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dc.contributor.authorEmery, Edward C.
dc.contributor.authorDiakogiannaki, Eleftheria
dc.contributor.authorGentry, Clive
dc.contributor.authorPsichas, Arianna
dc.contributor.authorHabib, Abdella M.
dc.contributor.authorBevan, Stuart
dc.contributor.authorFischer, Michael J.M.
dc.contributor.authorReimann, Frank
dc.contributor.authorGribble, Fiona M.
dc.contributor.illustrator
dc.date.accessioned2020-11-26T13:32:04Z
dc.date.available2020-11-26T13:32:04Z
dc.date.issued2014-10-16
dc.identifier.citationEmery EC, Diakogiannaki E, Gentry C, Psichas A, Habib AM, Bevan S, Fischer MJM, Reimann F, Gribble FM (2015) 'Stimulation of GLP-1 secretion downstream of the ligand-gated ion channel TRPA1', Diabetes, 64 (4), pp.1202-1210.en_US
dc.identifier.issn0012-1797
dc.identifier.pmid25325736
dc.identifier.doi10.2337/db14-0737
dc.identifier.urihttp://hdl.handle.net/10547/624684
dc.description.abstractStimulus-coupled incretin secretion from enteroendocrine cells plays a fundamental role in glucose homeostasis and could be targeted for the treatment of type 2 diabetes. Here, we investigated the expression and function of transient receptor potential (TRP) ion channels in enteroendocrine L cells producing GLP-1. By microarray and quantitative PCR analysis, we identified trpa1 as an L cell-enriched transcript in the small intestine. Calcium imaging of primary L cells and the model cell line GLUTag revealed responses triggered by the TRPA1 agonists allyl-isothiocyanate (mustard oil), carvacrol, and polyunsaturated fatty acids, which were blocked by TRPA1 antagonists. Electrophysiology in GLUTag cells showed that carvacrol induced a current with characteristics typical of TRPA1 and triggered the firing of action potentials. TRPA1 activation caused an increase in GLP-1 secretion from primary murine intestinal cultures and GLUTag cells, an effect that was abolished in cultures from trpa1-/- mice or by pharmacological TRPA1 inhibition. These findings present TRPA1 as a novel sensory mechanism in enteroendocrine L cells, coupled to the facilitation of GLP-1 release, which may be exploitable as a target for treating diabetes.en_US
dc.language.isoenen_US
dc.publisherAmerican Diabetes Association Inc.en_US
dc.relation.urlhttps://diabetes.diabetesjournals.org/content/64/4/1202.longen_US
dc.rightsBlue - can archive post-print (ie final draft post-refereeing) or publisher's version/PDF
dc.subjectDiabetesen_US
dc.subjectSubject Categories::C900 Others in Biological Sciencesen_US
dc.titleStimulation of GLP-1 secretion downstream of the ligand-gated ion channel TRPA1en_US
dc.typeArticleen_US
dc.contributor.departmentAddenbrooke’s Hospitalen_US
dc.contributor.departmentKing’s College Londonen_US
dc.contributor.departmentUniversity College Londonen_US
dc.contributor.departmentUniversity of Erlangen-Nurembergen_US
dc.identifier.journalDiabetesen_US
dc.identifier.pmcidPMC4375100
dc.date.updated2020-11-26T12:51:57Z
dc.description.notearticle is free to read on publisher site but no creative commons licence so not passing to repository. pre April 2016.


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