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Citations to this article

Molecular mediators of hepatic steatosis and liver injury
Jeffrey D. Browning, Jay D. Horton
Jeffrey D. Browning, Jay D. Horton
Published July 15, 2004
Citation Information: J Clin Invest. 2004;114(2):147-152. https://doi.org/10.1172/JCI22422.
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Molecular mediators of hepatic steatosis and liver injury

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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.

Authors

Jeffrey D. Browning, Jay D. Horton

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