Obesity induces an inflammatory state driven by adipose tissue and mononuclear phagocytes, contributing to complications such as insulin resistance, diabetes, and atherosclerosis.
Obesity 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.
Anthony W. Ferrante (Fri,) conducted a review in Obesity-induced inflammation. Obesity was evaluated. Obesity induces an inflammatory state driven by adipose tissue and mononuclear phagocytes, contributing to complications such as insulin resistance, diabetes, and atherosclerosis.