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1、www.biochemj.orgBiochem.J.(2010)425,1326(PrintedinGreatBritain)doi:10.1042/BJ2009118113REVIEWARTICLEMolecularmechanismsofmetabolicregulationbyinsulininDrosophilaAurelioA.TELEMAN1GermanCancerResearchCenter(DeutschesKrebsforschungszentrum),ImNeuenheimerFeld580,69
2、120Heidelberg,GermanyTheinsulinsignallingpathwayishighlyconservedfrommam-andcontrastingwiththemammaliansystem.IdiscussboththemalstoDrosophila.Insulinsignallinginthefly,asinmammals,intracellularsignallingnetwork,aswellasthecommunicationregulatesanumberofphysiolog
3、icalfunctions,includingcarbo-betweenorgansinthefly.hydrateandlipidmetabolism,tissuegrowthandlongevity.Inthepresentreview,IdiscussthemolecularmechanismsbywhichKeywords:Akt,Drosophilametabolism,insulinsignalling,targetinsulinsignallingregulatesmetabolisminDrosophi
4、la,comparingofrapamycin(TOR),totalbodyglucose,totalbodylipid.INTRODUCTIONINSULINMEDIATESMUCHOFTHENUTRIENT-DEPENDENTSIGNALLINGINDROSOPHILAInthepastdecade,DrosophilahasbeenoneoftheimportantmodelsystemsforstudyingtheinsulinandIGF(insulin-likeTwosetsofobservationss
5、upporttheconclusionthatmostofthegrowthfactor)/TOR(targetofrapamycin)signallingpathwaynutrientsensinginDrosophilatakesplaceviatheinsulinpathway.(Figure1).Forinstance,somecomponentsofthepathwaysuchFirst,mutationsincomponentsoftheinsulinpathwayphenocopyasRheb,Tsc1
6、(tuberoussclerosiscomplex1)andTsc2(tuberoustheeffectsofnutrientdeprivation.Forinstance,mutationofsclerosiscomplex2)werefirstplacedintotheTORpathwayinthethekinaseTORphenocopiesaminoaciddeprivation,leadingfly[1–5].Suchworkhasbeensupportedbythepowerfulgenetictoabloc
7、kintissuegrowth,reducednucleolarsizeandcelltoolsavailableinDrosophila,allowingresearcherstoquicklycyclearrestdespitethepresenceofnutrients[8].Asanothergenerateloss-of-functionanimalstoquerygenefunction,andexample,reductioninS6K[RPS6(ribosomalproteinS6)-p70-epis
8、tasisexperimentstoquerygenerelationships,bothofwhichproteinkinase]activityintheDrosophilabrainleadstosimilararefundamentalforelucidatingsignallingnetworks.changesinfeedingbe
