Fig. 7: Schematic figure of the effects of FXR on BA homeostasis and ethanol-induced injury.
From: Enhanced alcoholic liver disease in mice with intestine-specific farnesoid X receptor deficiency
Intestinal FGF15 is induced by activated FXR, released into portal circulation and transported to the liver where it binds to its receptor complex of FGFR4 and β-Klotho on the hepatocyte membrane to suppress BA synthesis. The activation of hepatic FXR by BAs leads to minor suppression of BA synthesis, promotion of liver regeneration and protection of the liver against cholestasis, steatosis, and inflammation. Intestinal FXR is crucial for maintaining intestinal barrier integrity and protecting the liver against influx of toxic gut endotoxins.
