ArticleEndocrinology2015
Bile Acids Trigger GLP-1 Release Predominantly by Accessing Basolaterally Located G Protein-Coupled Bile Acid Receptors.
Article in Endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 180 papers.
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Who cites it
180 citing papers in PubMed, 330 citations in OpenAlex.
- A short-term randomized clinical trial testing feasibility of and physiological responses to a Ruminococcus torques strain in healthy overweight humans.Genome medicine · 2026Trial
- Trial
- DuodenalGut · 2022Trial
- Effects of Manipulating Circulating Bile Acid Concentrations on Postprandial GLP-1 Secretion and Glucose Metabolism After Roux-en-Y Gastric Bypass.Frontiers in endocrinology · 2021 · on this mapTrial
- Ileo-colonic delivery of conjugated bile acids improves glucose homeostasis via colonic GLP-1-producing enteroendocrine cells in human obesity and diabetes.EBioMedicine · 2020Trial
- Chenodeoxycholic acid stimulates glucagon-like peptide-1 secretion in patients after Roux-en-Y gastric bypass.Physiological reports · 2017Trial
- Glucagon-like peptide-1: a critical link between gut microbiota dysbiosis and degenerative musculoskeletal diseases.Gut microbes · 2026Review
- How lipid ingestion is sensed: the mechanisms underlying intestinal hormone secretion.Clinical science (London, England : 1979) · 2026Review
- Integrated multi-omics and functional analyses reveal a GDCA-TGR5-mediated immunometabolic signature in anorexia nervosa.European archives of psychiatry and clinical neuroscience · 2026Article
- Targeting microbial bile salt hydrolase reprograms bile acid metabolism and ameliorates metabolic dysfunction-associated steatohepatitis in mice.Molecular metabolism · 2026Article
- Sphinganine as a novel stimulator of GLP-1 secretion.Diabetologia · 2026Article
- From Food Structure to L-Cell Exposure: How Processing and Digestion Shape Endogenous GLP-1 Responses.Molecules (Basel, Switzerland) · 2026Review
- From Structure to Dynamics: Activation Mechanism of the G Protein-Coupled Bile Acid Receptor 1‑GACS omega · 2026Article
- Bile acids in Alzheimer's disease: a double-edged sword in gut-liver-brain signaling and neurodegeneration.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Gut-liver metabolic and enterohormonal remodeling drives progression from metabolic dysfunction-associated steatotic liver disease to steatohepatitis.Metabolism: clinical and experimental · 2026Article
- Article
- GLP-1 agonists and the gut microbiome: A bidirectional relationship.British journal of clinical pharmacology · 2026Review
- Emerging Insights into the Liver-Pancreas Axis: A Central Hub in the Pathogenesis of Diabetes and Metabolic Diseases.Biomolecules · 2026Review
- Modulation of the gut-heart axis by exercise in diabetic cardiomyopathy: Microbial mechanisms and clinical implications.iScience · 2026Review
- Association of serum bile acid profiles with the risk of gastrointestinal autonomic neuropathy in patients with type 2 diabetes mellitus.World journal of diabetes · 2026Article
120 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 6 institutions in 3 countries.
Funding
Abstract
Bile acids are well-recognized stimuli of glucagon-like peptide-1 (GLP-1) secretion. This action has been attributed to activation of the G protein-coupled bile acid receptor GPBAR1 (TGR5), although other potential bile acid sensors include the nuclear farnesoid receptor and the apical sodium-coupled bile acid transporter ASBT. The aim of this study was to identify pathways important for GLP-1 release and to determine whether bile acids target their receptors on GLP-1-secreting L-cells from the apical or basolateral compartment. Using transgenic mice expressing fluorescent sensors specifically in L-cells, we observed that taurodeoxycholate (TDCA) and taurolithocholate (TLCA) increased intracellular cAMP and Ca(2+). In primary intestinal cultures, TDCA was a more potent GLP-1 secretagogue than taurocholate (TCA) and TLCA, correlating with a stronger Ca(2+) response to TDCA. Using small-volume Ussing chambers optimized for measuring GLP-1 secretion, we found that both a GPBAR1 agonist and TDCA stimulated GLP-1 release better when applied from the basolateral than from the luminal direction and that luminal TDCA was ineffective when intestinal tissue was pretreated with an ASBT inhibitor. ASBT inhibition had no significant effect in nonpolarized primary cultures. Studies in the perfused rat gut confirmed that vascularly administered TDCA was more effective than luminal TDCA. Intestinal primary cultures and Ussing chamber-mounted tissues from GPBAR1-knockout mice did not secrete GLP-1 in response to either TLCA or TDCA. We conclude that the action of bile acids on GLP-1 secretion is predominantly mediated by GPBAR1 located on the basolateral L-cell membrane, suggesting that stimulation of gut hormone secretion may include postabsorptive mechanisms.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.