Brain Transcriptional Responses to High-Fat Diet in Acads-Deficient Mice Reveal Energy Sensing Pathways 英文参考文献.docVIP

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Brain Transcriptional Responses to High-Fat Diet in Acads-Deficient Mice Reveal Energy Sensing Pathways 英文参考文献.doc

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Brain Transcriptional Responses to High-Fat Diet in Acads-Deficient Mice Reveal Energy Sensing Pathways 英文参考文献

BrainTranscriptionalResponsestoHigh-FatDietin Acads-DeficientMiceRevealEnergySensingPathways ClaudiaKruger1,K.GaneshKumar1¤,RandallL.Mynatt1,JuliaVolaufova2,BrendaK.Richards1* 1PenningtonBiomedicalResearchCenter,LouisianaStateUniversitySystem,BatonRouge,Louisiana,UnitedStatesofAmerica,2SchoolofPublicHealth,LouisianaState UniversityHealthSciencesCenter,NewOrleans,Louisiana,UnitedStatesofAmerica Abstract Background:Howsignalsfromfattyacidmetabolismaretranslatedintochangesinfoodintakeremainsunclear.Previously we reported that mice with a genetic inactivation of Acads (acyl-coenzyme A dehydrogenase, short-chain), the enzyme responsibleformitochondrialbeta-oxidationofC4–C6short-chainfattyacids(SCFAs),shiftconsumptionawayfromfatand towardcarbohydratewhenofferedachoicebetweendiets.Inthecurrentstudy,wesoughttoindentifycandidategenes andpathwaysunderlyingtheeffectsofSCFAoxidationdeficiencyonfoodintakeinAcads2/2mice. Methodology/PrincipalFindings:WeperformedatranscriptionalanalysisofgeneexpressioninbraintissueofAcads2/2 andAcads+/+ mice fedeither ahigh-fat (HF)or low-fat (LF) diet for2d.Ingenuity Pathway Analysis revealedthree top- scoring pathways significantly modified by genotype or diet: oxidative phosphorylation, mitochondrial dysfunction, and CREBsignalinginneurons.AcomparisonofstatisticallysignificantresponsesinHFAcads2/2vs.HFAcads+/+(3917)and Acads+/+HFvs.LFAcads+/+(3879)revealed2551genesorapproximately65%incommonbetweenthetwoexperimental comparisons.Allbutoneofthesegeneswereexpressedinoppositedirectionwithsimilarmagnitude,demonstratingthat HF-fedAcads-deficientmice displaytranscriptionalresponsesthatstronglyresemblethoseof Acads+/+mice fedLFdiet. Intriguingly, genes involved in both AMP-kinase regulation and the neural control of food intake followed this pattern. QuantitativeRT-PCRinhypothalamusconfirmedthedysregulationofgenesinthesepathways.Westernblottingshowedan increaseinhypothalamicAMP-kinaseinAcads2/2miceandHFdietincreased,akeyproteininanenergy-sensingca