Is adipose tissue lipolysis always an adaptive response to starvation?: implications for non-alcoholic fatty liver disease

Clinical Science
Seng Khee Gan, Gerald F Watts

Abstract

The physiological response to starvation involves increased muscle proteolysis and adipose tissue lipolysis that supply amino acids and non-esterified fatty acids ('free fatty acids') for gluconeogenesis, oxidation and ketogenesis. In the present issue of Clinical Science, Moller and co-workers show that, in humans, IHL (intrahepatic lipid) content, measured using (1)H-magnetic resonance spectroscopy, increases following 36 h of fasting, with a direct association with plasma levels of 3-hydroxybutyrate. The observation raises interesting questions as to how IHL levels increase in a situation of increased mitochondrial fatty acid oxidation and ketogenesis. Possible mechanisms for increased IHLs include reduced apoB-100 (apolipoprotein B-100) production and hepatic lipid export, and/or impaired mitochondrial function resulting from increased oxidative stress, with diversion of fatty acids for esterification. The accumulation of IHL during prolonged fasting may, therefore, reflect a maladaptive response to increased non-esterified fatty acid delivery to the liver that unmasks a subtle defect in mitochondrial function. This could have implications for the pathogenesis of the common human disorder of non-alcoholic fatty liver diseas...Continue Reading

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