Supporting the hypothesis that oxidative stress may be a significant factor in glucose intolerance, data from studies conducted in cell culture systems indicate that products of oxidative stress impair insulin-mediated translocation of GLUT4 in myotubes and adypocytes [21–23] and suppress gene transcription of adiponectin in adipocytes [24] and insulin in pancreatic β-cells [25]. This evidence concerns the gene INS and Glucose intolerance.