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Article

Unaltered diabetes presentation in NOD mice lacking the vitamin D receptor.

Diabetes - 1 Jan 2008

Gysemans Conny, van Etten Evelyne, Overbergh Lutgart, Giulietti Annapaula, Eelen Guy, Waer Mark, Verstuyf Annemieke, Bouillon Roger, Mathieu Chantal

Abstract excerpt

OBJECTIVE: Vitamin D deficiency increases risk for type 1 diabetes in genetically predisposed individuals, while high doses of 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] prevent insulitis and diabetes in NOD mice. RESEARCH DESIGN AND METHODS: Since 1,25(OH)(2)D(3) regulates gene transcription through the vitamin D receptor (VDR), we investigated the role of VDR in diabetes development by creating NOD mice...

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Share to Crosses, Genetic
Share to Diabetes Mellitus, Type 1

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mice, Inbred NOD

Share to Mice, Knockout

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Share to Receptors, Calcitriol

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Source

Identifiers

PMID: 17959935
DOI: 10.2337/db07-1095

Genes

VDR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

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