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Background  Accumulated evidence suggests that hydrogen peroxide (H 2 O 2 ) generated in cells during insulin stimulation plays an integral role in insulin receptor signal transduction. The role of insulin-induced H 2 O 2  in neuronal insulin receptor activation and the origin of insulin-induced H 2 O 2  in neurons remain unclear. The aim of the present study is to test the following hypotheses (1) whether insulin-induced H 2 O 2  is required for insulin receptor autophosphorylation in neurons, and (2) whether mitochondrial respiratory chain is involved in insulin-stimulated H 2 O 2  production, thus playing an integral role in insulin receptor autophosphorylation in neurons.    Results  Insulin stimulation elicited rapid insulin receptor autophosphorylation accompanied by an increase in H 2 O 2  release from cultured cerebellar granule neurons (CGN). N-acetylcysteine (NAC), a H 2 O 2  scavenger, inhibited both insulin-stimulated H 2 O 2  release and insulin-stimulated autophosphorylation of insulin receptor. Inhibitors of respiratory chain-mediated H 2 O 2  production, malonate and carbonyl cyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP), inhibited both insulin-stimulated H 2 O 2  release from neurons and insulin-stimulated autophosphorylation of insulin receptor. Dicholine salt of succinic acid, a respiratory substrate, significantly enhanced the effect of suboptimal insulin concentration on the insulin receptor autophosphorylation in CGN.    Conclusion  Results of the present study suggest that insulin-induced H 2 O 2  is required for the enhancement of insulin receptor autophosphorylation in neurons. The mitochondrial respiratory chain is involved in insulin-stimulated H 2 O 2  production, thus playing an integral role in the insulin receptor autophosphorylation in neurons.

bmc neuroscience

Mitochondrial respiratory chain is involved in insulin-stimulated hydrogen peroxide production and plays an integral role in insulin receptor autophosphorylation in neurons