Cytosolic, but not mitochondrial, oxidative stress likely contributes to cardiac hypertrophy resulting from cardiac specific GLUT4 deletion in mice

We hypothesized that oxidative stress may contribute to the development of hypertrophy observed in mice with cardiac specific ablation of the insulin sensitive glucose transporter gene (GLUT4, G4H-/-4 ). Measurements of oxidized glutathione (GSSG) in isolated mitochondria and whole heart homogenates were increased resulting in a lower ratio of reduced glutathione (GSH) to GSSG. Membrane translocation of the p67phox subunit of cardiac NOX2 was markedly increased in G4H-/- mice, suggesting elevated activity.