Bile acids are crucial for intestinal nutrient absorption and the secretion of lipids, toxic metabolites, and xenobiotics. They also serve as signaling molecules and metabolic regulators, activating nuclear receptors and G protein-coupled receptors (GPCRs) to maintain hepatic lipid, glucose, and energy homeostasis. The enterohepatic circulation of bile acids, regulated by nuclear receptors, is essential for nutrient absorption and metabolic regulation. Toxic bile acids can cause inflammation, apoptosis, and cell death, while bile acid-activated signaling protects against inflammation. Disorders in bile acid metabolism lead to cholestatic liver diseases, dyslipidemia, fatty liver diseases, cardiovascular diseases, and diabetes. Bile acids, their derivatives, and sequestrants are therapeutic agents for treating these conditions. The synthesis of bile acids involves 17 enzymes and two major pathways: the neutral (classic) pathway and the acidic pathway. Bile acids are conjugated with glycine or taurine and stored in the gallbladder before being secreted into the intestinal tract. The enterohepatic circulation of bile acids is highly efficient, with most bile acids being reabsorbed in the ileum and transported back to the liver. Bile acid synthesis is regulated by negative feedback mechanisms, with bile acids inhibiting cholesterol synthesis and CYP7A1 activity. Nutrients, such as cholesterol, insulin, and glucose, play a key role in regulating bile acid synthesis. Bile acid-activated nuclear receptors, including farnesoid X receptor (FXR), pregnane X receptor (PXR), and vitamin D receptor (VDR), regulate gene transcription and metabolic pathways. FXR, in particular, plays a critical role in bile acid synthesis, secretion, and uptake, and its activation by bile acids inhibits CYP7A1 expression. GPCR signaling, such as TGR5 and S1P2, also contributes to bile acid regulation, with TGR5 activating cAMP and AKT pathways and S1P2 activating ERK1/2 and AKT pathways. Bile acids are involved in inflammation, with hydrophobic bile acids causing inflammation and hydrophilic bile acids having anti-inflammatory effects. Bile acid signaling through FXR and TGR5 regulates lipid, glucose, and energy metabolism, and defects in bile acid metabolism can lead to various diseases, including cholestatic liver diseases and metabolic disorders.Bile acids are crucial for intestinal nutrient absorption and the secretion of lipids, toxic metabolites, and xenobiotics. They also serve as signaling molecules and metabolic regulators, activating nuclear receptors and G protein-coupled receptors (GPCRs) to maintain hepatic lipid, glucose, and energy homeostasis. The enterohepatic circulation of bile acids, regulated by nuclear receptors, is essential for nutrient absorption and metabolic regulation. Toxic bile acids can cause inflammation, apoptosis, and cell death, while bile acid-activated signaling protects against inflammation. Disorders in bile acid metabolism lead to cholestatic liver diseases, dyslipidemia, fatty liver diseases, cardiovascular diseases, and diabetes. Bile acids, their derivatives, and sequestrants are therapeutic agents for treating these conditions. The synthesis of bile acids involves 17 enzymes and two major pathways: the neutral (classic) pathway and the acidic pathway. Bile acids are conjugated with glycine or taurine and stored in the gallbladder before being secreted into the intestinal tract. The enterohepatic circulation of bile acids is highly efficient, with most bile acids being reabsorbed in the ileum and transported back to the liver. Bile acid synthesis is regulated by negative feedback mechanisms, with bile acids inhibiting cholesterol synthesis and CYP7A1 activity. Nutrients, such as cholesterol, insulin, and glucose, play a key role in regulating bile acid synthesis. Bile acid-activated nuclear receptors, including farnesoid X receptor (FXR), pregnane X receptor (PXR), and vitamin D receptor (VDR), regulate gene transcription and metabolic pathways. FXR, in particular, plays a critical role in bile acid synthesis, secretion, and uptake, and its activation by bile acids inhibits CYP7A1 expression. GPCR signaling, such as TGR5 and S1P2, also contributes to bile acid regulation, with TGR5 activating cAMP and AKT pathways and S1P2 activating ERK1/2 and AKT pathways. Bile acids are involved in inflammation, with hydrophobic bile acids causing inflammation and hydrophilic bile acids having anti-inflammatory effects. Bile acid signaling through FXR and TGR5 regulates lipid, glucose, and energy metabolism, and defects in bile acid metabolism can lead to various diseases, including cholestatic liver diseases and metabolic disorders.