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

J Intern Med. 2007 Oct;262(4):408-14. doi: 10.1111/j.1365-2796.2007.01852.x.

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adipose Tissue / immunology*
  • Animals
  • Cell Communication / physiology
  • Diabetes Mellitus, Type 2 / complications*
  • Diabetes Mellitus, Type 2 / immunology
  • Humans
  • Inflammation / complications
  • Inflammation / immunology
  • Inflammation / metabolism
  • Insulin Resistance / physiology*
  • Macrophages / immunology
  • Obesity / complications*
  • Obesity / immunology
  • Obesity / metabolism
  • Receptors, CCR2
  • Receptors, Chemokine / metabolism

Substances

  • CCR2 protein, human
  • Receptors, CCR2
  • Receptors, Chemokine