Mitochondrialuncouplingprotein-2isnotinvolvedin palmitate-induced impairmentofglucose-stimulatedinsulinsecretion in INS-1Einsulinomacellsandisnotneededfortheamplification of insulin release
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2015-03-27Author
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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.
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