Obesity-induced inflammation: a metabolic dialogue in the language of inflammation.
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.
Ferrante
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AW
Naomi Berrie Diabetes Center, Columbia University, New York, NY 10032, USA. awf7@columbia.edu
D000273:Adipose Tissue / Q000276:immunology*; D000818:Animals; D002450:Cell Communication / Q000502:physiology; D003924:Diabetes Mellitus, Type 2 / Q000150:complications* / Q000276:immunology; D006801:Humans; D007249:Inflammation / Q000150:complications / Q000276:immunology / Q000378:metabolism; D007333:Insulin Resistance / Q000502:physiology*; D008264:Macrophages / Q000276:immunology; D009765:Obesity / Q000150:complications* / Q000276:immunology / Q000378:metabolism; D054390:Receptors, CCR2; D019707:Receptors, Chemokine / Q000378:metabolism
C515334:CCR2 protein, human; D054390:Receptors, CCR2; D019707:Receptors, Chemokine