dc.contributorUniversidade Estadual Paulista (UNESP)
dc.creatorDe Paula, Flavia M. M.
dc.creatorBoschero, Antonio C.
dc.creatorCarneiro, Everardo M.
dc.creatorBosqueiro, José Roberto
dc.creatorRafacho, Alex
dc.date2014-05-20T13:26:07Z
dc.date2014-05-20T13:26:07Z
dc.date2011-01-01
dc.date.accessioned2017-04-05T20:04:35Z
dc.date.available2017-04-05T20:04:35Z
dc.identifierBiological Research. Santiago: Soc Biolgia Chile, v. 44, n. 3, p. 251-257, 2011.
dc.identifier0716-9760
dc.identifierhttp://hdl.handle.net/11449/8369
dc.identifierS0716-97602011000300006
dc.identifierWOS:000295952500006
dc.identifierS0716-97602011000300006-en.pdf
dc.identifierhttp://dx.doi.org/10.4067/S0716-97602011000300006
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/856747
dc.descriptionChronic administration of glucocorticoids induces insulin resistance that is compensated by an increase in beta-cell function and mass. Since insulin signaling is involved in the control of beta-cell function and mass, we investigated the content of insulin pathway proteins in pancreatic islets. Rats were made insulin resistant by daily administration of dexamethasone (1 mg/kg, b.w., i.p.) for 5 consecutive days (DEX), whilst control rats received saline (CTL). Circulating insulin and insulin released from isolated islets were measured by radioimmunoassay whereas the content of proteins was analyzed by Western blotting. DEX rats were hyperinsulinemic and exhibited augmented insulin secretion in response to glucose (P < 0.01). The IR alpha-subunit, IRS-1, Shc, AKT, p-p70(S6K), ERK1/2, p-ERK1/2, and glucocorticoid receptor protein levels were similar between DEX and CTL islets. However, the IR beta-subunit, p-IR beta-subunit, IRS-2, PI3-K, p-AKT and p70(S6K) protein contents were increased in DEX islets (P < 0.05). We conclude that IRS-2 may have a major role, among the immediate substrates of the insulin receptor, to link activated receptors to downstream signaling components related to islet function and growth in this insulin-resistant rat model.
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.languageeng
dc.publisherSoc Biolgia Chile
dc.relationBiological Research
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectdexamethasone
dc.subjectglucocorticoid
dc.subjectinsulin resistance
dc.subjectinsulin signaling
dc.subjectpancreatic islets
dc.titleInsulin signaling proteins in pancreatic islets of insulin-resistant rats induced by glucocorticoid
dc.typeOtro


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