dc.creatorZecchin, HG
dc.creatorBezerra, RMN
dc.creatorCarvalheira, JBC
dc.creatorCarvalho-Filho, MA
dc.creatorMetze, K
dc.creatorFranchini, KG
dc.creatorSaad, MJA
dc.date2003
dc.dateAPR
dc.date2014-11-20T05:23:14Z
dc.date2015-11-26T17:15:04Z
dc.date2014-11-20T05:23:14Z
dc.date2015-11-26T17:15:04Z
dc.date.accessioned2018-03-29T00:03:19Z
dc.date.available2018-03-29T00:03:19Z
dc.identifierDiabetologia. Springer-verlag, v. 46, n. 4, n. 479, n. 491, 2003.
dc.identifier0012-186X
dc.identifierWOS:000183198600006
dc.identifier10.1007/s00125-003-1073-0
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/60305
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/60305
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/60305
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1281953
dc.descriptionAims/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.
dc.description46
dc.description4
dc.description479
dc.description491
dc.languageen
dc.publisherSpringer-verlag
dc.publisherNew York
dc.publisherEUA
dc.relationDiabetologia
dc.relationDiabetologia
dc.rightsfechado
dc.rightshttp://www.springer.com/open+access/authors+rights?SGWID=0-176704-12-683201-0
dc.sourceWeb of Science
dc.subjectaging
dc.subjectobesity
dc.subjectinsulin resistance
dc.subjectaorta
dc.subjectphosphatidylinositol 3-kinase
dc.subjectMAP kinase
dc.subjectAkt
dc.subjectendothelial cell-nitric oxide synthase
dc.subjectSHR
dc.subjectNitric-oxide Production
dc.subjectPhosphatidylinositol 3-kinase
dc.subjectReceptor Substrate-1
dc.subjectEndothelial-cells
dc.subjectMesangial Cells
dc.subjectProtein
dc.subjectKinase
dc.subjectPhosphorylation
dc.subjectStimulation
dc.subjectSynthase
dc.titleInsulin signalling pathways in aorta and muscle from two animal models of insulin resistance - the obese middle-aged and the spontaneously hypertensive rats
dc.typeArtículos de revistas


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