Selenium and Diabetes

The relationship between selenium (Se) and diabetes remains an evolving field. Early studies were focused on antioxidant benefits of Se in diabetic animals and patients. However, the discovery of type 2 diabetes-like phenotype in the glutathione peroxidase (GPX) 1 overexpression mice and the pro-diabetic potential of Se supplementation in cancer subjects have provoked both research and public interests on its role in diabetes. Limited human data indicate a Se baseline--dependent risk for diabetes associated with Se supplementations: potentiating the risk for diabetes only in subjects with high-Se status. Among the 25 selenoproteins, GPX1 exhibits dual roles in insulin synthesis, secretion, and signaling via regulation of redox homeostasis, and selenoprotein P has the counteraction effect on insulin signaling. Both GPX3 and selenoprotein S may play roles in diabetic etiology via mediating inflammation. Dysregulations of the two endoplasmic reticulum (ER)resident selenoproteins, selenoproteins M and T, may disturb the redox homeostasis in ER, causing ER stress and increasing the diabetes risk. Iodothyronine deiodinases catalyze the metabolism of thyroid hormones and thus may affect the metabolism of glucose, lipids, and protein in the diabetic status. Polymorphism of selenoprotein genes in humans offers clues to the association of Se/selenoproteins and diabetes risk. In conclusion, effects of Se intake on the risk of diabetes are dose and baseline dependent. While underlying mechanisms for this paradox are partly understood through animal studies on the functions of several selenoproteins, appropriate Se intakes for the general public to prevent or treat diabetes warrant future research.