Insulin Signaling, Lipoproteins and Atherosclerosis
Insulin Signaling, Lipoproteins and Atherosclerosis
批准号:
7329715
负责人:
ALAN richard TALL
金额:
$55.25万
依托单位国家:
美国
项目类别:
财政年份:
2007
资助国家:
美国
项目状态:
已结题
起止时间:
2007-07-01 至 2012-06-30
关键词:
Apolipoproteins BApoptosisApoptoticAreaAtherosclerosisCD36 geneCaenorhabditis elegansCaloric RestrictionCellsCholesterolCollaborationsDataDiabetes MellitusEnzymesExclusionFailureFoam CellsGeneticGlucoseHepaticHepatocyteHistonesHyperinsulinismInduction of ApoptosisInsulinInsulin ReceptorInsulin ResistanceInsulin Signaling PathwayKnock-outLDL Cholesterol LipoproteinsLaboratoriesLeptinLesionLigationLinkLipoproteinsLiverLongevityLow-Density LipoproteinsMammalian CellMediatingMetabolicMetabolismModelingModificationMolecular TargetMusNecrosisNuclearNumbersOrthologous GenePeripheralPhosphorylationPlasmaPredispositionProtein OverexpressionProteinsReagentRegulationRoleSerumSignal PathwaySignal TransductionSirtuinsStimulusStressTLR4 geneTestingTransgenesVery low density lipoproteinWeekWorkbasebiological adaptation to stressdeprivationfeedingin vivoinsulin signalinginterestknock-downlipid biosynthesismacrophageoxidized low density lipoproteinresearch studyresponsescavenger receptortranscription factoruptake
中文摘要
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英文摘要
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of diabetes. In recent collaborative studies with the Tabas and Accili laboratories, we have shown that
Itmrancsrcorpiphtaiogneasl feroxmpreinssuiolin oref cCeDp3to6r a(InRd) SdeRfAic,ieinct rmeaicsedisupltaykedeofemctoivdeifieindsuLliDnLsiagndalincgr,eiansceredaseudscpeopstitb-ility
to apoptosis induced by FC loading and other stimuli. Apoptotic susceptibility is related to a failure to induce
IAinktot aLcDtiLvRity-/-dumrinceg trheesuEltRs isntrfeosrmsaretisopnoonfsea.dvAacnccoerdinlegslyio,nbsoncoenmtaainrrinogw itnracrnesapslaendtantuiomnbferorsmofIRapdoepfictoietinct mice
Idminecacrcerreaoaspsehedadgseaigsthneanrliondsgclalterhgroeosruigsnh.eTcprhoretiscuencrvoderedrslyh.ineIngpahtiycpoInRtvhse,rswsiseromefoftohduiesnl,dpLrtDojLehRcat-v/i-semtlhoiacweteinrwsVituhLliDnpLer/reLipsDhisLetarlaenlvceIRlswdaoenrfsidceinesncy and
Ifautrhtheerorsecvlearlousaiste, maceticnhganbiostmhsatlinthkeinlgevinesl uolfinthresviesstasneclewainll,mancdroaplshoaginetfhoeamlivecre.llTshteo parthopeorossacllwerilolsies,ekantod also
the relationship between insulin signaling in the liver and alterations in lipoprotein metabolism. In Aim 1we
Iwitllhcdoellafebcotrivaeteintosuilninvesigtingaltiengt.heInmpeacrthicaunliasrmwseawndill cdoentesremqiunencifedseocrfeinacsredasIRedsiagpnoaplintogsiasnidn lmowaecroApkhtaagcetsivity
leads to increased nuclear FoxO1/3 activity, increased ER stress/CHOP induction and apoptosis. In Aim 2
Iwleesiownilallemxtaecnrdopohuarginesvivinocrsetuadsiesmanadcrfouprhthaegreaxpoloprteosthiseahnydpoathesriosmthaactodmepfelecxtivtye. inRseullaintesdigsntuadliniegs in
Projects 1 and 3 will test the role of SRA and FoxOs in mediating these effects. In Aim 3 we will determine if
Idinecgreradsaetdionhewpiathtiicninthseulisnecsrigentoarlyinpgaltehawdasyt.oTdhecsreeaxspeedrhimepeantisc cFomxOpl1emacetnivtityhoasnedothf uPsroinjecrte3asexdamapinoinBg the
IipmropvaidcteonfehwepmatoiclecFuolxaOr i1nsoivgehrtsexipntroestshieoncaounsheespoaftidcialibpeidticanddysllipipoidperomteiainamndetiatsbovlaismcu.laTrhicsopmropjleicattimonasy.
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