Mitochondrialuncouplingprotein-2isnotinvolvedin palmitate-induced impairmentofglucose-stimulatedinsulinsecretion in INS-1Einsulinomacellsandisnotneededfortheamplification of insulin release
dc.contributor.author | hirschberg jensen, V | |
dc.contributor.author | Affourtit, Charles | |
dc.date.accessioned | 2015-07-09T08:10:24Z | |
dc.date.available | 2015-07-09T08:10:24Z | |
dc.date.issued | 2015-03-27 | |
dc.identifier.issn | 2405-5808 | |
dc.identifier.issn | 2405-5808 | |
dc.identifier.uri | http://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.extent | 8-15 | |
dc.format.medium | ||
dc.language | en | |
dc.language.iso | en | |
dc.publisher | Elsevier BV | |
dc.subject | BSA, bovine serum albumin | |
dc.subject | DAPI, 4′,6-diamidino-2-phenyl-indole | |
dc.subject | GSIS, glucose-stimulated insulin secretion | |
dc.subject | Glucolipotoxicity | |
dc.subject | Glucose-stimulated insulin secretion | |
dc.subject | Mitochondrial dysfunction | |
dc.subject | NEFA, non-esterified fatty acid | |
dc.subject | Pancreatic beta cells | |
dc.subject | Pseudoislets | |
dc.subject | UCP, uncoupling protein | |
dc.subject | Uncoupling protein-2 (UCP2) | |
dc.title | Mitochondrialuncouplingprotein-2isnotinvolvedin palmitate-induced impairmentofglucose-stimulatedinsulinsecretion in INS-1Einsulinomacellsandisnotneededfortheamplification of insulin release | |
dc.type | journal-article | |
dc.type | Article | |
plymouth.author-url | https://www.ncbi.nlm.nih.gov/pubmed/26339685 | |
plymouth.issue | 1 | |
plymouth.volume | 1 | |
plymouth.publication-status | Published | |
plymouth.journal | Biochemistry and Biophysics Reports | |
dc.identifier.doi | 10.1016/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.place | Netherlands | |
dcterms.dateAccepted | 2015-03-19 | |
dc.identifier.eissn | 2405-5808 | |
dc.rights.embargoperiod | No embargo | |
rioxxterms.versionofrecord | 10.1016/j.bbrep.2015.03.008 | |
rioxxterms.licenseref.uri | http://www.rioxx.net/licenses/all-rights-reserved | |
rioxxterms.type | Journal Article/Review | |
plymouth.funder | Why do pancreatic beta cells waste energy?::MRC |