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

Angela M. Hall, Brian N. Finck

Research output: Contribution to journalReview articlepeer-review

4 Scopus citations


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.

Original languageEnglish
Pages (from-to)2533-2535
Number of pages3
JournalJournal of Clinical Investigation
Issue number7
StatePublished - Jun 30 2017


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