Bile acids are essential physiological detergents that facilitate lipid, nutrient, and vitamin absorption in the intestine and regulate metabolic pathways through signaling. They act as ligands for nuclear receptors like FXR, PXR, and VDR, which control bile acid synthesis, lipid metabolism, and energy homeostasis. The enterohepatic circulation of bile acids plays a critical role in feedback inhibition of bile acid synthesis and whole-body lipid homeostasis. FXR, a key bile acid-activated receptor, regulates bile acid synthesis by inducing the small heterodimer partner (SHP), which inhibits CYP7A1, the rate-limiting enzyme in bile acid synthesis. In the intestine, FXR activates FGF19, which signals through FGFR4 to inhibit CYP7A1. However, the exact mechanism of FXR/FGF19/FGFR4 signaling in CYP7A1 inhibition remains unclear. Bile acids also regulate CYP7A1 through other pathways, including PXR and VDR activation, inflammatory cytokine signaling, and epigenetic mechanisms. These pathways collectively ensure bile acid homeostasis and metabolic regulation. Bile acids and their receptors are promising therapeutic targets for treating liver diseases, metabolic syndrome, and obesity. Recent studies highlight the importance of species differences in bile acid regulation between humans and mice, emphasizing the need for human-specific models in research. Advances in understanding bile acid signaling pathways offer potential for developing novel therapies for metabolic and liver diseases.Bile acids are essential physiological detergents that facilitate lipid, nutrient, and vitamin absorption in the intestine and regulate metabolic pathways through signaling. They act as ligands for nuclear receptors like FXR, PXR, and VDR, which control bile acid synthesis, lipid metabolism, and energy homeostasis. The enterohepatic circulation of bile acids plays a critical role in feedback inhibition of bile acid synthesis and whole-body lipid homeostasis. FXR, a key bile acid-activated receptor, regulates bile acid synthesis by inducing the small heterodimer partner (SHP), which inhibits CYP7A1, the rate-limiting enzyme in bile acid synthesis. In the intestine, FXR activates FGF19, which signals through FGFR4 to inhibit CYP7A1. However, the exact mechanism of FXR/FGF19/FGFR4 signaling in CYP7A1 inhibition remains unclear. Bile acids also regulate CYP7A1 through other pathways, including PXR and VDR activation, inflammatory cytokine signaling, and epigenetic mechanisms. These pathways collectively ensure bile acid homeostasis and metabolic regulation. Bile acids and their receptors are promising therapeutic targets for treating liver diseases, metabolic syndrome, and obesity. Recent studies highlight the importance of species differences in bile acid regulation between humans and mice, emphasizing the need for human-specific models in research. Advances in understanding bile acid signaling pathways offer potential for developing novel therapies for metabolic and liver diseases.