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Cited by 445

The DOI matches its Crossref record.

Impaired insulin secretory capacity in mice lacking a functional vitamin D receptor

Zeitz, Ute, Weber, Karin, Soegiarto, Desi W., Wolf, Eckhard, Balling, Rudi, Erben, Reinhold G.·2003·The FASEB Journal
DOI 10.1096/fj.02-0424fje
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Abstract

It was the aim of this study to further explore the functional role of vitamin D in the endocrine pancreas. By gene targeting, we have recently generated mice in which a lacZ reporter gene is driven by the endogenous vitamin D receptor (VDR) promoter. These mice express a functionally inactive mutant VDR. Pancreatic islets but not exocrine pancreas cells showed strong lacZ reporter gene expression in mutant mice. To rule out possible influences of hypocalcemia on pancreatic endocrine function, a rescue diet enriched with calcium, phosphorus, and lactose was fed to wild‐type (WT) and VDR mutant mice. The rescue diet normalized body weight and mineral homeostasis in VDR mutants. In glucose tolerance tests, baseline blood glucose levels were unchanged in fasting VDR mutants. However, blood glucose was elevated after oral or subcutaneous glucose loading, and maximum serum insulin levels were reduced by ~60% in VDR mutants vs. WT mice on either diet. In addition, insulin mRNA levels were decreased in VDR mutant mice on both diets, whereas pancreatic β cell mass, islet architecture, and islet neogenesis were normal. These findings clearly establish a molecular role of the VDR in pancreatic insulin synthesis and secretion in vivo.

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Metadata

Authors
Zeitz, U., Weber, K., Soegiarto, D. W., Wolf, E., Balling, R., & Erben, R. G.
Venue
The FASEB Journal
Publisher
Wiley
Published
2003-01-22
Volume
17
Issue
3
Pages
1-14
ISSN
  • 0892-6638 (ISSN-L)
  • 1530-6860
DOI
10.1096/fj.02-0424fje
OpenAlex
W1985297370
Cited by
445
References
0
FWCI
7.52
Type
journal article
Language
en
Open access
closed

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