Endocrinology Diabetes


A large number of pre-clinical and clinical studies have shown the relationship between a variety of free radical disorders and insufficient levels of glutathione (GSH). Recently published data imply that diabetic complications result from hyperglycemic episodes that promote oxidation of cellular enzymes and thus inactivate glutathione (GSH) synthesis pathways. The result is GSH deficiency in diabetics, which alters the homeostasis of the redox system (GSH / GSSG), explaining the appearance of cataracts, hypertension, occlusive atherosclerosis, and susceptibility to infections in these patients (1,2).