1. Introduction

Adipose tissue inflammation has been suggested to be crucially involved in the pathological mechanisms of obesity-associated cardiometabolic complications, including insulin resistance, type 2 diabetes, atherosclerosis, and non-alcoholic fatty liver disease (NAFLD). However, the underlying mechanisms of this process are still under investigation.

Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, © 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

© The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons

distribution, and eproduction in any medium, provided the original work is properly cited.

Adipocytes in an obesity setting, especially in morbid obesity, are characterized by hypertrophy and hypoxia, and they are the important sources to initialize adipose tissue inflammation. This inflammation is mediated by producing a large number of cytokines and chemokines, including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), monocyte chemotactic protein-1 (MCP-1), and regulated upon activation, normal T-cell expressed and secreted (RANTES). These cytokines and chemokines produced by adipocytes during hypertrophy and hypoxia significantly contribute to the development of obesity-associated adipose tissue inflammation. The capacity of constitutive and regulated release of immune mediators from adipocytes demonstrates a causal link between the biology of adipocytes and immune cells, such as macrophages and T cells. Moreover, the interplay of hypertrophic, hypoxia adipocytes and adipose tissue immune cells has been speculated to play the key regulatory role in the development of obesity-induced insulin resistance.

This review provides update evidence to emphasize the important role of adipocyte hypertrophy and hypoxia in the development of obesity-associated adipose tissue (AT) inflammation and insulin resistance and also discusses possible underlying mechanism.
