Efeitos da sepse nas etapas iniciais da sinalização insulinica em ratos

AUTOR(ES)
DATA DE PUBLICAÇÃO

2001

RESUMO

Sepsis is known to induce insulin resistance, but the exact molecular mechanism involved is unknown. In the present study we have examined the levels and phosphorylation state of the insulin receptor and insulin receptor substrate 1 (IRS-l), as well as the association between IRS-l and phosphatidylinositol 3-kinase (pI 3-kinase) in the liver, muscle,heart and fat of septic rats by immunoprecipitation and immunoblotting with anti-insulin receptor, anti-IRS-l, anti-PI 3-kinase and anti-phosphotyrosine antibodies. There were no changes in the insulin receptor concentration and phosphorylation levels in any tissue of septic rats. IRS-l protein levels were decreased to 61 ±12%(p <0.05) in musclebut not in other tissues of septicrats. In samples previously immunoprecipitated with anti-IRS-l antibody and blotted with antiphosphotyrosine antibody, the insulin-stimulated IRS-l phosphorylation levels in the muscle of septic rats decreased to 59±9% (p <0.05) and insulin-stimulated IRS-l association with PI 3-kinase decreased to 56±7% in muscle(p <0.05), but no changes were seen in liver, heart or fato These data suggest that there is a tissue-specific regulation of early steps of insulin signal transduction in septic rats, and the changes observed in muscle may have a role in the insulin resistance of these animaIs.

ASSUNTO(S)

insulina - receptores fisiologia septcemia

ACESSO AO ARTIGO

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