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Cell type-specific deletion in mice reveals roles for PAS kinase in insulin and glucagon production

dc.relation.isnodouble321e18cf-ef58-4b90-bad3-d6c147b73f34*
dc.relation.isnodouble66858f25-2364-4afc-81b3-e7b4d71b457c*
dc.relation.isnodouble00f003ca-a279-4ddc-91a2-85b889507c5d*
dc.contributor.authorSEMPLICI, F.
dc.contributor.authorMONDRAGON, A.
dc.contributor.authorMACINTYRE, B.
dc.contributor.authorMADEYSKI-BENGSTON, K.
dc.contributor.authorPERSSON-KRY, A.
dc.contributor.authorBARR, S.
dc.contributor.authorRAMNE, A.
dc.contributor.authorMARLEY, A.
dc.contributor.authorMCGINTY, J.
dc.contributor.authorFRENCH, P.
dc.contributor.authorSOEDLING, H.
dc.contributor.authorYOKOSUKA, R.
dc.contributor.authorGAITAN, Julien
dc.contributor.authorLANG, J.
dc.contributor.authorMIGRENNE-LI, S.
dc.contributor.authorPHILIPPE, E.
dc.contributor.authorHERRERA, P. L.
dc.contributor.authorMAGNAN, C.
dc.contributor.authorDA SILVA XAVIER, G.
dc.contributor.authorRUTTER, G. A.
dc.date.accessioned2020-09-03T07:56:07Z
dc.date.available2020-09-03T07:56:07Z
dc.date.issued2016
dc.identifier.issn0012-186x
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/10824
dc.description.abstractEnAIMS/HYPOTHESIS: Per-Arnt-Sim kinase (PASK) is a nutrient-regulated domain-containing protein kinase previously implicated in the control of insulin gene expression and glucagon secretion. Here, we explore the roles of PASK in the control of islet hormone release, by generating mice with selective deletion of the Pask gene in pancreatic beta or alpha cells. METHODS: Floxed alleles of Pask were produced by homologous recombination and animals bred with mice bearing beta (Ins1 Cre; PaskBKO) or alpha (Ppg Cre [also known as Gcg]; PaskAKO) cell-selective Cre recombinase alleles. Glucose homeostasis and hormone secretion in vivo and in vitro, gene expression and islet cell mass were measured using standard techniques. RESULTS: Ins1 Cre-based recombination led to efficient beta cell-targeted deletion of Pask. Beta cell mass was reduced by 36.5% (p < 0.05) compared with controls in PaskBKO mice, as well as in global Pask-null mice (38%, p < 0.05). PaskBKO mice displayed normal body weight and fasting glycaemia, but slightly impaired glucose tolerance, and beta cell proliferation, after maintenance on a high-fat diet. Whilst glucose tolerance was unaffected in PaskAKO mice, glucose infusion rates were increased, and glucagon secretion tended to be lower, during hypoglycaemic clamps. Although alpha cell mass was increased (21.9%, p < 0.05), glucagon release at low glucose was impaired (p < 0.05) in PaskAKO islets. CONCLUSIONS/INTERPRETATION: The findings demonstrate cell-autonomous roles for PASK in the control of pancreatic endocrine hormone secretion. Differences between the glycaemic phenotype of global vs cell type-specific null mice suggest important roles for tissue interactions in the control of glycaemia by PASK.
dc.language.isoen
dc.title.enCell type-specific deletion in mice reveals roles for PAS kinase in insulin and glucagon production
dc.title.alternativeDiabetologia
dc.typeArticle de revue
dc.identifier.doi10.1007/s00125-016-4025-1
dc.subject.halChimie/Matériaux
bordeaux.journalDiabetologia
bordeaux.page1938-1947
bordeaux.volume59
bordeaux.hal.laboratoriesInstitut de Chimie & de Biologie des Membranes & des Nano-objets (CBMN) - UMR 5248*
bordeaux.hal.laboratoriesInstitut de Chimie & de Biologie des Membranes & des Nano-objets (CBMN, UMR 5248)
bordeaux.issue9
bordeaux.institutionUniversité de Bordeaux
bordeaux.institutionBordeaux INP
bordeaux.COinSctx_ver=Z39.88-2004&amp;rft_val_fmt=info:ofi/fmt:kev:mtx:journal&amp;rft.jtitle=Diabetologia&amp;rft.date=2016&amp;rft.volume=59&amp;rft.issue=9&amp;rft.spage=1938-1947&amp;rft.epage=1938-1947&amp;rft.eissn=0012-186x&amp;rft.issn=0012-186x&amp;rft.au=SEMPLICI,%20F.&amp;MONDRAGON,%20A.&amp;MACINTYRE,%20B.&amp;MADEYSKI-BENGSTON,%20K.&amp;PERSSON-KRY,%20A.&amp;rft.genre=article


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