&&&deoxyribonucleic acid 在 有机化工 分类中
的翻译结果:
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&&&&Determination of Deoxyribonucleic Acid with Methylene Blue
by a Resonance Light-Scattering Method
&&&&亚甲基蓝共振光谱散射法测定脱氧核糖核酸
&&&&Analysis of Oxidative Deoxyribonucleic Acid Damage Marker,
8-Hydroxy-2′-deoxyguanosine,by High Performance
Liquid Chromatography with Electrochemical Detection
&&&&高效液相色谱-电化学检测法测定脱氧核糖核酸分子氧化损伤标志物8-羟基脱氧鸟苷
&&&&Determination of Deoxyribonucleic Acid with Acridine Orange by Resonance Light Scattering Technique
&&&&吖啶橙共振光散射法测定脱氧核糖核酸
&&&&The fluorescence spectra of 9-(3-aminoanilino)acridine(B2,m-APAA) with Deoxyribonucleic acid(DNA) has been studied, so a fluorescent method for the determination of DNA
&&&&对9-(3-氨基苯胺基)吖啶(B_2，简称m-APAA)与脱氧核糖核酸(DNA)作用的荧光光谱进行了研究，拟定了测定DNA的分析方法，探讨了反应机理，实验了最佳条件、干扰实验。
&&&&Using chelator
2 as the oxidative source of Fenton type reaction,reacting with calf thymus deoxyribonucleic acid (DNA) in vitro model. The yielded, 8
deoxyguanosine (8
OhdG), was analyzed by high performance liquid chromatography with electrochemical detection.
&&&&采用螯合剂 Fe2 + H2 O2 作为Fenton型反应的氧化源 ,与小牛胸腺脱氧核糖核酸反应生成 8 羟基脱氧鸟苷 ( 8 OhdG) ,建立脱氧核糖核酸 (DNA)分子氧化损伤的体外反应模型 ,用高效液相色谱 电化学检测方法对 8 OhdG进行定量。
&&&&Under optimal conditions, the calibration graphs are linear over the range of 0.09～9.00 mg/L for calf thymus
deoxyribonucleic acid (CT
DNA), 0.01～12.5 mg/L for fish sperm (FT)
DNA and 0.30～35 mg/L for yeast DNA respectively.
&&&&在最佳实验条件下,测定的线性范围分别为:小牛胸腺 (CT DNA) 0. 09 ~9mg/L; 鱼精DNA(FS DNA)0. 01~12. 5mg/L;
&&&&The fluorescence spectra of m-APAA with Deoxyribonucleic acid(DNA)was studied. It was shown that DNA has ability to quench the m-APAA fluorescence in 418 nm(λ_(ex)=256 nm),and the quenched intensity of fluorescence is proportional to the concentration DNA.
&&&&研究了该物质与DNA作用的荧光光谱,随着DNA的加入观察到418nm(λex=256nm)处的荧光峰猝灭,且其猝灭程度与DNA的浓度成正比,据此拟定了测定DNA的分析方法。 实验了最佳条件,干扰实验,确定了反应机理。
&&&&DETERMINATION OF PERCENTAGE OF GUANINE PLUS CYTOSINE IN DEOXYRIBONUCLEIC ACID BY USING 751-G SPECTROPHOTOMETER
&&&&使用国产仪器测定细菌DNA的GC百分含量的初步研究
&&&&Spetral Study on Biacridine Derivatives Interaction with Deoxyribonucleic Acid
&&&&双吖啶衍生物与核酸作用的光谱分析
&&&&Fluorescence Enhancing Method for the Determination of Deoxyribonucleic Acid with Bipyridyl-Cu(Ⅱ)? Complex
&&&&联吡啶-铜(Ⅱ)络合物荧光增强法测定核酸
查询“deoxyribonucleic acid”译词为用户自定义的双语例句&&&&我想查看译文中含有：的双语例句
为了更好的帮助您理解掌握查询词或其译词在地道英语中的实际用法，我们为您准备了出自英文原文的大量英语例句，供您参考。&&&&&&&&&&&&&&&&&&&& A simple method was described in detail for determining the percentage of guanine ( G ) plus cytosine ( C ) in Deoxyribonucleic Acid by using 751-G Spectrophotometer which did not have a Constant Temperature Water Circulation Device. The DMA samples were heated and equilibrated about 10 min at each selected temperature by JY-501 Constant Temperature Instrument. After heating, the optical desities of DNA samples at each temperature were read at 260 nm and divided by the value at 30℃. &&&&&&&&&&&&本文详细描述了一种测定脱氧核糖核酸(简称DNA)中鸟嘌吟(简称G)加胞嘧啶(简称C)百分含量的方法。将DNA样品分装于数支试管内,一起置于JY-501型超级恒温器中,加热至不同的预选温度并恒温10min,每次恒温后取出一支样品立即冰浴。然后测定其在260nm的吸收值。绘出温度与相对增色值之间的关系曲线,确定DNA的变性温度(Tm)并计算GC百分含量。对DNA的变性过程进行了电泳检查。本方法结果与前人报告的结果基本相符。&&&&&&&& The imaging mode and the development of tip technologies of atomic
force microscopy (AFM) are briefly surveyed. A review of the application of AFM in studying the structures
of biological macromolecules including deoxyribonucleic acid (DNA), proteins, polysaccharides etc. is presented. And the future prospect
of AFM in this field is outlooked. &&&&&&&&&&&&评述了原子力显微镜（ａｔｏｍｉｃ　ｆｏｒｃｅ　ｍｉｃｒｏｓｃｏｐｙ，ＡＦＭ）的成镜模式与探针技术的发展以及在脱氧核糖核酸、蛋白质和多糖等生物大分子结构研究中的应用进展，并展望了原子力显微镜在此领域的发展前景&&&&&&&& The resonance light
scattering (RLS) of methylene blue (MB) is greatly enhanced by deoxyribonucleic acid (DNA) in the pH range of 5.5～7.5. The enhanced intensity of RLS at 350 nm is proportional to the concentration of DNA in the range of 0.2～1.4×10
g/mL. The detection limit is 15×10
g/mL. This method is simple, rapid, It has been applied to the determination of DNA in synthetic sample with satisfactory results. &&&&&&&&&&&&基于脱氧核糖核酸 (DNA)对有机染料亚甲基蓝的共振光散射的增强效应 ,拟定了一种测定DNA的共振光散射法。在pH5.5～ 7.5范围内 ,亚甲基蓝在 350nm处的共振光散射增强与DNA浓度呈线性关系 ,线性范围为 2 0 0～ 140 0 μg L ,检出限可达 15μg L。该方法简便、快速 ,用于合成样品中DNA的测定 ,结果令人满意。&nbsp&&&&&&&&相关查询:
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Copyright (C) , .License: ICP NO.:Zhejiang ICPdeoxyribonucleic acid是什么意思_百度知道
deoxyribonucleic acid是什么意思
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The error: watson and crick discovered dna ( deoxyribonucleic acid)deoxyribonucleic acid脱氧核糖核酸 deoxyribonucleic acid脱氧核糖核酸. 误解; 例句:1：沃森和克里克发现了dna（脱氧核糖核酸）
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出门在外也不愁Deoxyribonucleic Acid Methylation and Gene04
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Deoxyribonucleic Acid Methylation and Gene04
ORIGINALEndocrine；ARTICLEResearch；DeoxyribonucleicAcidMeth；CharlotteBr?ns,*StineJac；StenoDiabetesCenter(C.B.；Context:Lowbirthweight(L；Design,Subjects,andMainO；Results:Whenchallenge
ORIGINALEndocrineARTICLEResearchDeoxyribonucleicAcidMethylationandGeneExpressionofPPARGC1AinHumanMuscleIsInfluencedbyHigh-FatOverfeedinginaBirth-Weight-DependentMannerCharlotteBr?ns,*StineJacobsen,*EmmaNilsson,TinaRo¨nn,ChristineB.Jensen,HeidiStorgaard,PernillePoulsen,LeifGroop,CharlotteLing,ArneAstrup,andAllanVaagStenoDiabetesCenter(C.B.,S.J.,E.N.,C.B.J.,H.S.,P.P.,A.V.),Type2DiabetesPathophysiology,2820Gentofte,DDepartmentofHumanNutrition(C.B.,A.A.),FacultyofLifeSciences,UniversityofCopenhagen,1958Frederiksberg,DandDepartmentofClinicalSciences(T.R.,L.G.,C.L.,A.V.),DiabetesandEndocrinologyResearchUnit,LundUniversity,Malmo¨UniversityHospital,S-20502Malmo¨,SwedenContext:Lowbirthweight(LBW)andunhealthydietsareriskfactorsofmetabolicdiseaseincludingtype2diabetes(T2D).Genetic,nongenetic,andepigeneticdataproposearoleofthekeymetabolicregulatorperoxisomeproliferator-activatedreceptor?,coactivator1?(PPARGC1A)inthedevelopmentofT2D.Objective:OurobjectivewastoinvestigategeneexpressionandDNAmethylationofPPARGC1Aandcoregulatedoxidativephosphorylation(OXPHOS)genesinLBWandnormalbirthweight(NBW)subjectsduringcontrolandhigh-fatdiets.Design,Subjects,andMainOutcomeMeasures:TwentyyounghealthymenwithLBWand26matchedNBWcontrolswerestudiedafter5dhigh-fatoverfeeding(?50%calories)andafteracontroldietinarandomizedmanner.Hyperinsulinemic-euglycemicclampswereperformedandskeletalmusclebiopsiesexcised.DNAmethylationandgeneexpressionweremeasuredusingbisulfitesequencingandquantitativereal-timePCR,respectively.Results:Whenchallengedwithhigh-fatoverfeeding,LBWsubjectsdevelopedperipheralinsulinresistanceandreducedPPARGC1AandOXPHOS(P?0.05)geneexpression.PPARGC1Amethyl-ationwassignificantlyhigherinLBWsubjects(P?0.0002)duringthecontroldiet.However,PPARGC1AmethylationincreasedinonlyNBWsubjectsafteroverfeedinginareversiblemanner.DNAmethylationofPPARGC1AdidnotcorrelatewithmRNAexpression.Conclusions:LBWsubjectsdevelopedperipheralinsulinresistanceanddecreasedgeneexpressionofPPARGC1AandOXPHOSgeneswhenchallengedwithfatoverfeeding.TheextenttowhichourfindingofaconstitutivelyincreasedDNAmethylationinthePPARGC1ApromoterinLBWsubjectsmaycon-tributeneedstobedetermined.WeprovidethefirstexperimentalsupportinhumansthatDNAmethylationinducedbyoverfeedingisreversible.(JClinEndocrinolMetab95:10)Individualsbornwithlowbirthweight(LBW)areatin-creasedriskofdevelopinginsulinresistance,type2diabetes(T2D),andthemetabolicsyndromelaterinlife(1).WehavepreviouslyidentifiednumerousmetabolicabnormalitiesrelevanttothepathophysiologyofT2Dinhealthy,youngLBWmenincludingimpairedinsulin-stim-Abbreviations:BMI,BFFA,LBW,NBW,OXPHOS,oxidT2D,type2diabetes.ISSNPrintXISSNOnlinePrintedinU.S.A.Copyright?2010byTheEndocrineSocietydoi:10.1210/jc.ReceivedNovember11,2009.AcceptedMarch18,2010.FirstPublishedOnlineApril21,2010*C.B.andS.J.contributedequallytothiswork.3048jcem.endojournals.orgJClinEndocrinolMetab,June):JClinEndocrinolMetab,June):ulatedglucoseuptakeintheforearmmuscle(2),decreasedwhole-bodyinsulin-stimulatedglycolyticflux(3),hepaticinsulinresistance(3),andchangesinmuscleandfatinsu-lin-signalingproteins(4,5).Theincreaseddiseasesuscep-tibilityinLBWsubjectshaslongbeenspeculatedtoin-volveepigeneticprogramminginutero,andrecentstudieshaveprovidedpreliminaryevidenceofaconnectionbe-tweenmaternalnutritionandhealthononesideandofDNAmethylationintheoffspringontheother(6C8).OneofthebestcharacterizedepigeneticmechanismsisDNAmethylation,whichmayaffectgeneexpression(9)andgenomestability(10).DNAmethylationsoccurthroughoutthegenomebutaremostlystudiedandthoughttobeimportantatCpGdinucleotides,whicharefoundinhighdensitiesandoftenunmethylatedingenepromoters,referredtoasCpGislands(11).DNAmethy-lationsareinfluencedbyenvironmentalfactorsasevidentbydivergingepigeneticpatternswithincreasingageinmonozygotictwinpairs(12),higherDNAmethylationofcytochrome-c-oxidasesubunitVIIapolypeptide1(COX7A1)(13),andNADHdehydrogenase-1?subcom-plex,6(NDUFB6)inoldcomparedwithyoungsubjects(14)andbyagenerallyhigherDNAmethylationwitholderageofCpGislandsacrossmultipletissues(15).Decreasedexpressionofperoxisomeproliferator-acti-vatedreceptor-?,coactivator-1?(PPARGC1A)maycauseinsulinresistancebyinterferingwithmultiplekeycellularfunctionsincludingmitochondrialfunction(16),lipidoxidation(17),angiogenesis,andmicrovascularflow(18)aswellasoxidativestress(19).PPARGC1Amayalsoplayaroleinregulationofpancreaticinsulinsecretion(20).DecreasedexpressionofPPARGC1Aandoxidativephosphorylation(OXPHOS)genesinskeletalmusclehasbeenobservedinsome(16,21,22),butnotall(23),studiesofT2Dpatients.Recentstudieshaveshownincreasedpro-moterDNAmethylationanddecreasedgeneexpressionofPPARGC1Ainbothpancreaticislets(20)andskeletalmusclebiopsies(24)frompatientswithT2D.Importantly,wehavefoundthatdecreasedexpressionofPPARGC1AinskeletalmuscleisassociatedwithLBWinelderly,butnotyoung,twins(25).AnotherrecentstudyshowedthatmaternalobesityisassociatedwithDNAmethylationofPPARGC1AincordbloodfromthenewbornoffspringpointingtowardapotentialkeyroleofPPARGC1Ameth-ylationinprogrammingofobesity,T2D,andthemeta-bolicsyndrome(6).Recentstudieshavesuggestedthatepigenetictraitsareinfluencedbydifferentdietaryconditionsandinterven-tionsincludingcalorierestrictioninhumans(26).Studiesinrodentshaveshownthathigh-fatdietsincreaseDNAmethylationoftheleptinpromoter(27)andprolongthepresenceofDNAmethylationinliverandlungtissueafterjcem.endojournals.org3049treatmentwithacarcinogenicagent(28,29).AstudyofhumanskeletalmusclecellculturesshowedahigherdegreeofmethylationofPPARGC1Awhenincubatedwithfreefattyacids(FFA)(24).Interestingly,sustainedcellularexposuretosaturatedfattyacids(30)aswellas3dintakeofahigh-fatdietresultedinreducedexpressionofPPARGC1Ainyoungmen(31).WehypothesizedthatyoungandhealthyLBWmenexhibitalteredDNAmethylationinthepromoterregionofPPARGC1Ainskeletalmuscleasaresultoffetalpro-grammingresemblingthatseeninpatientswithovertT2D.TounmaskmetabolicabnormalitiespotentiallyconferringsusceptibilitytoT2DinLBWsubjects,LBWaswellasnormalbirthweight(NBW)subjectswerestudiedbothduringacontroldietaswellasafterexposuretoadiethighinfatandcaloriesfora5-dperiod.SubjectsandMethodsSubjectsTwenty-sixhealthy,young,leanmalevolunteerswithLBW(?10thpercentile)and20subjectswithNBW(50C90thpercen-tile)wererecruitedaspreviouslydescribed(2C4,32).Allsubjectswerebornatterm,andthegroupswerematchedaccordingtoageandbodymassindex(BMI).Thesubjectshadnofamilyhistoryofdiabetesintwogenerations,andsubjectswithaBMIhigherthan30kg/m2orahighphysicalactivitylevel(?10h/wk)wereexcluded.ControlinvivodataincludingmuscleOXPHOSgeneexpressionandmetabolicresponsestohigh-fatoverfeedinginNBWsubjects(notinLBWsubjects)werepublishedpreviously(3,33).TheprotocolconformedtotheDeclarationofHelsinkiandwasapprovedbytheethicscommitteeforCopenhagenCounty,andallsubjectssignedaninformedconsentform.ExperimentalprotocolThestudywasarandomizedcrossoverstudy,withawashoutperiodof6C8wk,aspreviouslyreportedfortheNBWcontrolsubjects(33).Inbrief,subjectswereexaminedtwicewithahy-perinsulinemic-euglycemicclampafterintakeofa3-dcontroldietincluding30%fat(mean11.9?1.1MJ)andaftera5-dhigh-fatoverfeedingdiet(mean17.6?1.4MJ)containing50%extracaloriesand60%fat.Hyperinsulinemic-euglycemicclampTheclampwasperformedandanalyzedaspreviouslyde-scribed(3).Aprimedcontinuousinfusionoftritiated[3-3H]glu-cosewasinitiatedat0h,andaninsulininfusionof80mU/m2?minwasusedthroughoutthe180-minclamptomaintaineuglycemia.Glucoseandfatoxidationratesweremeasuredbyindirectcalorimetry(34),andbasalandinsulin-stimulatedbi-opsieswereexcisedfrommusculusvastuslateralisin35ofthe46subjectsusingaBergstro¨mneedle.Thetissuewasimmediatelyfrozeninliquidnitrogenandstoredat?80C.Bodycompositionwasassessedbydual-energyx-rayabsorptiometryscanning(Lu-narRadiation,Madison,WI).3050Br?nsetal.TranscriptionofPPARGC1AinYoungMenJClinEndocrinolMetab,June):Quantitativereal-time-PCRTotalRNAwasextractedfromthemusclebiopsiesusingTRIreagent(Sigma-Aldrich,St.Louis,MO).cDNAwassynthesizedusingQuantiTectreversetranscriptionkit(QIAGEN,Valencia,CA).mRNAlevelsweredetectedwiththeABI7900sequencedetectionsystem(AppliedBiosystems,FosterCity,CA)usinggene-specificprobe/primerpairsforNDUFB6(Hs),ubiquinol-cytochromecreductasebindingprotein(UQCRB)(Hs),COX7A1(Hs),ATPsynthase,H?transporting,mitochondrialF1complex,Osubunit(ATP5O)(Hs),andPPARGC1A(Hs)(Ap-pliedBiosystems).Allsampleswereruninduplicateandthestan-dardcurveapproachusedforquantification.Thetranscriptquan-titywasnormalizedtomRNAlevelsofcyclophilinA(PPIA)(4326316E;AppliedBiosystems).DNAmethylationGenomicDNAwasextractedcollectivelywithRNAfrommus-clebiopsiesandpartitionedintoaseparatefractionforfurtherprocessing.BisulfiteconversionwascompletedusingtheEZDNAmethylationkit(ZymoResearch,Orange,CA)andamplifiedusingforwardandreverseprimersdesignedbyMethPrimer(35).ThePPARGC1ApromotersequencecontainsfourCpGsitesandisidenticaltothatstudiedbyLingetal.(20)in?-cellsfromT2Dpatientsandwaslocated624C867bpupstreamfromthetran-scriptionstartandamplifiedusingforwardprimer5?-TATTTTA-AGGTAGTTAGGGAGGAAA-3?andreverseprimer5?-CCCATAACAATAAAAAATACCAACTC-3?(Fig.1A).WeincludedNDUFB6asacontrolgenebecauseitisnotdirectlyinvolvedintranscriptionalactivities,isreducedinT2D,andispossiblyregulatedbyepigeneticfactors(14).TheNDUFB6sequencewaslocated392C611bpupstreamfromthetranscrip-tionstartandamplifiedwithforwardprimer5?-GTTGTTTTTT-GATTGTTGTATTATAATTTA-3?andreverseprimer5?-AAAATACCCTAAACAACTATCTCAT-3?.TheNDUFB6sequencecontainsthreeCpGsitesandonepolymorphismcreatingapossiblemethylationsite(rs629566,A/G).Theampliconswerevisualizedafterelectrophoresisthrougha2%ethidiumbro-mide-stainedagarosegel.SmallfragmentswereremovedbyExoSAP-ITtreatment(USBCorp.,Cleveland,OH).DNAwasprecipitatedwithethanolandsequencingPCRper-formedusingBigDyeTerminatorversion3.1cyclesequenc-ingkit(AppliedBiosystems).ThesamplesweresequencedwiththeABI3130xlgeneticanalyzer(AppliedBiosystems).TracefilesweresubjecttoqualitycontrolandanalysisusingtheESMEsoftware(Epigenomics,Berlin,Germany)(Fig.1B)(36).StatisticalanalysisStatisticalanalyseswereperformedwithSASStatisticalAnal-ysisPackage(SASInstitute,Cary,NC;version8.2).NormalitywasevaluatedbyKolmogorov-Smirnov’stestandnormalityplots.Dataarepresentedasmean?SDorSEM,wheneverappro-priate.Basalandinsulin-stimulatedgeneexpressionwascom-binedbecausenoeffectofinsulinongeneexpressionwasob-served.Two-sidedStudent’sttestwasusedtoidentifysignificantdifferencesbetweenNBWandLBWsubjects(unpaired)andbe-tweendiets(paired).P?0.05wasconsideredsignificant.Cor-relationswerecalculatedusingPearson’scorrelationcoefficient.FIG.1.SequencingofasubsetofthePPARGC1Apromoter.A,VisualizationofthespecificsectionofthepromoterregionofPPARGC1A,whichwassequenced,stretchingfrom?624to?867upstreamofthetranscriptionstart(arrow).ThefourCpGsitesinvestigatedaremarkedwithaperpendicularline.B,ESMEoutputfileofmethylationsitesanddegreeofmethylation(site?841,17%;site?816,16%;andsite?783,11%,respectively)inthePPARGC1Apromoter.Thesamplesequenceisalignedtoagenomicdatabasereferencesequence.Methylationsitesareidentifiedbyunconvertedcytosine(C)basesinthesamplesequence.JClinEndocrinolMetab,June):TABLE1.SubjectcharacteristicsoftheNBWandLBWgroupsatbaseline(controldiet)NBWLBWBirthweight(g)?269Age(yr)24.6?1.024.2?0.5Height(m)1.83?0.071.77?0.05bWeight(kg)78.3?9.177.7?10.9BMI(kg/m2)23.4?2.424.8?3.7Trunkfatmass/total0.50?0.040.53?0.04afatmass(g)Legfatmass/total0.37?0.040.34?0.03afatmass(g)Trunkfatmass/total1.09?0.181.23?0.17afatmass(%)Dataaremean?SD.a-cNBW(n?26)vs.LBW(n?20):aP?0.05;bP?0.01;cP?0.001.Interactionofbirthweightanddietwasinvestigatedbyanormalmixedmodel.ESMEanalysissoftwareversion3.2.1(Epigenom-ics,Berlin,Germany)wasemployedinqualitycontrolandanal-ysisofthemethylationdata.Inbrief,ESMEalignthebisulfiteconvertedsequencetoareferencesequenceandprovidesanav-eragedegreeofmethylationateachCpGsiteaccordingtothefluorescentsignaldetectedfrommethylatedandunmethylatedcytosines.ThemeanmethylationsobtainedforthesameCpGsiteusingforwardandreverseprimerswereusedtoexpresstheCpGsite-specificdegreeofmethylation.ResultsSubjectscharacteristicsTheLBWsubjectsweresmalleratbirth,hadasignifi-cantlylowerfinalheight,andweremoreabdominallyobesecomparedwithNBWsubjects(Table1),whichisinaccordancewithpreviousfindings(3).Weightandbodycompositionwerenotaffectedbyoverfeeding(datanotshown).InvivometabolismTheLBWsubjectshadelevatedfastingglucoseandin-sulinlevelscomparedwithNBWsubjectsonthecontroldiet(Table2).Inresponsetohigh-fatoverfeeding,bothgroupshadsignificantlyincreasedfastingbloodglucoseandC-peptidelevels(NBWonly)anddecreasedFFAlev-els,whereastherewerenochangesinseruminsulin.Aspreviouslypublished,LBWandNBWsubjectshadasim-ilardegreeofperipheralinsulinaction(M-value)afterthecontroldiet(3).Likewise,basalandinsulin-stimulatedratesofwhole-bodyfatandglucoseoxidation(Table2)andhepaticglucoseproductionweresimilarinthetwogroupsonthecontroldiet(3).Nevertheless,incontrasttotheNBWsubjects(33),theLBWsubjectsdevelopedasignificantdeteriorationofperipheralinsulinaction(Ta-ble2),whenexposedto5daysofoverfeeding.Moreover,jcem.endojournals.org3051TABLE2.Invivodatafromthehyperinsulinemic-euglycemicclampexaminationincludingglucose,insulin,andC-peptideconcentrationsandmetabolicfluxdataafterthecontrolandoverfeedingdietDietNBWLBWFasting(baseline)Bloodglucose(mmol/liter)Control4.59?0.464.96?0.46aOverfeeding5.05?0.40c5.18?0.33bSeruminsulin(pmol/liter)Control30.9?14.140.7?14.4aOverfeeding43.4?29.242.9?18.8SerumC-peptide(pmol/liter)Control408?Overfeeding521?269b530?174PlasmaFFA(mmol/liter)Control334?Overfeeding205?82c188?91cGlucoseoxidation(mg/kgFFM?min)Control2.41?0.831.96?0.74Overfeeding2.43?0.902.20?0.56Fatoxidation(mg/kgFFM?min)Control0.98?0.391.12?0.51Overfeeding0.94?0.391.17?0.33aInsulinstimulated(clamp)Bloodglucose(mmol/liter)Control5.11?0.315.06?0.30Overfeeding5.17?0.305.07?0.30Seruminsulin(pmol/liter)Control870?Overfeeding867?SerumC-peptide(pmol/liter)Control406?Overfeeding453?PlasmaFFA(mmol/liter)Control9.3?4.49.6?4.8Overfeeding12.4?6.414.4?7.8bM-value(mg/kgFFM?min)Control13.73?2..98Overfeeding13.29?3..57bGlucoseoxidation(mg/kgFFM?min)Control5.18?0.804.89?0.93Overfeeding4.83?1.344.74?0.82Fatoxidation(mg/kgFFM?min)Control0.02?0.250.14?0.44Overfeeding0.15?0.290.37?0.34a,bDataaremean?SDandareshownforNBW(n?26)vs.LBW(n?20)subjects.FFM,Fat-freemass.aSignificantdifferencesbetweenNBWandLBWsubjectsatP?0.05.b,cPairedcomparisonsbetweencontrolandoverfeedingincluden?25(NBW)andn?18(LBW)subjects.Significantdifferencesbetweenthecontrolandoverfeedingdietareindicatedasfollows:bP?0.05;cP?0.001.theLBWsubjectsshowedanincreasedrateofinsulin-stimulatedfatoxidationafteroverfeeding,whichwasalsohigherthantheNBWsubjectsduringboththecontrolandoverfeedingdiet.Inotherwords,thehigh-fatoverfeeding3052Br?nsetal.TranscriptionofPPARGC1AinYoungMenJClinEndocrinolMetab,June):A1.81.61.41.21.00.80.60.40.20.0B1.81.61.41.21.00.80.60.40.20.0p=0.02mRNA/PPIAmRNA/PPIANDUFB6UQCRBCOX7A1ATP50PPARGC1ANDUFB6UQCRBCOX7A1ATP50PPARGC1ACmRNA/PPIA1.81.61.41.21.00.80.60.40.20.0p=0.04D1.81.61.4mRNA/PPIA1.21.00.80.60.40.20.0NDUFB6UQCRBCOX7A1ATP50PPARGC1ANDUFB6UQCRBCOX7A1ATP50PPARGC1AFIG.2.PPARGC1AandOXPHOSgeneexpressionnormalizedtoPPIAinNBW(white)andLBW(hatched)subjectsduringcontrol(grey)andoverfeeding(black)diets.A,GeneexpressioninNBW(n?21)andLBW(n?17)subjectsduringthecontroldiet.B,GeneexpressioninNBW(n?21)andLBW(n?13)subjectsduringoverfeeding.CandD,EffectofoverfeedingongeneexpressionwithintheNBW(C)(n?20)andtheLBW(D)(n?13)subjects.Dataaremean?SEM.challengeunmaskedaselectiveriskofdevelopinginsulinresistanceandelevatedfatoxidationinonlytheLBWsubjects.GeneexpressionTheNBWandLBWsubjectshadsimilargeneexpres-siononthecontroldiet(Fig.2A).Whenexposedtohigh-fatoverfeeding,mRNAlevelsofNDUFB6,UQCRB,andATP5O(allP?0.02)aswellasofPPARGC1A(P?0.05)weresignificantlylowerbyapproximately25%inskeletalmusclefromLBWcomparedwithNBWsubjects(Fig.2B).AsimilartrendwasobservedforCOX7A1(P?0.12)(Fig.2B).ThedifferencearoseastheNBWsubjectsshowedatrendtowardhigherexpressionaftertheover-feedingdiet,beingstatisticallysignificantonlyforNDUFB6(P?0.04)(Fig.2C),whereastheLBWsubjectsremainedunchangedwithatendencytowarddecreasedexpression(Fig.2D).Thedietaryinterventionwasper-formedinarandomizedcrossovermanner,enablingustodocumentreversibilityofchangesofgeneexpressionin-ducedbythehigh-fatdiet.Wewere,however,unabletoidentifyanyreversibilityofgeneexpressioninducedbytheoverfeedingdietofeitherPPARCG1AorOXPHOSgenes(datanotshown).OXPHOSgenesareconsideredtobetightlyregulatedbyPPARGC1A,whichwassupportedbysignificantpositivecorrelationsbetweenPPARGC1AandtheOXPHOSgenesduringboththecontrol(r?0.56C0.83,P?0.01)andoverfeeding(r?0.50C0.63;P?0.01)diets.Aspreviouslypublished(3),skeletalmus-clePPARGC1AandOXPHOSmRNAexpressionwassimilarinthetwogroupsduringthecontroldiet(Fig.2A).ThegeneexpressionlevelofPPARGC1AaswellasoftheOXPHOSgenedidnotcorrelatewithwhole-bodyinsulinaction(M-value)orwiththeratesofglucoseorfatoxi-dation,asassessedduringeitherthebasalortheinsulin-stimulatedstate.DNAmethylationDNAmethylationwasinvestigatedinthepromoterre-gionofPPARGC1AatfourCpGsites(Fig.1A).ThemeanDNAmethylationwassignificantlyhigherintheLBWthanNBWsubjectsafterthecontroldiet(P?0.0002).ThedifferencesbetweenNBWandLBWsubjectsweresignificantatthreeCpGsitesduringthecontroldiet(Fig.3A)(site?841:32%,P?0.05;site?816:59%,P?0.001;site?783:59%,P?0.008;site?652:41%,P?0.42).MeasuresofthefourthCpGsite(?652)wereobtainedforonlyhalfofthesubjects,resultinginalesspowerfulanalysis.Whenexposedtooverfeeding,meth-ylationofPPARGC1AincreasedintheNBWonly,andthedifferencesbetweenthegroupsweresubsequentlyat-tenuated(Fig.3B).Thechangeinmethylationduringover-feedinginNBWsubjectsreachedstatisticalsignificancefortwoCpGsites(site?841:30%,P?0.01;site?816:31%,P?0.10;site?783:43%,P?0.008;site?652:6%,P?0.93)(Fig.3C).TheLBWsubjectsshowedsimilarPPARGC1Amethylationduringthetwodiets(Fig.3D).WheninvestigatingthereversibilityoftheDNAmethyl-包含各类专业文献、文学作品欣赏、高等教育、应用写作文书、行业资料、幼儿教育、小学教育、各类资格考试、Deoxyribonucleic 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