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dc.contributor.CRUESPUniversidade Estadual de Campinaspt_BR
dc.typeArtigo de periódicopt_BR
dc.titleInsulin signalling pathways in aorta and muscle from two animal models of insulin resistance - the obese middle-aged and the spontaneously hypertensive ratspt_BR
dc.contributor.authorZecchin, HGpt_BR
dc.contributor.authorBezerra, RMNpt_BR
dc.contributor.authorCarvalheira, JBCpt_BR
dc.contributor.authorCarvalho-Filho, MApt_BR
dc.contributor.authorMetze, Kpt_BR
dc.contributor.authorFranchini, KGpt_BR
dc.contributor.authorSaad, MJApt_BR
unicamp.authorUniv Estadual Campinas, Fac Ciencias Med, Dept Clin Med, BR-13083970 Campinas, SP, Brazil Univ Estadual Campinas, Fac Ciencias Med, Dept Anat Patol, BR-13083970 Campinas, SP, Brazilpt_BR
dc.subjectagingpt_BR
dc.subjectobesitypt_BR
dc.subjectinsulin resistancept_BR
dc.subjectaortapt_BR
dc.subjectphosphatidylinositol 3-kinasept_BR
dc.subjectMAP kinasept_BR
dc.subjectAktpt_BR
dc.subjectendothelial cell-nitric oxide synthasept_BR
dc.subjectSHRpt_BR
dc.subject.wosNitric-oxide Productionpt_BR
dc.subject.wosPhosphatidylinositol 3-kinasept_BR
dc.subject.wosReceptor Substrate-1pt_BR
dc.subject.wosEndothelial-cellspt_BR
dc.subject.wosMesangial Cellspt_BR
dc.subject.wosProteinpt_BR
dc.subject.wosKinasept_BR
dc.subject.wosPhosphorylationpt_BR
dc.subject.wosStimulationpt_BR
dc.subject.wosSynthasept_BR
dc.description.abstractAims/hypothesis. The aim of this study was to investigate insulin signalling pathways directly in vivo in skeletal muscle and thoracic aorta from obese middle-aged (12-month-old) rats, which have insulin resistance but not cardiovascular disease, and from spontaneously hypertensive rats (SHR), an experimental model of insulin resistance and cardiovascular disease. Methods. We have used in vivo insulin infusion, followed by tissue extraction, immunoprecipitation and immunoblotting. Results. Obese middle-aged rats and the SHR showed marked insulin resistance, which parallels the reduced effects of this hormone in the insulin signalling cascade in muscle. In aortae from obese middle-aged rats, the PI 3-kinase/Akt pathway is preserved, leading to a normal,activation of endothelial nitric oxide synthase. In SHR this pathway is severely blunted, with reductions in eNOS protein concentration and activation. Both animals, however, showed higher concentrations and higher tyrosine phosphorylation of mitogen-activated protein (MAP) kinase isoforms in aortae. Conclusions/interpretation. Alterations in the IRS/PI 3-K/Akt pathway in muscle of 12-month-old rats and SHR could be involved in the insulin resistance of these animals. The preservation of this pathway in aorta of 12-month-old rats, apart from increases in MAP kinase protein concentration and activation, could be a factor that contributes to explaining the absence of cardiovascular disease in this animal model. However, in aortae of SHR, the reduced insulin signalling through IRS/PI 3-kinase/Akt/eNOS pathway could contribute to the endothelial dysfunction of this animal.pt
dc.relation.ispartofDiabetologiapt_BR
dc.relation.ispartofabbreviationDiabetologiapt_BR
dc.publisher.cityNew Yorkpt_BR
dc.publisher.countryEUApt_BR
dc.publisherSpringer-verlagpt_BR
dc.date.issued2003pt_BR
dc.date.monthofcirculationAPRpt_BR
dc.identifier.citationDiabetologia. Springer-verlag, v. 46, n. 4, n. 479, n. 491, 2003.pt_BR
dc.language.isoenpt_BR
dc.description.volume46pt_BR
dc.description.issuenumber4pt_BR
dc.description.firstpage479pt_BR
dc.description.lastpage491pt_BR
dc.rightsfechadopt_BR
dc.rights.licensehttp://www.springer.com/open+access/authors+rights?SGWID=0-176704-12-683201-0pt_BR
dc.sourceWeb of Sciencept_BR
dc.identifier.issn0012-186Xpt_BR
dc.identifier.wosidWOS:000183198600006pt_BR
dc.identifier.doi10.1007/s00125-003-1073-0pt_BR
dc.date.available2014-11-20T05:23:14Z
dc.date.available2015-11-26T17:15:04Z-
dc.date.accessioned2014-11-20T05:23:14Z
dc.date.accessioned2015-11-26T17:15:04Z-
dc.description.provenanceMade available in DSpace on 2014-11-20T05:23:14Z (GMT). No. of bitstreams: 1 WOS000183198600006.pdf: 679046 bytes, checksum: f9c9e9b314a513cc55c40558b0610e85 (MD5) Previous issue date: 2003en
dc.description.provenanceMade available in DSpace on 2015-11-26T17:15:04Z (GMT). No. of bitstreams: 2 WOS000183198600006.pdf: 679046 bytes, checksum: f9c9e9b314a513cc55c40558b0610e85 (MD5) WOS000183198600006.pdf.txt: 50168 bytes, checksum: fa740f16282c91a3bbf254c27e11bbb1 (MD5) Previous issue date: 2003en
dc.identifier.urihttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/60305pt_BR
dc.identifier.urihttp://www.repositorio.unicamp.br/handle/REPOSIP/60305
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/60305-
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