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dc.contributor.authorAcebes Vindel, Ángel José 
dc.contributor.authorTriñanes, J.
dc.contributor.authorRodríguez Rodríguez, A.E.
dc.contributor.authorBrito Casillas, Y.
dc.contributor.authorWagner, A.
dc.contributor.authorDe Vries, A.P.J.
dc.contributor.authorCuesto, G.
dc.contributor.authorSalido, E.
dc.contributor.authorTorres, A.
dc.contributor.authorPorrini, E.
dc.date.accessioned2024-01-29T21:06:04Z
dc.date.available2024
dc.date.issued2017
dc.identifier.issn2829–2840
dc.identifier.urihttp://riull.ull.es/xmlui/handle/915/35809
dc.description.abstractb Cell transcription factors such as fork head box proteinO1(FoxO1), v-maf musculoaponeurotic fibrosarcoma oncogene homologA (MafA), pancreatic and duodenal homeobox1, and neuronal differentiation 1, are dysfunctional in type 2 diabetes mellitus (T2DM). Posttransplant diabetes mellitus resembles T2DMandreflectsinteractionbetweenpretransplant insulin resistanceand immunosuppressants ,mainly calcineurininhibitors(CNIs).We evaluated the effect of tacrolimus(TAC),cyclosporineA(CsA),and metabolic stressors (glucose plus palmitate) on insulinomab cells invitro and in pancreata of obeseand lean Zucker rats.Cellswereculturedfor5dayswith 100lMpalmitateand22mMglucose;CsA(250ng/ mL)orTAC(15ng/mL)were added in the last48h.
dc.format.mimetypeapplication/pdf
dc.language.isoen
dc.relation.ispartofseriesAmerican Journal of Transplantation, 2017;17.
dc.rightsLicencia Creative Commons (Reconocimiento-No comercial-Sin obras derivadas 4.0 Internacional)
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/deed.es_ES
dc.titleDeciphering tacrolimus-induced toxicity in pancreatic ß-cells.
dc.typeinfo:eu-repo/semantics/article
dc.identifier.doi10.1111/ajt.14323
dc.subject.keywordPancreatic b Cellsen
dc.subject.keywordToxicityen
dc.subject.keywordTacrolimus-Induceden


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Licencia Creative Commons (Reconocimiento-No comercial-Sin obras derivadas 4.0 Internacional)
Except where otherwise noted, this item's license is described as Licencia Creative Commons (Reconocimiento-No comercial-Sin obras derivadas 4.0 Internacional)