The Role of Vitamin D in the Pathogenesis of NOD Mouse Diabetes

The existence of β-cell dysfunction and insulin resistance in vitamin D-deficient individuals on top of the demonstrated presence of receptors for 1,25-dihydroxyvitamin D3, the active metabolite of vitamin D, in pancreatic islet β- cells and immune cells have lead to scientific and clinical interest in vitamin D with respect to its potential role in the pathogenesis of type 1 diabetes. Also, its therapeutic potential in the prevention of type 1 diabetes has been studied, especially since the availability of synthetic analogues of the molecule that lack its calcemic effects. Solid evidence is available on the detrimental effects of vitamin D deficiency on insulin synthesis and secretion in animal models as well as in humans. Interventions with pharmacological doses of 1,25-dihydroxyvitamin D3 are able to delay onset of autoimmune diabetes in NOD mice mainly through immune modulation.