Visceral fat and metabolic inflammation: the portal theory revisited

Obes Rev. 2012 Dec;13 Suppl 2:30-9. doi: 10.1111/j.1467-789X.2012.01035.x.

Abstract

Abdominal (central) obesity strongly correlates with (hepatic) insulin resistance and type 2 diabetes. Among several hypotheses that have been formulated, the 'portal theory' proposes that the liver is directly exposed to increasing amounts of free fatty acids and pro-inflammatory factors released from visceral fat into the portal vein of obese patients, promoting the development of hepatic insulin resistance and liver steatosis. Thus, visceral obesity may be particularly hazardous in the pathogenesis of insulin resistance and type 2 diabetes. Herein, we will critically review existing evidence for a potential contribution of portally drained free fatty acids and/or cytokines to the development of hepatic insulin resistance.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Body Composition / physiology
  • Body Constitution / physiology
  • Diabetes Mellitus, Type 2 / epidemiology*
  • Diabetes Mellitus, Type 2 / etiology
  • Fatty Liver / epidemiology
  • Fatty Liver / etiology
  • Humans
  • Inflammation / metabolism*
  • Insulin Resistance*
  • Intra-Abdominal Fat / metabolism
  • Intra-Abdominal Fat / physiopathology*
  • Obesity, Abdominal / metabolism
  • Obesity, Abdominal / physiopathology*