ArticleThe Journal of physiology2013
Ursodeoxycholic acid attenuates colonic epithelial secretory function.
Article in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- Addition of a Gastrointestinal Microbiome Modulator to Metformin Improves Metformin Tolerance and Fasting Glucose Levels.Journal of diabetes science and technology · 2015 · on this mapTrial
- Effect of bile salts on intestinal epithelial function in gilthead seabream (Sparus aurata).Fish physiology and biochemistry · 2024Article
- Determination of Bile Acids in Canine Biological Samples: Diagnostic Significance.Metabolites · 2024Review
- Bile Acid and Gut Microbiota in Irritable Bowel Syndrome.Journal of neurogastroenterology and motility · 2022Review
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- Bile acid detergency: permeability, inflammation, and effects of sulfation.American journal of physiology. Gastrointestinal and liver physiology · 2022Review
- Contributions of bile acids to gastrointestinal physiology as receptor agonists and modifiers of ion channels.American journal of physiology. Gastrointestinal and liver physiology · 2022Article
- Bile acids modulate colonic MAdCAM-1 expression in a murine model of combined cholestasis and colitis.Mucosal immunology · 2021Article
- Modulating bile acid pathways and TGR5 receptors for treating liver and GI diseases.Current opinion in pharmacology · 2017Review
- The Effect of Deoxycholic Acid on Secretion and Motility in the Rat and Guinea Pig Large Intestine.Journal of neurogastroenterology and motility · 2017Article
- The Yin and Yang of bile acid action on tight junctions in a model colonic epithelium.Physiological reports · 2017Article
- Helminths and intestinal barrier function.Tissue barriers · 2017Review
- Reduction of epithelial secretion in male rat distal colonic mucosa by bile acid receptor TGR5 agonist, INT-777: role of submucosal neurons.Neurogastroenterology and motility · 2016Article
- Therapeutic targeting of bile acids.American journal of physiology. Gastrointestinal and liver physiology · 2015Review
- Bile acid effects are mediated by ATP release and purinergic signalling in exocrine pancreatic cells.Cell communication and signaling : CCS · 2015Article
- Effect of increased bile acid synthesis or fecal excretion in irritable bowel syndrome-diarrhea.The American journal of gastroenterology · 2014Article
- Key discoveries in bile acid chemistry and biology and their clinical applications: history of the last eight decades.Journal of lipid research · 2014Review
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dihydroxy bile acids, such as chenodeoxycholic acid (CDCA), are well known to promote colonic fluid and electrolyte secretion, thereby causing diarrhoea associated with bile acid malabsorption. However, CDCA is rapidly metabolised by colonic bacteria to ursodeoxycholic acid (UDCA), the effects of which on epithelial transport are poorly characterised. Here, we investigated the role of UDCA in the regulation of colonic epithelial secretion. Cl(-) secretion was measured across voltage-clamped monolayers of T84 cells and muscle-stripped sections of mouse or human colon. Cell surface biotinylation was used to assess abundance/surface expression of transport proteins. Acute (15 min) treatment of T84 cells with bilateral UDCA attenuated Cl(-) secretory responses to the Ca(2+) and cAMP-dependent secretagogues carbachol (CCh) and forskolin (FSK) to 14.0 ± 3.8 and 40.2 ± 7.4% of controls, respectively (n = 18, P < 0.001). Investigation of the molecular targets involved revealed that UDCA acts by inhibiting Na(+)/K(+)-ATPase activity and basolateral K(+) channel currents, without altering their cell surface expression. In contrast, intraperitoneal administration of UDCA (25 mg kg(-1)) to mice enhanced agonist-induced colonic secretory responses, an effect we hypothesised to be due to bacterial metabolism of UDCA to lithocholic acid (LCA). Accordingly, LCA (50-200 μm) enhanced agonist-induced secretory responses in vitro and a metabolically stable UDCA analogue, 6α-methyl-UDCA, exerted anti-secretory actions in vitro and in vivo. In conclusion, UDCA exerts direct anti-secretory actions on colonic epithelial cells and metabolically stable derivatives of the bile acid may offer a new approach for treating intestinal diseases associated with diarrhoea.
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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.