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• W2022790546 abstract "Proinflammatory cytokines are well-known to inhibit insulin signaling to result in insulin resistance. IL-1α is also one of the proinflammatory cytokines, but the mechanism of how IL-1α induces insulin resistance remains unclear. We have now examined the effects of IL-1α on insulin signaling in 3T3-L1 adipocytes. Prolonged IL-1α treatment for 12 to 24 hours partially decreased the protein levels as well as the insulin-stimulated tyrosine phosphorylation of IRS-1 and Akt phosphorylation. mRNA for SOCS3, an endogenous inhibitor of insulin signaling, was dramatically augmented 4 hours after IL-1α treatment. Concomitantly, the level of IL-6 in the medium and STAT3 phosphorylation were increased by the prolonged IL-1α treatment. Addition of anti-IL-6 neutralizing antibody to the medium or overexpression of dominant-negative STAT3 decreased the IL-1α-stimulated STAT3 activation and SOCS3 induction, and ameliorated insulin signaling. These results suggest that the IL-1α-mediated deterioration of insulin signaling is largely due to the IL-6 production and SOCS3 induction in 3T3-L1 adipocytes." @default.
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• W2022790546 date "2008-01-01" @default.
• W2022790546 modified "2023-10-04" @default.
• W2022790546 title "Long-term Interleukin-1α Treatment Inhibits Insulin Signaling via IL-6 Production and SOCS3 Expression in 3T3-L1 Adipocytes" @default.
• W2022790546 doi "https://doi.org/10.1055/s-2007-1004515" @default.
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