Molecular Mechanisms Of Insulin Resistance.

dc.creatorSaad, M J
dc.date1994-Apr
dc.date2015-11-27T12:18:30Z
dc.date2015-11-27T12:18:30Z
dc.date.accessioned2018-03-29T00:51:17Z
dc.date.available2018-03-29T00:51:17Z
dc.identifierBrazilian Journal Of Medical And Biological Research = Revista Brasileira De Pesquisas Médicas E Biológicas / Sociedade Brasileira De Biofísica ... [et Al.]. v. 27, n. 4, p. 941-57, 1994-Apr.
dc.identifier0100-879X
dc.identifier
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/8087096
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/193783
dc.identifier8087096
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1294016
dc.description1. Insulin stimulates tyrosine phosphorylation of the insulin receptor and of an endogenous substrate of approximately 185 kDa (insulin receptor substrate 1 or IRS-1). IRS-1 fulfills the criteria of a direct substrate of the insulin receptor, and tyrosine phosphorylation of IRS-1 leads to another step in insulin action, i.e., an association of phosphorylated IRS-1 with the enzyme PI3-kinase activating this enzyme. Using antipeptide antibodies to insulin receptor, to IRS-1 and to PI 3-kinase together with anti-phosphotyrosine antibodies it is possible to study insulin-stimulated insulin receptor phosphorylation, IRS-1 phosphorylation and the association/activation of IRS-1/PI 3-kinase. 2. In this review we describe alterations in these three early steps of insulin action after binding in animal models of insulin resistance, i.e., streptozotocin-induced diabetes (STZ diabetes), fasting, spontaneously hypertensive rats, the ob/ob mice, dexamethasone-treated rats, and the chronic effect of insulin on Fao cells in culture. 3. In states of insulin resistance with hypoinsulinemia (STZ diabetes and fasting) there is an increase in these early steps of insulin action. In animal models of insulin resistance with hyperinsulinemia there is a decrease in these steps of insulin action, indicating molecular post-receptor defects. Since we could reproduce the decrease in these three early steps of insulin action in cells in culture by chronic treatment with insulin, we postulate that these defects may be a consequence of the hyperinsulinemia of these animals.
dc.description27
dc.description941-57
dc.languageeng
dc.relationBrazilian Journal Of Medical And Biological Research = Revista Brasileira De Pesquisas Médicas E Biológicas / Sociedade Brasileira De Biofísica ... [et Al.]
dc.relationBraz. J. Med. Biol. Res.
dc.rightsaberto
dc.rights
dc.sourcePubMed
dc.subjectAmino Acid Sequence
dc.subjectAnimals
dc.subjectDexamethasone
dc.subjectDiabetes Mellitus, Experimental
dc.subjectFasting
dc.subjectInsulin
dc.subjectInsulin Receptor Substrate Proteins
dc.subjectInsulin Resistance
dc.subjectLiver
dc.subjectMice
dc.subjectMolecular Sequence Data
dc.subjectMuscles
dc.subjectPhosphatidylinositol 3-kinases
dc.subjectPhosphoproteins
dc.subjectPhosphorylation
dc.subjectPhosphotransferases (alcohol Group Acceptor)
dc.subjectRats
dc.subjectRats, Inbred Shr
dc.subjectReceptor, Insulin
dc.subjectTyrosine
dc.titleMolecular Mechanisms Of Insulin Resistance.
dc.typeArtículos de revistas


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