胰岛素信号传导、脂蛋白和动脉粥样硬化-猫眼课题宝

胰岛素信号传导、脂蛋白和动脉粥样硬化

批准号：

7329715

负责人：

ALAN richard TALL

金额：

$55.25万

依托单位：

COLUMBIA UNIVERSITY HEALTH SCIENCES

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

来源：

https://reporter.nih.gov/project-details/7329715

关键词：

Apolipoproteins B Apoptosis Apoptotic Area Atherosclerosis CD36 gene Caenorhabditis elegans Caloric Restriction Cells Cholesterol Collaborations Data Diabetes Mellitus Enzymes Exclusion Failure Foam Cells Genetic Glucose Hepatic Hepatocyte Histones Hyperinsulinism Induction of Apoptosis Insulin Insulin Receptor Insulin Resistance Insulin Signaling Pathway Knock-out LDL Cholesterol Lipoproteins Laboratories Leptin Lesion Ligation Link Lipoproteins Liver Longevity Low-Density Lipoproteins Mammalian Cell Mediating Metabolic Metabolism Modeling Modification Molecular Target Mus Necrosis Nuclear Numbers Orthologous Gene Peripheral Phosphorylation Plasma Predisposition Protein Overexpression Proteins Reagent Regulation Role Serum Signal Pathway Signal Transduction Sirtuins Stimulus Stress TLR4 gene Testing Transgenes Very low density lipoprotein Week Work base biological adaptation to stress deprivation feeding in vivo insulin signaling interest knock-down lipid biosynthesis macrophage oxidized low density lipoprotein research study response scavenger receptor transcription factor uptake

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中文摘要

翻译

IAmtehcehroasncislemrostiacrevapsocourlayrudnisdearsteooisd.aImnsaujloinr与oartbthideitycealnludladrelaevthelincaduiasbeestemsa，的关系不同于传统的管理方式糖尿病的症状。在最近与Tabas和Accili实验室的合作研究中，我们表明 [中英文摘要][晓雨-0920交稿]这是一种新的rmeaicsedisupltaykedeofemctoivdeifieindsuLliDnLsiagndalincgr，检测方法。对Fc负荷等刺激诱导的细胞凋亡有明显的抑制作用。细胞凋亡的易感性与未能诱导 Iinktot aLcDtiLvRity-/-哑巴isntrfeosrmsaretisopnoonfsea.dvAacnccoerdinlegslyio，nbsoncoenmtaainrrinogw itnracrnesapslaendtantuiomnbferorsmofIRapdoepfictoietinct小鼠 Idminecacrcerreaoaspsehedadgseaigsthneanrliondsgclalterhgroeosruigsnh.eTcprhoretiscuencrvoderedrslyh.ineIngpahtiycpoInRtvhse，rswsiseromefoftohduiesnl、dpLrtDojLehRcat-v/i-semtlhoiacweteinrwsVituhLliDnpLer/reLipsDhisLetarlaenlvceIRlswdaoenrfsidceinesncy和如果他们或安全的话，他们可能会受到威胁，他们也会受到威胁，也会受到威胁。肝脏胰岛素信号与脂蛋白代谢改变的关系。在AIM 1WE中 Iwitllhcdoellafebcotrivaeteintosuilninvesigtingaltiengt.heInmpeacrthicaunliasrmwseawndill cdoentesremqiunencifedseocrfeinacsredasIRedsiagpnoaplintogsiasnidn ImowaecroApkhtaagcetty 导致核FoxO1/3活性增加，内质网应激/CHOP诱导和细胞凋亡增加。在AIM 2 Iwleesiownilallemxtaecnrdopohuarginesvivinocrsetuadsiesmanadcrfouprhthaegreaxpoloprteosthiseahnydpoathesriosmthaactodmepfelecxtivtye.在RseullaintsDigstuadlinegs中项目1和3将测试SRA和FoxO在调节这些影响方面的作用。在目标3中，我们将确定 Idinecgreradsaetdionhewpiathtiicninthseulisnecsrigentoarlyinpgaltehawdasyt.oTdhecsreeaxspeedrhimepeantisc cFomxOpl1emacetnivtiyasnedothofuPsroinrte3asexDamapinoinBg IipmropvaidcteonfehwepmatoiclecFuolxaor i1nsoivgehrtsexipntroestshieoncaounsheespoaftidcialibpeidticanddysllipipoidperomteiainamndetiatsbovlaismcu.laTrhicsopmropjleicattimonasy.

英文摘要

IAmtehcehroasncislemrostiacrevapsocourlayrudnisdearsteooisd.aImnsaujloinr creasuisetaonfcme oartbthideitycealnludladrelaevthelincaduiasbeestemsa,nbyutotfhteheucnodmerplylicnagtions 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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