Molecular mediators of hepatic steatosis and liver injury

J Clin Invest. 2004 Jul;114(2):147-52. doi: 10.1172/JCI22422.

Abstract

Obesity and its associated comorbidities are among the most prevalent and challenging conditions confronting the medical profession in the 21st century. A major metabolic consequence of obesity is insulin resistance, which is strongly associated with the deposition of triglycerides in the liver. Hepatic steatosis can either be a benign, noninflammatory condition that appears to have no adverse sequelae or can be associated with steatohepatitis: a condition that can result in end-stage liver disease, accounting for up to 14% of liver transplants in the US. Here we highlight recent advances in our understanding of the molecular events contributing to hepatic steatosis and nonalcoholic steatohepatitis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • AMP-Activated Protein Kinases
  • Disease Progression
  • Fatty Liver / epidemiology
  • Fatty Liver / metabolism*
  • Fatty Liver / physiopathology
  • Humans
  • Insulin Resistance / physiology
  • Lipid Peroxidation
  • Liver / metabolism*
  • Liver / pathology
  • Liver / physiopathology
  • Mitochondria / metabolism
  • Multienzyme Complexes / metabolism
  • Obesity / complications
  • Obesity / physiopathology*
  • Oxidative Stress
  • Protein-Serine-Threonine Kinases / metabolism
  • Triglycerides / metabolism

Substances

  • Multienzyme Complexes
  • Triglycerides
  • Protein-Serine-Threonine Kinases
  • AMP-Activated Protein Kinases