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Visceral fat and metabolic inflammation: the portal theory revisited


Item, F; Konrad, D (2012). Visceral fat and metabolic inflammation: the portal theory revisited. Obesity Reviews, 13(2 Suppl):30-39.

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.

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.

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Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > University Children's Hospital Zurich > Medical Clinic
04 Faculty of Medicine > Center for Integrative Human Physiology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:2012
Deposited On:01 Nov 2012 14:31
Last Modified:05 Apr 2016 16:03
Publisher:Wiley-Blackwell
ISSN:1467-7881
Publisher DOI:https://doi.org/10.1111/j.1467-789X.2012.01035.x
PubMed ID:23107257

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