Bile acids are essential for intestinal nutrient absorption and biliary secretion of lipids, toxic metabolites, and xenobiotics. They also act as signaling molecules that regulate hepatic lipid, glucose, and energy homeostasis through nuclear receptors and G protein-coupled receptors (GPCRs). Bile acid metabolism is crucial for maintaining cholesterol homeostasis and preventing liver and organ damage. The enterohepatic circulation of bile acids, regulated by a complex membrane transport system, plays a central role in nutrient absorption, metabolic regulation, and homeostasis. Toxic bile acids can cause inflammation, apoptosis, and cell death, while bile acid-activated signaling protects against inflammation in the liver, intestine, and macrophages. 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 used to treat chronic liver diseases, obesity, and diabetes. Bile acids are derived from cholesterol and have a specific structure. Their synthesis involves multiple enzymes located in the cytosol, endoplasmic reticulum, mitochondria, and peroxisomes. Two major pathways are involved in bile acid synthesis: the neutral (classic) pathway and the acidic (alternative) pathway. The neutral pathway starts with cholesterol 7α-hydroxylase (CYP7A1), the rate-limiting enzyme in bile acid synthesis, and produces two primary bile acids, cholic acid (CA) and chenodeoxycholic acid (CDCA). The acidic pathway starts with sterol 27-hydroxylase (CYP27A1) and contributes about 9% of total bile acid synthesis in human hepatocytes. Bile acids are conjugated with amino acids such as glycine or taurine to increase solubility. Conjugated bile acids are reabsorbed in the ileum and transported back to the liver via portal blood circulation. The enterohepatic circulation of bile acids is highly efficient in humans and is important for nutrient absorption, xenobiotic disposal, and metabolic homeostasis. Bile acid feedback inhibition of its own synthesis has been studied for over 50 years, but the underlying molecular mechanism remains unclear. Recent studies have shown that bile acids are endogenous ligands of the nuclear receptor farnesoid X receptor (FXR), providing insight into their role in gene transcription regulation. FXR-dependent pathways are critical for maintaining metabolic homeostasis. Bile acid-activated G protein-coupled receptors, such as TGR5 and S1P2, play roles in energy metabolism, protecting the liver and intestine from inflammation and steatosis, and improving insulin sensitivity. These receptors are involved in the regulation of lipid, glucose, and energy metabolism. Bile acid synthesis is regulated by various factors, including nutrient availability, hormonal signals,Bile acids are essential for intestinal nutrient absorption and biliary secretion of lipids, toxic metabolites, and xenobiotics. They also act as signaling molecules that regulate hepatic lipid, glucose, and energy homeostasis through nuclear receptors and G protein-coupled receptors (GPCRs). Bile acid metabolism is crucial for maintaining cholesterol homeostasis and preventing liver and organ damage. The enterohepatic circulation of bile acids, regulated by a complex membrane transport system, plays a central role in nutrient absorption, metabolic regulation, and homeostasis. Toxic bile acids can cause inflammation, apoptosis, and cell death, while bile acid-activated signaling protects against inflammation in the liver, intestine, and macrophages. 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 used to treat chronic liver diseases, obesity, and diabetes. Bile acids are derived from cholesterol and have a specific structure. Their synthesis involves multiple enzymes located in the cytosol, endoplasmic reticulum, mitochondria, and peroxisomes. Two major pathways are involved in bile acid synthesis: the neutral (classic) pathway and the acidic (alternative) pathway. The neutral pathway starts with cholesterol 7α-hydroxylase (CYP7A1), the rate-limiting enzyme in bile acid synthesis, and produces two primary bile acids, cholic acid (CA) and chenodeoxycholic acid (CDCA). The acidic pathway starts with sterol 27-hydroxylase (CYP27A1) and contributes about 9% of total bile acid synthesis in human hepatocytes. Bile acids are conjugated with amino acids such as glycine or taurine to increase solubility. Conjugated bile acids are reabsorbed in the ileum and transported back to the liver via portal blood circulation. The enterohepatic circulation of bile acids is highly efficient in humans and is important for nutrient absorption, xenobiotic disposal, and metabolic homeostasis. Bile acid feedback inhibition of its own synthesis has been studied for over 50 years, but the underlying molecular mechanism remains unclear. Recent studies have shown that bile acids are endogenous ligands of the nuclear receptor farnesoid X receptor (FXR), providing insight into their role in gene transcription regulation. FXR-dependent pathways are critical for maintaining metabolic homeostasis. Bile acid-activated G protein-coupled receptors, such as TGR5 and S1P2, play roles in energy metabolism, protecting the liver and intestine from inflammation and steatosis, and improving insulin sensitivity. These receptors are involved in the regulation of lipid, glucose, and energy metabolism. Bile acid synthesis is regulated by various factors, including nutrient availability, hormonal signals,