Molecular mediators of hepatic steatosis and liver injury.
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.
Browning
Jeffrey D
JD
Department of Internal Medicine, University of Texas Southwestern Medical Center at Dallas, 75390-9046, USA.
Horton
Jay D
JD
D055372:AMP-Activated Protein Kinases; D018450:Disease Progression; D005234:Fatty Liver / Q000453:epidemiology / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology; D015227:Lipid Peroxidation; D008099:Liver / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D008928:Mitochondria / Q000378:metabolism; D009097:Multienzyme Complexes / Q000378:metabolism; D009765:Obesity / Q000150:complications / Q000503:physiopathology*; D018384:Oxidative Stress; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism; D014280:Triglycerides / Q000378:metabolism
D009097:Multienzyme Complexes; D014280:Triglycerides; D017346:Protein Serine-Threonine Kinases; D055372:AMP-Activated Protein Kinases