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Molecular Mechanisms of the Diabetogenic Effects of Arsenic: Inhibition of Insulin Signaling by Arsenite and Methylarsonous Acid

机译:砷致糖尿病作用的分子机制:砷和甲基亚砷酸抑制胰岛素信号传导

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摘要

Background Increased prevalences of diabetes mellitus have been reported among individuals chronically exposed to inorganic arsenic (iAs). However, the mechanisms underlying the diabetogenic effects of iAs have not been characterized. We have previously shown that trivalent metabolites of iAs, arsenite (iAsIII) and methylarsonous acid (MAsIII) inhibit insulin-stimulated glucose uptake (ISGU) in 3T3-L1 adipocytes by suppressing the insulin-dependent phosphorylation of protein kinase B (PKB/Akt).
机译:背景技术据报道,长期暴露于无机砷(iAs)的个体中,糖尿病的患病率上升。但是,尚未确定iA的致糖尿病作用的潜在机制。先前我们已经证明iAs,亚砷酸盐(iAs III )和甲基亚砷酸(MAs III )的三价代谢物会抑制3T3-L1脂肪细胞中胰岛素刺激的葡萄糖摄取(ISGU)通过抑制胰岛素依赖性蛋白激酶B(PKB / Akt)的磷酸化。

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