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1、糖皮质激素影响肉仔鸡骨骼肌脂肪代谢的机制研究treatments:1μMDEX,100nMinsulin,1μMDEX+100nMinsulinorcontrolfor2hours.Althoughnotstatisticsignificantly,DEXinducedtheincreasedmRNAlevelofAMPKα2andL-CPT1,whiledecreasedmTORexpression.ThemRNAlevelofAMPKα和L-CPT1weredown-regulatedbyinsulin.Whencellswe
2、retreatedbycooperationofDEXandinsulin,mRNAlevelofAMPKα2andL-CPT1wereretarded,whilemTORexpressionwasup-regulated.TheresultshowedthatfattyacidoxidationinmyoblastswasimprovedbyDEX,whiledecreasedbyinsulin.ThecooperationofDEXandinsulininducedtheretardedlipidutilizationinch
3、ickenskeletammuscle.ThepathwayofglucocorticoidsandinsulinregulatinglipidmetabolisminchickenmyoblastMyoblastswaspreparedfromSPFchickenembryos(11-dold),thensubjectedtofollowingtreatments:1μMDEX,10μMAMPKinhibitor,100nMinsulin,20μMAKTinhibitororcontrolfor12hours.Theexpres
4、sionsofGR,AMPKa2andL-CPT1wereelevatedwhilemTORwasdecreasedbyDEX,andrestoredtonormalbyAMPKinhibitor,exceptforGR.AKT1expressionwasnotaffectedbyDEX,butitsexpressionwasenhancedbyAMPKinhibitor.InsulininducedtheincreasedAKT1andmTORtranscriptionandtendedtodecreaseAMPKa2mRNAl
5、evel,andtheyallrestoredtonormalbyAKTinhibitor.TheresultsshowedthatDEXmediatedmyoblastlipidmetabolismthroughregulationofAMPKandmTOR,independentofAKT,whileinsulinexertitseffectviaAKT-mTORandAKT-AMPK-mTORpathway.Inconclusion,glucocorticoidsadministrationdistributeslipidt
6、oaccumulation,ratherthanutilization.Glucocorticoidsmaypromoteintramyocellularlipidaccumulationbyincreasedfattyaciddenovosynthesisandavailabilitytotissue,inturnthedecreasedcellularAMP:ATPratio.Thefollowingdown-regulatedAMPKinducestheactivemTORsignal,finallytheretardedl
7、ipidoxidation.TheelevatedcirculatinginsulinimprovesAKT1pathway,butnotassociatedwithmTORactivation.TheinvitroresultsshowthatglucocorticoidsaloneincreasefataccumulationthroughregulationofAMPKandmTOR,independentofAKT,whileinsulinexertsitseffectviaAKT-mTORandAKT-AMPK-mTOR
8、pathway.Keywords:Broilerchickens;Fattyaciduptake;Fattyacidoxidation;Glucocorticoids;Skeletalmuscle6PDF文件使用"pdfFactoryPro"试用版
