Bile Acid Physiology.
Level 5 - mechanism / opinion, no new human data
Narrative review describing physiological and metabolic mechanisms without original empirical data or systematic review methodology.
PubMed 29080336 · doi:10.5604/01.3001.0010.5493
What was done
This is a narrative review summarizing the synthesis, enterohepatic circulation, microbiome biotransformation, and endocrine signaling mechanisms of bile acids, focusing on farnesoid X receptor (FXR) and G-protein-coupled bile acid receptor-1 (GPBAR-1/TGR5) activation.
What was found
The abstract reports no numerical data. It summarizes the physiological pathway: liver synthesis of primary bile acids from cholesterol, conjugation with glycine or taurine, gallbladder storage, meal-stimulated intestinal release, secondary bile acid conversion by colonic microbiota, and ileal/colonic reabsorption. It also details how bile acid signaling through FXR and GPBAR-1 modulates lipid and glucose metabolism, gene expression, and epithelial cell proliferation across the liver, intestine, muscle, and brown adipose tissue.
Why it matters
It highlights the broader role of bile acids as systemic metabolic signaling molecules rather than passive fat-emulsifying agents.
Limits
The abstract contains no primary data, quantitative findings, or systematic search methodology. It provides broad mechanistic overview rather than testing specific clinical outcomes or interventions.
Cited by
- supports Bile is synthesized in the liver and concentrated and stored in the gallbladder until released during digestion.