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Molecular mediators of hepatic steatosis and liver injury Browning JD; Horton JDJ Clin Invest 2004[Jul]; 114 (2): 147-52Obesity 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.|AMP-Activated Protein Kinases[MESH]|Disease Progression[MESH]|Fatty Liver/epidemiology/*metabolism/physiopathology[MESH]|Humans[MESH]|Insulin Resistance/physiology[MESH]|Lipid Peroxidation[MESH]|Liver/*metabolism/pathology/physiopathology[MESH]|Mitochondria/metabolism[MESH]|Multienzyme Complexes/metabolism[MESH]|Obesity/complications/*physiopathology[MESH]|Oxidative Stress[MESH]|Protein Serine-Threonine Kinases/metabolism[MESH]|Triglycerides/metabolism[MESH] |
