The effect of insulin-stimulated pentose phosphate cycle activity on cellular glutathione content in rat adipocytes.
Insulin is known to stimulate intracellular H2O2 production in rat adipocytes. This H2O2 could in turn stimulate the pentose phosphate cycle by oxidizing GSH and shifting the redox state of the cells. However, insulin had no effects on cell GSH content or GSSG in buffer other than as related to changes in medium glucose. On the contrary, in the presence of an active pentose phosphate cycle, insulin tended to reverse the fall in glutathione content induced with the catalase inhibitor 3-amino-1,2,4-triazole, the oxidant t-butyl hydroperoxide and the sulfhydryl blocker N-ethylmaleimide. It was also found that insulin-stimulated H2O2 production could be blocked under conditions in which the effect of the hormone on the pentose phosphate cycle persisted. These results suggest that stimulation of the pentose phosphate cycle by insulin is not related to increased H2O2 generation, rather that activation of the pentose phosphate cycle by the hormone may provide NADPH for regeneration of depleted GSH.
D000273:Adipose Tissue / Q000032:analysis* / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D005978:Glutathione / Q000032:analysis*; D006861:Hydrogen Peroxide / Q000378:metabolism; D066298:In Vitro Techniques; D007328:Insulin / Q000494:pharmacology*; D008297:Male; D010428:Pentosephosphates / Q000378:metabolism*; D051381:Rats
D007328:Insulin; D010428:Pentosephosphates; D006861:Hydrogen Peroxide; D005978:Glutathione