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- W2016089130 abstract "Insulin receptor substrate (IRS)-2 has been implicated in the promotion of β-cell survival. Here we tested the hypothesis that the novel analog [LysB3, GluB29] insulin (insulin glulisine, IG) might mediate an enhanced β-cell protective effect due to its unique property of preferential IRS-2 phosphorylation. We assessed IRS activation by IG and its anti-apoptotic activity against cytokines or palmitic acid in comparison to insulin, insulin analogs, and insulin-like growth factor (IGF)-I using INS-1 cells. IG induced a prominent IRS-2 activation without significant IRS-1 stimulation. The marked cytokine- and fatty acid-induced apoptosis was strongly (55–60%) inhibited by IG both at the level of caspase 3 activation and nucleosomal release, with only 15% inhibition of apoptosis by regular insulin. At 1 nM, insulin, insulin aspart, and insulin lispro were much less effective compared to IG. In conclusion, the prominent anti-apoptotic activity of insulin glulisine might serve to counteract autoimmune- and lipotoxicity-induced β-cell destruction." @default.
- W2016089130 created "2016-06-24" @default.
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- W2016089130 date "2003-10-01" @default.
- W2016089130 modified "2023-10-18" @default.
- W2016089130 title "[LysB3, GluB29] insulin: a novel insulin analog with enhanced β-cell protective action" @default.
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- W2016089130 doi "https://doi.org/10.1016/j.bbrc.2003.09.090" @default.
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