Vitamin D Receptor overexpression in β-cells ameliorates diabetes in mice.

Vitamin D deficiency has been associated with increased incidence of diabetes, both in humans and in animal models. In addition, an association between vitamin D receptor (VDR) gene polymorphisms and diabetes has also been described. However, the involvement of VDR in the development of diabetes, specifically in pancreatic beta-cells, has not been elucidated yet. Here, we aimed to study the role of VDR in beta-cells in the pathophysiology of diabetes. Our results indicate that Vdr expression was modulated by glucose in healthy islets and decreased in islets from both type 1 diabetes and type 2 diabetes mouse models. In addition, transgenic mice overexpressing VDR in beta-cells were protected against streptozotocin-induced diabetes and presented a preserved beta-cell mass and a reduction in islet inflammation. Altogether, these results suggest that sustained VDR levels in beta-cells may preserve beta-cell mass and beta-cell function and protect against diabetes.