Farnesoid X receptor; Takeda G protein-coupled receptor 5 (FXR; TGR5)

Farnesoid X receptor is a nuclear hormone receptor (NR1H4) primarily expressed in the liver, intestine, and kidney. It acts as a ligand-activated transcription factor central to bile acid, cholesterol, glucose, and lipid homeostasis, and also modulates inflammation, fibrosis, and metabolic/energy balance. FXR is a validated therapeutic target for liver diseases, metabolic diseases, and certain cancers, with several agonists in clinical use or investigation. TGR5 (G protein-coupled bile acid receptor 1, GPBAR1) is a membrane-bound G protein-coupled receptor activated by bile acids. It is expressed in diverse tissues (including liver, intestines, adipose tissue, and immune cells) and is involved in energy expenditure, glucose regulation, and anti-inflammatory signaling. TGR5 is emerging as a target in metabolic disorders, osteoporosis, and inflammation. Some synthetic compounds target both FXR and TGR5 to achieve synergistic therapeutic effects. Summary of key distinctions: FXR is a nuclear receptor and transcription factor; TGR5 is a cell surface GPCR. Both bind bile acids, but with different mechanisms and tissue distributions; they have overlapping but distinct biological roles. Recommendation: For structured data, separate entries for "Farnesoid X receptor" and "Takeda G protein-coupled receptor 5" (TGR5) should be maintained for accuracy. This entry combines information for two distinct receptors due to the input query's format, hence marked as incorrect.

Other names

FXRNR1H4G protein-coupled bile acid receptor 1GPBAR1M-BARBG37

FXR-agonists: Activation represses bile acid synthesis, reduces plasma triglyceride, cholesterol and glucose levels, modulates gene expression controlling metabolism and inflammation. TGR5-agonists: Activation stimulates energy expenditure, decreases blood glucose, mediates thyroid hormone activation, inhibits osteoclast differentiation. Dual FXR/TGR5 activation: Synergistic effects on bone remodeling, atherosclerosis reduction, and metabolic regulation.