Please use this identifier to cite or link to this item: https://hdl.handle.net/11000/3815
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dc.contributor.authorVettorazzi, Jean Franciesco-
dc.contributor.authorRibeiro, Rosane Aparecida-
dc.contributor.authorBorck, Patricia Cristine-
dc.contributor.authorSouto Branco, Renato Chaves-
dc.contributor.authorSoriano, Sergi-
dc.contributor.authorMerino Antolín, Beatriz-
dc.contributor.authorBoschero, Antonio Carlos-
dc.contributor.authorNadal Navajas, Ángel-
dc.contributor.authorQuesada Moll, Iván-
dc.contributor.authorCarneiro, Everardo M.-
dc.contributor.otherDepartamentos de la UMH::Biología Aplicadaes
dc.date.accessioned2017-09-08T15:23:27Z-
dc.date.available2017-09-08T15:23:27Z-
dc.date.created2016-03-
dc.date.issued2017-09-08-
dc.identifier.urihttp://hdl.handle.net/11000/3815-
dc.description.abstractObjective While bile acids are important for the digestion process, they also act as signaling molecules in many tissues, including the endocrine pancreas, which expresses specific bile acid receptors that regulate several cell functions. In this study, we investigated the effects of the conjugated bile acid TUDCA on glucose-stimulated insulin secretion (GSIS) from pancreatic β-cells. Methods Pancreatic islets were isolated from 90-day-old male mice. Insulin secretion was measured by radioimmunoassay, protein phosphorylation by western blot, Ca2 + signals by fluorescence microscopy and ATP-dependent K+ (KATP) channels by electrophysiology. Results TUDCA dose-dependently increased GSIS in fresh islets at stimulatory glucose concentrations but remained without effect at low glucose levels. This effect was not associated with changes in glucose metabolism, Ca2 + signals or KATP channel activity; however, it was lost in the presence of a cAMP competitor or a PKA inhibitor. Additionally, PKA and CREB phosphorylation were observed after 1-hour incubation with TUDCA. The potentiation of GSIS was blunted by the Gα stimulatory, G protein subunit-specific inhibitor NF449 and mimicked by the specific TGR5 agonist INT-777, pointing to the involvement of the bile acid G protein-coupled receptor TGR5. Conclusion Our data indicate that TUDCA potentiates GSIS through the cAMP/PKA pathway.es
dc.description.sponsorshipThis work was by grants from the Spanish Ministerio de Ciencia e Innovación (BFU2013-42789-P; BFU2011-28358)-
dc.description.sponsorshipThis work was supported by grants from Fundacão de Amparo á Pesquisa do Estado de São Paulo (FAPESP 2013/01318-4)-
dc.description.sponsorshipThis work was supported by grants from Conselho Nacional para o Desenvolvimento Científico e Tecnológico (CNPq 200030/2014-0)-
dc.formatapplication/pdfes
dc.format.extent36es
dc.language.isoenges
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.subjectβ-celles
dc.subjectBile acidses
dc.subjectInsulin secretiones
dc.subjectTUDCAes
dc.subject.other577 - Bioquímica. Biología molecular. Biofísicaes
dc.titleThe bile acid TUDCA increases glucose-induced insulin secretion via the cAMP/PKA pathway in pancreatic beta cellses
dc.typeinfo:eu-repo/semantics/articlees
dc.identifier.doi10.1016/j.metabol.2015.10.021-
dc.relation.publisherversionhttps://doi.org/10.1016/j.metabol.2015.10.021-
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