Role of Vitamin D in Diabetes

Abstract

    The role of vitamin D in the pathogenesis and prevention of diabetes has sparked widespread interest. Vitamin D receptors are present in both pancreatic beta-cells and immune cells. Beside its classical role as the major regulator for calcium absorption, vitamin D mediates the activity of beta-cell calcium-dependent endopeptidases promotes conversion of proinsulin to insulin and increases insulin output. In peripheral insulin target tissues, vitamin D enhances insulin action via regulation of the calcium pool. Vitamin D also acts as a potent immunosuppressor. It tends to down-regulate the transcription of various proinflammatory cytokine genes like Interleukin-2, Interlukin-12 and Tumor Necrosis Factor-alpha. It promotes the induction of regulatory T-lymphocytes, the production of anti-inflammatory cytokines and protects beta-cell from destruction. Vitamin D deficiency predisposes to type 1 diabetes in animal models and in humans. It is probable that a similar relationship exists for type 2 diabetes. Vitamin D deficiency impairs insulin secretion and induces glucose intolerance. Several vitamin D related genes are associated with different pathogenetic traits of the disease. Vitamin D supplementation has shown to reduce the risk of developing type 1 diabetes. Vitamin D has also been shown to reduce the risk of diabetes associated complications. Prospective clinical studies on vitamin D are required to firmly establish the role of vitamin D in the prevention and management of diabetes.




 doi:10.4021/jem23w