Visceral fat and metabolic inflammation: the portal theory revisited

Summary 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 re...

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Bibliographic Details
Published in:Obesity reviews 2012-12, Vol.13 (S2), p.30-39
Main Authors: Item, F., Konrad, D.
Format: Article
Language:English
Subjects:
Body Composition - physiology
Body Constitution - physiology
Diabetes Mellitus, Type 2 - epidemiology
Diabetes Mellitus, Type 2 - etiology
Fatty Liver - epidemiology
Fatty Liver - etiology
Free fatty acid
hepatic insulin resistance
Humans
Inflammation - metabolism
Insulin Resistance
Intra-Abdominal Fat - metabolism
Intra-Abdominal Fat - physiopathology
lipid metabolism
obesity
Obesity, Abdominal - metabolism
Obesity, Abdominal - physiopathology
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Summary:Summary 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.
ISSN:1467-7881
1467-789X
DOI:10.1111/j.1467-789X.2012.01035.x