Additional factors that contribute to the development of diabetes by STZ are the decrease in the pancreatic GSH level with a corresponding increase in GSSG [35,39], and the inhibitory action of the diabetogenic agent on the activity of islet O-GlcNAcase, an enzyme that cleaves terminal β-O-GlcNAc residues from modified nucleocytoplasmic proteins acting as a glucose sensor [40,42]. This evidence concerns the gene OGA and diabetes mellitus.