FXR deletion in hepatocytes does not affect the severity of alcoholic liver disease in mice.

ABSTRACT: Emerging evidence has shown that FXR activation ameliorates the development of alcoholic liver diseases (ALD) while whole-body deficiency of FXR in mice leads to more severe ALD. However, it's unknown whether the enhanced susceptibility to ALD development in FXR^-/- mice is due to deficiency of hepatic FXR or increased toxicity secondary to increased bile acid (BA) levels. Hepatocyte-specific FXR knockout mice (FXR^hep-/-) present similar BA levels compared to wild-type mice, and are therefore a useful model to study a direct role of hepatic FXR in ALD development. FXR^hep-/- mice were subject to an ALD model with chronic plus binge drinking of alcohol to determine the effects of hepatic FXR deficiency on ALD development. The FXR^hep-/- mice showed a

SUBMITTER: Zhang M 

PROVIDER: S-EPMC6168334 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature