Functions of the Gallbladder.
Level 5 - mechanism / opinion, no new human data
Narrative review of gallbladder physiology and related pathology without systematic search or meta-analysis.
PubMed 27347902 · doi:10.1002/cphy.c150050
What was done
This narrative physiological review synthesized existing literature on the regulatory mechanisms of gallbladder motor function, epithelial fluid and mucin transport, bile acid handling, and the downstream metabolic and clinical consequences of gallbladder dysfunction and cholecystectomy.
What was found
The abstract provides a qualitative summary of physiological mechanisms without quantitative metrics or effect estimates. Gallbladder filling and emptying are regulated by bile acid receptors (TGR5) and neurohormonal peptides such as cholecystokinin (triggering emptying) and FGF15/19 (triggering refilling). Epithelial mucin and bicarbonate secretion, regulated by cAMP- and calcium-dependent pathways, provide cytoprotection against bile acids. The review notes that cholecystectomy accelerates enterohepatic recirculation of bile acids, which is associated with increased risks of nonalcoholic fatty liver disease, cirrhosis, and small-intestine carcinoid.
Why it matters
It provides a comprehensive physiological framework showing that the gallbladder is an active metabolic and secretory organ rather than a passive reservoir. This mechanistic understanding supports the evaluation of gallbladder-preserving strategies over routine cholecystectomy in selected patients.
Limits
The abstract reports no sample size, search protocol, quantitative risk estimates, or primary patient data. As a narrative review, it reflects descriptive physiological models and associations rather than standardized comparative outcomes.
Cited by
- supports Bile is synthesized in the liver and concentrated and stored in the gallbladder until released during digestion.