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Texto completo SciELO Chile
Boschero, Antonio C
Carneiro, Everardo M
Texto completo
Id: lil-608621
Autor: De Paula, Flávia MM; Boschero, Antonio C; Carneiro, Everardo M; Bosqueiro, José R; Rafacho, Alex.
Título: Insulin signaling proteins in pancreatic islets of insulin-resistant rats induced by glucocorticoid
Fonte: Biol. Res;44(3):251-257, 2011. ilus.
Idioma: en.
Resumo: Chronic administration of glucocorticoids induces insulin resistance that is compensated by an increase in p-cell function and mass. Since insulin signaling is involved in the control of p-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 (1mg/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 IRa-subunit, IRS-1, Shc, AKT, p-p70S6K, ERK1/2, p-ERK1/2, and glucocorticoid receptor protein levels were similar between DEX and CTL islets. However, the IRp-subunit, p-IRp-subunit, IRS-2, PI3-K, p-AKT and p70S6K 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.
Descritores: Dexametasona/efeitos adversos
Glucocorticoides/efeitos adversos
Resistência à Insulina
Proteínas Substratos do Receptor de Insulina/metabolismo
Insulina/metabolismo
Ilhotas Pancreáticas/efeitos dos fármacos
-Insulina
Ilhotas Pancreáticas/metabolismo
Ratos Wistar
Transdução de Sinais
Proteínas Adaptadoras da Sinalização Shc/metabolismo
Limites: Animais
Masculino
Ratos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME



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