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Baishideng Publishing Group, World Journal of Gastroenterology, 2(14), p. 193, 2008

DOI: 10.3748/wjg.14.193

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Nonalcoholic fatty liver disease and mitochondrial dysfunction

Journal article published in 2008 by R. Scott Rector, Yongzhong Wei, John P. Thyfault, Jamal A. Ibdah ORCID
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

Nonalcoholic fatty liver disease (NAFLD) includes hepatic steatosis, nonalcoholic steatohepatitis (NASH), fibrosis, and cirrhosis. NAFLD is the most common liver disorder in the United States and worldwide. Due to the rapid rise of the metabolic syndrome, the prevalence of NAFLD has recently dramatically increased and will continue to increase. NAFLD has also the potential to progress to hepatocellular carcinoma (HCC) or liver failure. NAFLD is strongly linked to caloric overconsumption, physical inactivity, insulin resistance and genetic factors. Although significant progress in understanding the pathogenesis of NAFLD has been achieved in years, the primary metabolic abnormalities leading to lipid accumulation within hepatocytes has remained poorly understood. Mitochondria are critical metabolic organelles serving as “cellular power plants”. Accumulating evidence indicate that hepatic mitochondrial dysfunction is crucial to the pathogenesis of NAFLD. This review is focused on the significant role of mitochondria in the development of NAFLD.