Morró, MeritxellVilà Prats, LaiaFranckhauser, SylvieMallol, CristinaElias, GemmaFerré Masferrer, TuraMolas Laplana, MariaCasana, EstefaníaRodó Tomás, JordiPujol, AnnaTéllez, NoèliaBosch i Tubert, FàtimaCasellas, Alba2025-01-222025-01-2220200012-1797https://hdl.handle.net/2445/217807Vitamin 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 b-cells, has not been elucidated yet. Here, we aimed to study the role of VDR in b-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 b-cells were protected against streptozotocin-induced diabetes and presented a preserved b-cell mass and a reduction in islet inflammation. Altogether, these results suggest that sustained VDR levels in b-cells may preserve b-cell mass and b-cell function and protect against diabetes13 p.application/pdfengcc-by-nc-nd (c) American Diabetes Association, 2020http://creativecommons.org/licenses/by-nc-nd/4.0/DiabetisVitamina DDiabetesVitamin Dinfo:eu-repo/semantics/article7524632025-01-22info:eu-repo/semantics/openAccess