Bile acids are essential physiological detergents that facilitate lipid, nutrient, and vitamin absorption and transport in the intestine. They also act as signaling molecules and inflammatory agents, rapidly activating nuclear receptors and cell signaling pathways that regulate lipid, glucose, and energy metabolism. The enterohepatic circulation of bile acids plays a critical role in feedback inhibition of bile acid synthesis and whole-body lipid homeostasis. In the liver, bile acids activate the farnesoid X receptor (FXR), which induces an atypical nuclear receptor, small heterodimer partner (SHP), which inhibits nuclear receptors such as liver-related homolog-1 and hepatocyte nuclear factor 4α, leading to inhibition of the critical regulatory gene in bile acid synthesis, cholesterol 7α-hydroxylase (CYP7A1). In the intestine, FXR induces fibroblast growth factor 15 (FGF15; or FGF19 in humans), which activates hepatic FGF receptor 4 (FGFR4) signaling to inhibit bile acid synthesis. However, the mechanism by which FXR/FGF19/FGFR4 signaling inhibits CYP7A1 remains unclear. Bile acids can induce FGF19 in human hepatocytes, and the FGF19 autocrine pathway may exist in human livers. Bile acids and their receptors are therapeutic targets for treating cholestatic liver diseases, fatty liver diseases, diabetes, obesity, and metabolic syndrome. Bile acids are derived from cholesterol and play a central role in bile acid synthesis, which is the primary metabolic pathway for cholesterol catabolism in humans. Hydroxylation and modification of cholesterol to bile acids convert a hydrophobic membrane constituent into amphipathic molecules that serve as physiological detergents and signaling molecules. Bile acids bind to the ligand-binding domain of FXR, which forms a heterodimer with retinoid X receptor and binds to the inverted repeat of AGGTCa-like sequence in the promoters of FXR target genes to stimulate gene transcription. FXR plays a central role in regulating bile acid synthesis, excretion, and transport, as well as lipid, glucose, and energy metabolism. Hydrophobic bile acids, such as chenodeoxycholic acid (CDCA), are the most effective endogenous FXR ligands, while hydrophilic bile acids, such as ursodeoxycholic acid and muricholic acids, do not activate FXR. Bile acids also bind and activate PXR and VDR, which play important roles in detoxification of bile acids, drugs, and xenobiotics. Bile acids modulate cellular signaling pathways, including calcium mobilization, cyclic AMP synthesis, and protein kinase C activation. Bile acids stimulate secretion of pro-inflammatory cytokines, such as tumor necrosis factor α (TNFα) and interleukin-1β (ILBile acids are essential physiological detergents that facilitate lipid, nutrient, and vitamin absorption and transport in the intestine. They also act as signaling molecules and inflammatory agents, rapidly activating nuclear receptors and cell signaling pathways that regulate lipid, glucose, and energy metabolism. The enterohepatic circulation of bile acids plays a critical role in feedback inhibition of bile acid synthesis and whole-body lipid homeostasis. In the liver, bile acids activate the farnesoid X receptor (FXR), which induces an atypical nuclear receptor, small heterodimer partner (SHP), which inhibits nuclear receptors such as liver-related homolog-1 and hepatocyte nuclear factor 4α, leading to inhibition of the critical regulatory gene in bile acid synthesis, cholesterol 7α-hydroxylase (CYP7A1). In the intestine, FXR induces fibroblast growth factor 15 (FGF15; or FGF19 in humans), which activates hepatic FGF receptor 4 (FGFR4) signaling to inhibit bile acid synthesis. However, the mechanism by which FXR/FGF19/FGFR4 signaling inhibits CYP7A1 remains unclear. Bile acids can induce FGF19 in human hepatocytes, and the FGF19 autocrine pathway may exist in human livers. Bile acids and their receptors are therapeutic targets for treating cholestatic liver diseases, fatty liver diseases, diabetes, obesity, and metabolic syndrome. Bile acids are derived from cholesterol and play a central role in bile acid synthesis, which is the primary metabolic pathway for cholesterol catabolism in humans. Hydroxylation and modification of cholesterol to bile acids convert a hydrophobic membrane constituent into amphipathic molecules that serve as physiological detergents and signaling molecules. Bile acids bind to the ligand-binding domain of FXR, which forms a heterodimer with retinoid X receptor and binds to the inverted repeat of AGGTCa-like sequence in the promoters of FXR target genes to stimulate gene transcription. FXR plays a central role in regulating bile acid synthesis, excretion, and transport, as well as lipid, glucose, and energy metabolism. Hydrophobic bile acids, such as chenodeoxycholic acid (CDCA), are the most effective endogenous FXR ligands, while hydrophilic bile acids, such as ursodeoxycholic acid and muricholic acids, do not activate FXR. Bile acids also bind and activate PXR and VDR, which play important roles in detoxification of bile acids, drugs, and xenobiotics. Bile acids modulate cellular signaling pathways, including calcium mobilization, cyclic AMP synthesis, and protein kinase C activation. Bile acids stimulate secretion of pro-inflammatory cytokines, such as tumor necrosis factor α (TNFα) and interleukin-1β (IL