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Molecular mediators of hepatic steatosis and liver injury

Journal of Clinical Investigation · 2004 · Vol. 114(2) · pp. 147–152
Jeffrey D. BrowningJay D. Horton

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.

Liver Disease Diagnosis and TreatmentPancreatic function and diabetesDiet, Metabolism, and DiseaseSteatosisSteatohepatitisInsulin resistanceObesityMedicineNonalcoholic fatty liver diseaseFatty liverGastroenterologyInternal medicineNonalcoholic steatohepatitis

MeSH terms

Fatty LiverHumansInsulin ResistanceLiverMitochondriaMultienzyme ComplexesObesityTriglyceridesLipid PeroxidationProtein Serine-Threonine KinasesOxidative StressDisease ProgressionAMP-Activated Protein Kinases

Funding

  • American Liver Foundation
  • National Institutes of Health
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