• A W Ferrante.
• Naomi Berrie Diabetes Center, Columbia University, New York, NY 10032, USA. awf7@columbia.edu
• J. Intern. Med. 2007 Oct 1; 262 (4): 408414408-14.

AbstractObesity induces an inflammation state that is implicated in many clinically important complications, including insulin resistance, diabetes, atherosclerosis and non-alcoholic fatty liver disease. Although the cause and the molecular participants in this process remain incompletely defined, adipose tissue has a central role. Obesity-induced production of pro-inflammatory molecules, typified by TNF-alpha was recognized more than a dozen years ago, and since then more than two dozen other pro-inflammatory molecules induced by obesity have been identified. More recently a critical role for immune cells, specifically mononuclear phagocytes, in generating the obesity-induced inflammation has been identified. Defining the molecular and cellular components of obesity-induced inflammation offers the potential of identifying therapeutic targets that can ameliorate the complications associated with obesity.

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