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dc.rights.licenseopenen_US
dc.contributor.authorGUILLEMAIN, Ghislaine
hal.structure.identifierChimie et Biologie des Membranes et des Nanoobjets [CBMN]
dc.contributor.authorKHEMTEMOURIAN, Lucie
dc.contributor.authorBREHAT, Juliette
dc.contributor.authorMORIN, Didier
dc.contributor.authorMOVASSAT, Jamileh
dc.contributor.authorTOURREL-CUZIN, Cecile
dc.contributor.authorLACAPERE, Jean-Jacques
dc.date.accessioned2025-01-14T11:37:31Z
dc.date.available2025-01-14T11:37:31Z
dc.date.issued2024-06-20
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/204259
dc.description.abstractEnAmyloidosis forms a large family of pathologies associated with amyloid deposit generated by the formation of amyloid fibrils or plaques. The amyloidogenic proteins and peptides involved in these processes are targeted against almost all organs. In brain they are associated with neurodegenerative disease, and the Translocator Protein (TSPO), overexpressed in these inflammatory conditions, is one of the target for the diagnostic. Moreover, TSPO ligands have been described as promising therapeutic drugs for neurodegenerative diseases. Type 2 diabetes, another amyloidosis, is due to a beta cell mass decrease that has been linked to hIAPP (human islet amyloid polypeptide) fibril formation, leading to the reduction of insulin production. In the present study, in a first approach, we link overexpression of TSPO and inflammation in potentially prediabetic patients. In a second approach, we observed that TSPO deficient rats have higher level of insulin secretion in basal conditions and more IAPP fibrils formation compared with wild type animals. In a third approach, we show that diabetogenic conditions also increase TSPO overexpression and IAPP fibril formation in rat beta pancreatic cell line (INS-1E). These data open the way for further studies in the field of type 2 diabetes treatment or prevention.
dc.language.isoENen_US
dc.subject.enAmyloid proteins
dc.subject.enPancreas
dc.subject.enTSPO
dc.subject.enType 2 diabetes
dc.title.enTSPO in pancreatic beta cells and its possible involvement in type 2 diabetes
dc.typeArticle de revueen_US
dc.identifier.doi10.1016/j.biochi.2024.06.007en_US
dc.subject.halChimie/Matériauxen_US
dc.identifier.pubmed38908539en_US
bordeaux.journalBiochimieen_US
bordeaux.page104-113en_US
bordeaux.volume224en_US
bordeaux.hal.laboratoriesCBMN : Chimie & de Biologie des Membranes & des Nano-objets - UMR 5248en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionBordeaux INPen_US
bordeaux.institutionCNRSen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.popularnonen_US
hal.audienceInternationaleen_US
hal.exportfalse
dc.rights.ccCC BYen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Biochimie&rft.date=2024-06-20&rft.volume=224&rft.spage=104-113&rft.epage=104-113&rft.au=GUILLEMAIN,%20Ghislaine&KHEMTEMOURIAN,%20Lucie&BREHAT,%20Juliette&MORIN,%20Didier&MOVASSAT,%20Jamileh&rft.genre=article


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