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β 细胞中维生素 D 受体过表达可改善小鼠糖尿病。

Vitamin D Receptor Overexpression in β-Cells Ameliorates Diabetes in Mice.

机构信息

Center of Animal Biotechnology and Gene Therapy, Universitat Autònoma de Barcelona, Bellaterra, Spain.

Department of Biochemistry and Molecular Biology, Universitat Autònoma de Barcelona, Bellaterra, Spain.

出版信息

Diabetes. 2020 May;69(5):927-939. doi: 10.2337/db19-0757. Epub 2020 Feb 21.

DOI:10.2337/db19-0757
PMID:32086292
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7171966/
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 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.

摘要

维生素 D 缺乏与糖尿病的发病率增加有关，无论是在人类还是在动物模型中。此外，维生素 D 受体 (VDR) 基因多态性与糖尿病之间也存在关联。然而，VDR 在糖尿病的发展中，特别是在胰岛β细胞中的作用尚未阐明。在这里，我们旨在研究 VDR 在糖尿病病理生理学中β细胞中的作用。我们的结果表明，在健康胰岛中，葡萄糖调节 VDR 的表达，而在 1 型和 2 型糖尿病小鼠模型的胰岛中则减少。此外，过表达 VDR 的转基因小鼠对链脲佐菌素诱导的糖尿病具有保护作用，β细胞的质量和胰岛炎症减少。总之，这些结果表明，β细胞中持续的 VDR 水平可能有助于维持β细胞的质量和功能，并预防糖尿病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a816/7171966/e21e535daf1a/db190757f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a816/7171966/47047bfe2bf5/db190757f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a816/7171966/240fd0cfa1d7/db190757f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a816/7171966/ea5f59e3696e/db190757f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a816/7171966/73da466051ae/db190757f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a816/7171966/5b52c3fa6c78/db190757f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a816/7171966/4f83e6dcb62f/db190757f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a816/7171966/318a55eb8399/db190757f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a816/7171966/e21e535daf1a/db190757f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a816/7171966/47047bfe2bf5/db190757f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a816/7171966/240fd0cfa1d7/db190757f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a816/7171966/ea5f59e3696e/db190757f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a816/7171966/73da466051ae/db190757f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a816/7171966/5b52c3fa6c78/db190757f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a816/7171966/4f83e6dcb62f/db190757f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a816/7171966/318a55eb8399/db190757f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a816/7171966/e21e535daf1a/db190757f8.jpg

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