The evolving role of inflammation in obesity and the metabolic syndrome

Curr Diab Rep. 2005 Feb;5(1):70-5. doi: 10.1007/s11892-005-0071-7.


Advances in adipose tissue biology over the past 10 years have led to an improved understanding of the mechanisms linking obesity with the metabolic syndrome and other complications. Obesity is characterized by a chronic, systemic low-grade state of inflammation. Biomarkers of inflammation, such as the leukocyte count, tumor necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6), and C-reactive protein, are increased in obesity, associated with insulin resistance, and predict the development of type 2 diabetes and cardiovascular disease. It is now clear that the adipocyte is an active participant in the generation of the inflammatory state in obesity. Adipocytes secrete a variety of cytokines, including IL-6 and TNF-alpha, that promote inflammation. Moreover, recent studies suggest that obesity is associated with an increase in adipose tissue macrophages, which also participate in the inflammatory process through the elaboration of cytokines. An improved understanding of the role of adipose tissue in the activation of inflammatory pathways may suggest novel treatment and prevention strategies aimed at reducing obesity-associated morbidities and mortality.

Publication types

  • Review

MeSH terms

  • Arteriosclerosis / physiopathology
  • Diabetes Mellitus, Type 2 / physiopathology
  • Diabetic Angiopathies / physiopathology
  • Humans
  • Inflammation / physiopathology*
  • Insulin Resistance / physiology
  • Metabolic Syndrome / physiopathology*
  • Obesity / physiopathology*