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

pre-printWe 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