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, Fàtima Bosch, Alba Casellas*

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

17 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)927-939
Number of pages13
Issue number5
Publication statusPublished - 1 May 2020


Dive into the research topics of 'Vitamin D receptor overexpression in β-cells ameliorates diabetes in mice'. Together they form a unique fingerprint.

Cite this