The lipogenic transcription factor ChREBP dissociates hepatic steatosis from insulin resistance in mice and humans.

ABSTRACT: Nonalcoholic fatty liver disease (NAFLD) is associated with all features of the metabolic syndrome. Although deposition of excess triglycerides within liver cells, a hallmark of NAFLD, is associated with a loss of insulin sensitivity, it is not clear which cellular abnormality arises first. We have explored this in mice overexpressing carbohydrate responsive element-binding protein (ChREBP). On a standard diet, mice overexpressing ChREBP remained insulin sensitive, despite increased expression of genes involved in lipogenesis/fatty acid esterification and resultant hepatic steatosis (simple fatty liver). Lipidomic analysis revealed that the steatosis was associated with increased accumulation of

SUBMITTER: Benhamed F 

PROVIDER: S-EPMC3366390 | biostudies-literature | 2012 Jun

REPOSITORIES: biostudies-literature