Pei-Chi Chan

By Pei-Chi Chan and Po-Shiuan Hsieh

Adipose tissue inflammation has been suggested to play a central role in the pathogenesis of many obesity-associated complications including insulin resistance and type 2 diabetes. Adipocyte hypertrophy and hypoxia especially in morbid obesity are the important sources for the development of 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). Of note, these cytokines and chemokines produced by adipocytes during hypertrophy and hypoxia are crucially involved in the initiation and development of obesity-associated inflammatory response in adipose tissue. 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 synergistic effect of hypertrophic, hypoxia adipocytes, and adipose tissue immune cells has also been implicated in the development of obesity-induced insulin resistance. This chapter provides the overall review and update evidence to highlight the important role and possible underlying mechanism of adipocyte hypertrophy and hypoxia in the development of obesity-associated adipose tissue (AT) inflammation and insulin resistance.

Part of the book: Adiposity