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Published on: May 11, 2015
Vitamin D Receptor Overexpression in β-Cells Ameliorates Diabetes in Mice
Meritxell Morró1,2,3, Laia Vilà1,3, Sylvie Franckhauser1,3
1Center of Animal Biotechnology and Gene Therapy, Universitat Autònoma de Barcelona, Bellaterra, Spain.
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.
Insights
Vitamin D receptor (VDR) plays a crucial role in pancreatic beta-cells, protecting against diabetes. Maintaining VDR levels in beta-cells preserves their mass and function, offering protection from diabetes.
Area of Science:
- Endocrinology
- Molecular Biology
- Metabolic Diseases
Background:
- Vitamin D deficiency is linked to increased diabetes incidence in humans and animal models.
- Vitamin D receptor (VDR) gene polymorphisms are associated with diabetes, but its specific role in pancreatic beta-cells remains unclear.
Purpose of the Study:
- To investigate the role of the vitamin D receptor (VDR) in pancreatic beta-cells concerning the pathophysiology of diabetes.
- To elucidate the impact of VDR modulation on beta-cell function and diabetes development.
Main Methods:
- Studied VDR expression in pancreatic islets from healthy and diabetic mouse models (type 1 and type 2 diabetes).
- Utilized transgenic mice overexpressing VDR specifically in beta-cells.
- Assessed protection against streptozotocin-induced diabetes, beta-cell mass, and islet inflammation.
Main Results:
- VDR expression in islets was modulated by glucose and decreased in diabetic mouse models.
- Overexpression of VDR in beta-cells protected mice against streptozotocin-induced diabetes.
- VDR overexpression preserved beta-cell mass and reduced islet inflammation.
Conclusions:
- Sustained VDR levels in pancreatic beta-cells are critical for maintaining beta-cell mass and function.
- VDR in beta-cells plays a protective role against diabetes development.
- Targeting VDR may offer a therapeutic strategy for diabetes prevention and management.
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