Gut microbiota and bile acid metabolic pathways (GM-BA axis)

The gut microbiota and bile acid metabolic pathways represent a complex bidirectional signaling axis that plays a fundamental role in host metabolism and immune homeostasis. Bile acids are synthesized from cholesterol in the liver and secreted into the intestine, where they are chemically modified by gut bacteria through processes such as deconjugation via bile salt hydrolase (BSH) and 7α-dehydroxylation to form secondary bile acids (1.4.1, 1.4.4). These molecules act as potent signaling ligands for host receptors, most notably the farnesoid X receptor (FXR) and the Takeda G protein-coupled receptor 5 (TGR5), which regulate glucose, lipid, and energy metabolism (1.1.4, 1.4.2). Dysregulation of this axis, often characterized by microbial dysbiosis and an altered bile acid pool, is strongly associated with metabolic disorders like type 2 diabetes, obesity, and non-alcoholic fatty liver disease, as well as gastrointestinal conditions like inflammatory bowel disease and C. difficile infection (1.2.3, 1.3.3). Therapeutic strategies targeting this pathway include the use of FXR agonists like obeticholic acid, probiotics to restore microbial balance, and drugs like metformin that modulate the microbiota-bile acid pool to improve metabolic outcomes (1.2.1, 1.5.1).

Other names

Gut-microbiota-bile acid axisBile acid-gut microbiome axisEnterohepatic circulation-microbiota axisMicrobiota-bile acid-FXR axis

Modulation of the bile acid pool composition through microbial enzymes like bile salt hydrolase (BSH), activation of the farnesoid X receptor (FXR) and Takeda G protein-coupled receptor 5 (TGR5), and regulation of the FGF19/FGFR4 signaling pathway to maintain metabolic and immune homeostasis.