Commentary 10.1172/JCI95008

ChREBP refines the hepatic response to fructose to protect the liver from injury

Angela M. Hall and Brian N. Finck

Division of Geriatrics and Nutritional Sciences, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.

Address correspondence to: Brian N. Finck, Washington University School of Medicine, 660 S. Euclid Ave., Box 8031, St. Louis, Missouri 63110, USA. Phone: 314.362.8963; Email: bfinck@wustl.edu.

Find articles by Hall, A. in: JCI | PubMed | Google Scholar

Division of Geriatrics and Nutritional Sciences, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.

Address correspondence to: Brian N. Finck, Washington University School of Medicine, 660 S. Euclid Ave., Box 8031, St. Louis, Missouri 63110, USA. Phone: 314.362.8963; Email: bfinck@wustl.edu.

Find articles by Finck, B. in: JCI | PubMed | Google Scholar

First published June 19, 2017 - More info

Published in Volume 127, Issue 7 (June 30, 2017)
J Clin Invest. 2017;127(7):2533–2535. doi:10.1172/JCI95008.
Copyright © 2017, American Society for Clinical Investigation

First published June 19, 2017

See the related article at Lipogenic transcription factor ChREBP mediates fructose-induced metabolic adaptations to prevent hepatotoxicity.

Overconsumption of fructose and other sugars has been linked to nonalcoholic fatty liver disease (NAFLD); however, the sugar-associated effects that lead to disease are poorly defined. In this issue of the JCI, Zhang and colleagues show that the carbohydrate response element–binding protein (ChREBP) coordinates an adaptive response to a high-fructose diet in mice and that loss of this transcription factor leads to hepatic inflammation and early signs of fibrosis. Intriguingly, ChREBP-dependent effects were due to an exaggerated activation of the proapoptotic arms of the endoplasmic reticulum stress response that is probably secondary to inappropriate derepression of cholesterol biosynthesis. These findings suggest that a previously unknown link exists between ChREBP and the regulation of cholesterol synthesis that affects liver injury.

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