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dc.contributor.authorhirschberg jensen, V
dc.contributor.authorAffourtit, C
dc.date.accessioned2015-07-09T08:10:24Z
dc.date.available2015-07-09T08:10:24Z
dc.date.issued2015-03-27
dc.identifier.issn2405-5808
dc.identifier.issn2405-5808
dc.identifier.urihttp://hdl.handle.net/10026.1/3416
dc.description.abstract

WehaverecentlyshownthatovernightexposureofINS-1Einsulinomacellstopalmitateinthepresence of highglucosecausesdefectsinbothmitochondrialenergymetabolismandglucose-stimulatedinsulin secretion (GSIS).Herewereportexperimentsdesignedtotesttheinvolvementofmitochondrial uncoupling protein-2(UCP2)intheseglucolipotoxiceffects.Measuringreal-timeoxygenconsumption in siRNA-transfectedINS-1Ecells,weshowthatdeleteriouseffectsofpalmitateontheglucosesensitivity of mitochondrialrespirationandonthecouplingefficiency ofoxidativephosphorylationareindepen- dent ofUCP2.Consistently,palmitateimpairsGSIStothesameextentincellswithandwithoutUCP2. Furthermore,weknockeddownUCP2inspheroidINS-1Ecellclusters(pseudoislets)totestwhetheror not UCP2regulatesinsulinsecretionduringprolongedglucoseexposure.Wedemonstratethatthereare no differencesintemporalGSISkineticsbetweenperifusedpseudoisletswithandwithoutUCP2.We conclude thatUCP2isnotinvolvedinpalmitate-inducedimpairmentofGSISinINS-1Einsulinomacells and isnotneededfortheamplification ofinsulinrelease.Theseconclusionsinformongoingdebateon the disputedbiochemicalandphysiologicalfunctionsofthebetacellUCP2.

dc.format.extent8-15
dc.format.mediumPrint
dc.languageen
dc.language.isoen
dc.publisherElsevier BV
dc.subjectBSA, bovine serum albumin
dc.subjectDAPI, 4′,6-diamidino-2-phenyl-indole
dc.subjectGSIS, glucose-stimulated insulin secretion
dc.subjectGlucolipotoxicity
dc.subjectGlucose-stimulated insulin secretion
dc.subjectMitochondrial dysfunction
dc.subjectNEFA, non-esterified fatty acid
dc.subjectPancreatic beta cells
dc.subjectPseudoislets
dc.subjectUCP, uncoupling protein
dc.subjectUncoupling protein-2 (UCP2)
dc.titleMitochondrialuncouplingprotein-2isnotinvolvedin palmitate-induced impairmentofglucose-stimulatedinsulinsecretion in INS-1Einsulinomacellsandisnotneededfortheamplification of insulin release
dc.typejournal-article
dc.typeArticle
plymouth.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/26339685
plymouth.issue1
plymouth.volume1
plymouth.publisher-urlhttp://dx.doi.org/10.1016/j.bbrep.2015.03.008
plymouth.publication-statusPublished
plymouth.journalBiochemistry and Biophysics Reports
dc.identifier.doi10.1016/j.bbrep.2015.03.008
plymouth.organisational-group/Plymouth
plymouth.organisational-group/Plymouth/Faculty of Health
plymouth.organisational-group/Plymouth/Faculty of Health/School of Biomedical Sciences
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA/UoA01 Clinical Medicine
plymouth.organisational-group/Plymouth/Research Groups
plymouth.organisational-group/Plymouth/Research Groups/Institute of Translational and Stratified Medicine (ITSMED)
plymouth.organisational-group/Plymouth/Research Groups/Institute of Translational and Stratified Medicine (ITSMED)/CBR
plymouth.organisational-group/Plymouth/Users by role
plymouth.organisational-group/Plymouth/Users by role/Academics
dc.publisher.placeNetherlands
dcterms.dateAccepted2015-03-19
dc.identifier.eissn2405-5808
dc.rights.embargoperiodNo embargo
rioxxterms.versionofrecord10.1016/j.bbrep.2015.03.008
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.typeJournal Article/Review
plymouth.funderWhy do pancreatic beta cells waste energy?::MRC


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