Vitamin D Receptor Overexpression in β-Cells Ameliorates Diabetes in Mice
Meritxell Morró, Laia Vilà, Sylvie Franckhauser, Cristina Mallol, Gemma Elias, Tura Ferré, Maria Molas, Estefanía Casana, Jordi Rodó, Anna Pujol, Noèlia Téllez, Fátima Bosch, Alba Casellas
Abstract
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 β-cells, has not been elucidated yet. Here, we aimed to study the role of VDR in β-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 β-cells were protected against streptozotocin-induced diabetes and presented a preserved β-cell mass and a reduction in islet inflammation. Altogether, these results suggest that sustained VDR levels in β-cells may preserve β-cell mass and β-cell function and protect against diabetes.