Fig. 3

a dynamic balance of BAs. Intestinal and hepatic FXR work synergistically to regulate BAs, reducing their synthesis and promoting excretion. Activation of hepatic FXR leads to an upregulation of SHP, which in turn inhibits various transcription factors, including LXR, LRH-1, and HNF-4α, thereby impacting the activities of enzymes such as CYP7A1 and CYP8B1 involved in BA synthesis. Additionally, MAFG, influenced by FXR, may affect the CDCA: CA ratio, thereby influencing the hydrophobicity of BAs without altering the overall BA pool size. b BAs regulate blood glucose levels through FXR. BAs activate FXR within pancreatic β cells, which in turn promotes the release of insulin while inhibiting the release of glucagon and the production of glucose in the liver. SHP competes with HNF-4α, thereby suppressing the expression of genes related to gluconeogenesis. FXR’s direct interaction with ChREBP helps maintain glucose balance by reducing glycolysis and stimulating the storage of glycogen following a meal