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《The beta-3 adrenergic agonist (CL-316,243)restores the expression of down-regulated fattyacid oxidation genes in type 2 diabetic miceβ-3肾上腺素能激动剂（CL—316243） 下调下调脂肪的表达 2型糖尿病小鼠的酸氧化基因》由会员上传分享，免费在线阅读，更多相关内容在学术论文-天天文库。
1、Kumaretal.Nutrition&Metabolism(2015)12:8DOI10.1186/s12986-015-0003-8RESEARCHOpenAccessThebeta-3adrenergicagonist(CL-316,243)restorestheexpressionofdown-regulatedfattyacidoxidationgenesintype2diabeticmice1,2123*AmitKumar,JosephShiloach,MichaelJBetenbaughandEmilyJGa
2、llagherAbstractBackground:ThehallmarkofType2diabetes(T2D)ishyperglycemia,althoughtherearemultipleothermetabolicabnormalitiesthatoccurwithT2D,includinginsulinresistanceanddyslipidemia.ToadvanceT2Dpreventionanddeveloptargetedtherapiesforitstreatment,agreaterundersta
3、ndingofthealterationsinmetabolictissuesassociatedwithT2Disnecessary.Theaimofthisstudywastousemicroarrayanalysisofgeneexpressioninmetabolictissuesfromamousemodelofpre-diabetesandT2DtofurtherunderstandthemetabolicabnormalitiesthatmaycontributetoT2D.Wealsoaimedtounco
4、verthenovelgenesandpathwaysregulatedbytheinsulinsensitizingagent(CL-316,243)toidentifykeypathwaysandtargetgenesinmetabolictissuesthatcanreversethediabeticphenotype.Methods:MaleMKRmiceonanFVB/nbackgroundandagematchedwild-type(WT)FVB/nmicewereusedinallexperiments.Sk
5、eletalmuscle,liverandfatwereisolatedfromprediabetic(3weekold)anddiabetic(8weekold)MKRmice.MaleMKRmiceweretreatedwithCL-316,243.Skeletalmuscle,liverandfatwereisolatedafterthetreatmentperiod.RNAwasisolatedfromthemetabolictissuesandsubjectedtomicroarrayandKEGGdatabas
6、eanalysis.Results:SignificantdecreasesintheexpressionofmitochondrialandperoxisomalfattyacidoxidationgeneswerefoundintheskeletalmuscleandadiposetissueofadultMKRmice,andtheliverofpre-diabeticMKRmice,comparedtoWTcontrols.AftertreatmentwithCL-316,243,thecirculatingglu
7、coseandinsulinconcentrationsintheMKRmiceimproved,anincreaseintheexpressionofperoxisomalfattyacidoxidationgeneswasobservedinadditiontoadecreaseintheexpressionofretinaldehydedehydrogenases.ThesegeneswerenotpreviouslyknowntoberegulatedbyCL-316,243treatment.Conclusion
8、s:ThisstudyuncoversnovelgenesthatmaycontributetopharmacologicalreversalofinsulinresistanceandT2Dandmaybetargetsfortreatment.Inaddition,itexplainsthelowe
