Recent studies have revealed that inflammatory responses contribute to the development of a variety of common diseases, including atherosclerosis and metabolic diseases, including diabetes mellitus. On the other hand, adipose tissue has been recognized to secrete bioactive substances that relate to inflammation. TNF-a is a typical cytokine that plays a major role in inflammatory cellular phenomena. Since Uysal et al. first reported that adipose tissue secretes this cytokine and proposed it as one of the candidates for molecules inducing insulin resistance (25), TNF-a has come to be recognized as an important adipocytokine. It has been shown that adipose TNF-a mRNA and plasma TNF-a protein are increased in most animal models and in humans with obesity and insulin resistance (25,26). Neutralizing TNF-a in obese rats with a soluble TNF-a receptor-immunoglobulin G fusion protein markedly improves insulin resistance (27).
These results indicate that higher production of TNF-a in accumulated adipose tissue may be causative for obesity-associated insulin resistance. In addition to TNF-a, inter-leukin (IL)-1P, IL-6, macrophage migration factor, nerve growth factor, and haptoglobin have been shown to be secreted from adipose tissue and linked to inflammation and the inflammatory response. More recently one typical marker of inflammation, C-reactive protein (CRP), was found to be produced in adipose tissue and CRP mRNA expression was found to be enhanced in adipose tissue in adiponectin KO mice (28).
The elevated production of these inflammation-related adipocytokines is increasingly considered to be important in the development of diseases linked to obesity, particularly type 2 diabetes and cardiovascular disease. Namely, adipose tissue is involved in extensive crosstalk with other organs and multiple metabolic systems through the various adipocytokines.
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