Visceral fat and metabolic inflammation: the portal theory revisited

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.