ArticleThe Journal of physiology2010
Hydrophobic bile salts inhibit gallbladder smooth muscle function via stimulation of GPBAR1 receptors and activation of KATP channels.
Article in The Journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 123 citations in OpenAlex.
- Bile acids as a "new hormone" in aging-related liver disease.Life medicine · 2026Review
- Gut Microbiome Dysbiosis Promotes Gallstone Formation via Bile Acid Metabolic Disorder: A Multiomics Study.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Can bile salts affect the contractile oesophageal activity associated with gastroesophageal reflux disease?World journal of gastroenterology · 2026Article
- The role of bile acid-activated receptor TGR5 in inflammation and liver diseases.Frontiers in physiology · 2026Review
- Targeting of a Bile Acid Receptor, Takeda G Protein Receptor 5 [TGR5], by a Novel First-in-Class Competitive Antagonist, SBI-364, Diminishes Hepatic and Renal Cystogenesis in Polycystic Liver and Kidney Disease.ACS pharmacology & translational science · 2025Article
- Ultrasonographic assessment of gastric and gallbladder dynamics in human health and disease.Internal and emergency medicine · 2025Review
- Biological Actions of Bile Acids via Cell Surface Receptors.International journal of molecular sciences · 2025Review
- Inhibition of hepatic bile salt uptake by Bulevirtide reduces atherosclerosis in Oatp1a1Journal of lipid research · 2024Article
- Smooth muscle cells, interstitial cells and neurons in the gallbladder (GB): Functional syncytium of electrical rhythmicity and GB motility (Review).International journal of molecular medicine · 2023Review
- TGR5 agonists induce peripheral and central hypersensitivity to bladder distension.Scientific reports · 2022Article
- Synthesis of Novel C/D Ring Modified Bile Acids.Molecules (Basel, Switzerland) · 2022Article
- Functional, Diagnostic and Therapeutic Aspects of Bile.Clinical and experimental gastroenterology · 2022Article
- Notoginsenoside Ft1 acts as a TGR5 agonist but FXR antagonist to alleviate high fat diet-induced obesity and insulin resistance in mice.Acta pharmaceutica Sinica. B · 2021Article
- TGR5 controls bile acid composition and gallbladder function to protect the liver from bile acid overload.JHEP reports : innovation in hepatology · 2021Article
- TGR5 Signaling in Hepatic Metabolic Health.Nutrients · 2020Review
- Compound 18 Improves Glucose Tolerance in a Hepatocyte TGR5-dependent Manner in Mice.Nutrients · 2020Article
- An update on the pathogenesis of cholesterol gallstone disease.Current opinion in gastroenterology · 2018Review
- Recent advances in understanding and managing cholesterol gallstones.F1000Research · 2018Review
- Article
- Glucagon-like peptide-2 promotes gallbladder refilling via a TGR5-independent, GLP-2R-dependent pathway.Molecular metabolism · 2017Article
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8 authors at 3 institutions in 1 country.
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Abstract
Hydrophobic bile salts are thought to contribute to the disruption of gallbladder smooth muscle (GBSM) function that occurs in gallstone disease, but their mechanism of action is unknown. The current study was undertaken to determine how hydrophobic bile salts interact with GBSM, and how they reduce GBSM activity. The effect of hydrophobic bile salts on the activity of GBSM was measured by intracellular recording and calcium imaging using wholemount preparations from guinea pig and mouse gallbladder. RT-PCR and immunohistochemistry were used to evaluate expression of the G protein-coupled bile acid receptor, GPBAR1. Application of tauro-chenodeoxycholate (CDC, 50-100 microm) to in situ GBSM rapidly reduced spontaneous Ca(2+) flashes and action potentials, and caused a membrane hyperpolarization. Immunoreactivity and transcript for GPBAR1 were detected in gallbladder muscularis. The GPBAR1 agonist, tauro-lithocholic acid (LCA, 10 microm) mimicked the effect of CDC on GBSM. The actions of LCA were blocked by the protein kinase A (PKA) inhibitor, KT5720 (0.5-1.0 microm) and the K(ATP) channel blocker, glibenclamide (10 microm). Furthermore, LCA failed to disrupt GBSM activity in Gpbar1(/) mice. The findings of this study indicate that hydrophobic bile salts activate GPBAR1 on GBSM, and this leads to activation of the cyclic AMP-PKA pathway, and ultimately the opening of K(ATP) channels, thus hyperpolarizing the membrane and decreasing GBSM activity. This inhibitory effect of hydrophobic bile salt activation of GPBAR1 could be a contributing factor in the manifestation of gallstone disease.
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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.