Hmgcs2-mediated ketogenesis modulates high-fat diet-induced hepatosteatosis.

ABSTRACT:

Objective

Aberrant ketogenesis is correlated with the degree of steatosis in non-alcoholic fatty liver disease (NAFLD) patients, and an inborn error of ketogenesis (mitochondrial HMG-CoA synthase deficiency) is commonly associated with the development of the fatty liver. Here we aimed to determine the impact of Hmgcs2-mediated ketogenesis and its modulations on the development and treatment of fatty liver disease.

Methods

Loss- and gain-of-ketogenic function models, achieved by Hmgcs2 knockout and overexpression, respectively, were utilized to investigate the role of ketogenesis in the hepatic lipid accumulation during postnatal development and in a high-fat diet-induced NAFLD mouse model.

Results

Ketogenic function was decreased in NAFLD mice with a reduction in Hmgc

SUBMITTER: Asif S 

PROVIDER: S-EPMC9039870 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature