the expression of these adipokines occurs in a variety of conditions, such as obesity, and can lead to various metabolic abnormalities, including hyperglycemia and hyperlipidemia. In turn, this can contribute to insulin resistance (IR) and heart diseases. Adipose endoplasmic reticulum (ER) stress is increasingly recognized as the primary factor governing these conditions, which ultimately result in the initiation of IR or the aggravation of pre existing IR. Studies have suggested that a number of conditions, including obesity, nutrient overload and metabolic syndromes, can initiate or enhance this process in a multi dimensional manner. This review focuses on the mechanism by which ER stress in AT can contribute to IR.