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      Obesity-induced inflammation: a metabolic dialogue in the language of inflammation.

      Journal of Internal Medicine
      Adipose Tissue, immunology, Animals, Cell Communication, physiology, Diabetes Mellitus, Type 2, complications, Humans, Inflammation, metabolism, Insulin Resistance, Macrophages, Obesity, Receptors, CCR2, Receptors, Chemokine

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          Abstract

          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.

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