Mechanism of ER Stress and Inflammation for Hepatic Insulin Resistance in Obesity

Ann Nutr Metab. 2015;67(4):218-27. doi: 10.1159/000440905. Epub 2015 Oct 10.

Abstract

Background: Obesity is a major risk factor in the development of hepatic insulin resistance, which is characterized by an impairment of insulin ability to inhibit glucose output. Although the underlying mechanism for the link between obesity and insulin resistance in the liver is unclear, it has been widely reported and suggested that hepatic endoplasmic reticulum (ER) stress and inflammation induced by obesity lead to the development of hepatic insulin resistance and gluconeogenesis.

Summary: This review addresses the aspects of ER stress and inflammation currently understood to be involved in metabolic disease, including their role in obesity, hepatic insulin resistance, and hyperglycemia.

Publication types

  • Review

MeSH terms

  • Endoplasmic Reticulum Stress / physiology*
  • Humans
  • Hyperglycemia / complications
  • Hyperglycemia / physiopathology
  • Inflammation / complications
  • Inflammation / physiopathology*
  • Insulin Resistance / physiology*
  • Liver / physiopathology*
  • Obesity / complications
  • Obesity / physiopathology*