Neuro-humoral signalling by bile acids and the TGR5 receptor in the gastrointestinal tract
Open accessAbstract
In addition to their role in the digestion and absorption of dietary fats, bile acids (BAs) are tightly regulated signalling molecules. Their levels in the intestinal lumen, circulation and tissues fluctuate after feeding and fasting, and as a result of certain diseases and therapies. BAs regulate many cell types in the gut wall and beyond by activating nuclear and plasma membrane receptors. Of these, the G protein-coupled receptor TGR5 has emerged as a key mediator of the non-genomic actions of BAs. TGR5 is a cell-surface receptor that couples to Gαs, formation of cAMP, activation of protein kinase A and extracellular signal-regulated kinases, and inhibition of inflammatory signalling pathways. TGR5 has been implicated in mediating the actions of BAs on secretion of glucagon-like peptide 1 and glucose homeostasis, gastrointestinal motility and transit, electrolyte and fluid transport in the colon, bile formation and secretion, sensory transduction and inflammation. TGR5 agonists have been developed as treatments for metabolic, inflammatory and digestive disorders, and emerging evidence suggests that TGR5 mutations are associated with inflammatory diseases. Thus, TGR5 plays an important role in the normal processes of digestion and is a new therapeutic target for important digestive diseases.
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Bile acids stimulate the release of 5-hydroxytryptamine and calcitonin gene-related peptide from enterochromaffin cells and intrinsic primary afferent neurons by activating TGR5, leading to the bowel peristaltic reflex.
“BAs are known to stimulate the release of 5-hydroxytryptamine (5-HT) and calcitonin gene-related peptide from enterochromaffin cells and intrinsic primary afferent neurons by activating the G protein-coupled BA receptor (TGR5), leading to the bowel peristaltic reflex [ 38 , 39 ].”
From Role of gut microbiota in functional constipation (2021) · cites this paper as [39]
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- Authors
- Bunnett, N. W.
- Affiliations
- The University of Melbourne (AU)
- Corresponding author
- Bunnett, Nigel W.
- ORCID
- Bunnett, Nigel W.
- Venue
- The Journal of Physiology
- Publisher
- Wiley
- Published
- 2014-04-14
- Volume
- 592
- Issue
- 14
- Pages
- 2943-2950
- ISSN
- 0022-3751 (ISSN-L)
- 1469-7793
- PMC
- PMC4214650
- OpenAlex
- W1581234793
- Cited by
- 110
- References
- 35
- Citations by year
- 2026: 10 · 2025: 8 · 2024: 14 · 2023: 9 · 2022: 10 · 2021: 14 · 2020: 7 · 2019: 10 · 2018: 8 · 2017: 7 · 2016: 5 · 2015: 6 · 2014: 2
- FWCI
- 0.76
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- NHMRC (63303, 1049682, 1031886)
- Monash University
- Topics
- Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Keywords
- bile acids, TGR5, G protein-coupled receptors, gastrointestinal tract, cAMP signaling, protein kinase A, ERK activation, glucagon-like peptide-1, glucose homeostasis, gastrointestinal motility, bile formation, intestinal inflammation, TGR5 agonists, gastrointestinal diseases
- MeSH terms
- Animals, Bile Acids and Salts, Humans, Gastrointestinal Tract, Receptors, G-Protein-Coupled
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