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Updated: Mar 22, 2026

Optimized Analysis of In Vivo and In Vitro Hepatic Steatosis
Published on: March 11, 2017
Pathogenesis and Prevention of Hepatic Steatosis
Fatiha Nassir1, R Scott Rector1, Ghassan M Hammoud1
1Dr Nassir is an assistant research professor of medicine in the Division of Gastroenterology and Hepatology at the University of Missouri School of Medicine in Columbia, Missouri. Dr Rector is an assistant professor of medicine in the Division of Gastroenterology and Hepatology and the Department of Nutrition and Exercise Physiology at the University of Missouri School of Medicine; he is also a research health scientist in the Research Service at the Harry S. Truman Memorial Veterans' Hospital in Columbia, Missouri. Dr Hammoud is an associate professor of clinical medicine in the Division of Gastroenterology and Hepatol ogy at the University of Missouri School of Medicine. Dr Ibdah is a professor of medicine in the Division of Gastroenterology and Hepatology and the Department of Nutrition and Exercise Physiology at the University of Missouri School of Medicine, where he is also the director of the Division of Gastroenterology and Hepatology; in addition, he is a research health scientist in the Research Service at the Harry S. Truman Memorial Veterans' Hospital.
Abstract:
Hepatic steatosis is defined as intrahepatic fat of at least 5% of liver weight. Simple accumulation of triacylglycerols in the liver could be hepatoprotective; however, prolonged hepatic lipid storage may lead to liver metabolic dysfunction, inflammation, and advanced forms of nonalcoholic fatty liver disease. Nonalcoholic hepatic steatosis is associated with obesity, type 2 diabetes, and dyslipidemia. Several mechanisms are involved in the accumulation of intrahepatic fat, including increased flux of fatty acids to the liver, increased de novo lipogenesis, and/or reduced clearance through β-oxidation or very-low-density lipoprotein secretion. This article summarizes the mechanisms involved in the accumulation of triacylglycerols in the liver, the clinical implications, and the prevention of hepatic steatosis, with a focus on the role of mitochondrial function and lifestyle modifications.
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