Increased activin bioavailability enhances hepatic insulin sensitivity while inducing hepatic steatosis in male mice.

ABSTRACT: The development of insulin resistance is tightly linked to fatty liver disease and is considered a major health concern worldwide, although their mechanistic relationship remains controversial. Activin has emerging roles in nutrient homeostasis, but its metabolic effects on hepatocytes remain unknown. In this study, we investigated the effects of increased endogenous activin bioactivity on hepatic nutrient homeostasis by creating mice with inactivating mutations that deplete the circulating activin antagonists follistatin-like-3 (FSTL3) or the follistatin 315 isoform (FST315; FST288-only mice). We investigated liver histology and lipid content, hepatic insulin sensitivity, and metabolic gene expression including the HepG2 cell and primary hepatocyte response to activin treatment. Both FSTL

SUBMITTER: Ungerleider NA 

PROVIDER: S-EPMC3740489 | biostudies-literature | 2013 Jun

REPOSITORIES: biostudies-literature