Visceral fat and metabolic inflammation: the portal theory revisited

Authors

  • F. Item,

    1. Division of Pediatric Endocrinology and Diabetology, University Children's Hospital, Zurich, Switzerland
    2. Children Research's Centre, University Children's Hospital, Zurich, Switzerland
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  • D. Konrad

    Corresponding author
    1. Children Research's Centre, University Children's Hospital, Zurich, Switzerland
    2. Zurich Center for Integrative Human Physiology, University of Zurich, Zurich, Switzerland
    • Division of Pediatric Endocrinology and Diabetology, University Children's Hospital, Zurich, Switzerland
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Address for correspondence: Professor D Konrad, Department of Endocrinology and Diabetology, University Children's Hospital, Steinwiesstrasse 75, CH-8032 Zurich, Switzerland.

E-mail: daniel.konrad@kispi.uzh.ch

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.

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