Title : Insulin generates free radicals by an NAD(P)H, phosphatidylinositol 3'-kinase-dependent mechanism in human skin fibroblasts ex vivo.

Pub. Date : 2004 May

PMID : 15111505






4 Functional Relationships(s)
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1 Insulin treatment significantly increased intracellular superoxide anion (O(2)(-)) production, an effect completely abolished by Tiron, a cell-permeable superoxide dismutase (SOD) mimetic and by polyethylene glycol (PEG)-SOD, but not by PEG catalase. Superoxides insulin Homo sapiens
2 Furthermore, insulin-induced O(2)(-) production was attenuated by the NAD(P)H inhibitor apocynin, but not by rotenone or oxypurinol. Superoxides insulin Homo sapiens
3 Inhibition of the phosphatidylinositol 3"-kinase (PI 3"-kinase) pathway with LY294002 blocked insulin-stimulated O(2)(-) production, suggesting a direct involvement of PI 3"-kinase in the activation of NAD(P)H oxidase. Superoxides insulin Homo sapiens
4 In conclusion, these findings provided direct evidence that elevated insulin levels generate O(2)(-) by an NAD(P)H-dependent mechanism that involves the activation of PI 3"-kinase and stimulates ERK-1- and ERK-2-dependent pathways. Superoxides insulin Homo sapiens