Evidence map›Paper›PMID 21952242›Full record

ArticleEndocrinology2011

Calcium insufficiency accelerates type 1 diabetes in vitamin D receptor-deficient nonobese diabetic (NOD) mice.

John P Driver, Deanna J Lamont, Conny Gysemans, Chantal Mathieu, David V Serreze

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Vitamin D and Beta Cells in Type 1 Diabetes: A Systematic Review.International journal of molecular sciences · 2022
    Pooled it
  2. Article
  3. Article
  4. Article
  5. PTH and Vitamin D.Comprehensive Physiology · 2016
    Review
  6. Article
  7. Article
  8. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

John P DriverThe Jackson Laboratory, 600 Main Street, Bar Harbor, Maine 04609, USA.
Deanna J Lamont
Conny Gysemans
Chantal Mathieu
David V Serreze
Jackson Laboratory · USKU Leuven · BE

Funding

Shared Resource ManagementP30CA034196 · NCI · JACKSON LABORATORY · PI William Carl Skarnes · 1985 to 2026
$61.9M
Diabetogenic Role of MHC Class I Alleles in NOD MiceR01DK046266 · NIDDK · JACKSON LABORATORY · PI SERREZE, DAVID V · 2000 to 2018
$7.2M
DIABETOGENIC ROLE OF H-2G7 CLASS I ALLELES IN NOD MICER29DK046266 · NIDDK · JACKSON LABORATORY · PI SERREZE, DAVID V. · 1993 to 1998
–
NCI NIH HHS CA34196NCI NIH HHS P30 CA034196NIDDK NIH HHS DK-46266NIDDK NIH HHS DK-75000NIDDK NIH HHS R01 DK046266NIDDK NIH HHS R29 DK046266NLM NIH HHS N01 DK075000
6 · The paper itself

Abstract

Vitamin D exerts important regulatory effects on the endocrine and immune systems. Autoimmune type 1 diabetes (T1D) development in the inbred NOD mouse strain can be accelerated by vitamin D insufficiency or suppressed by chronic treatment with high levels of 1α,25-dihydroxyvitamin D(3). Consequently, a report that T1D development was unaffected in NOD mice genetically lacking the vitamin D receptor (VDR) was unexpected. To further assess this result, the mutant stock was imported to The Jackson Laboratory, backcrossed once to NOD/ShiLtJ, and progeny rederived through embryo transfer. VDR-deficient NOD mice of both sexes showed significant acceleration of T1D. This acceleration was not associated with alterations in immune cells targeting pancreatic β-cells. Rather, the capacity of β-cells to produce and/or secrete insulin was severely impaired by the hypocalcaemia developing in VDR-deficient NOD mice fed a standard rodent chow diet. Feeding a high-lactose calcium rescue diet that circumvents a VDR requirement for calcium absorption from the intestine normalized serum calcium levels, restored β-cell insulin secretion, corrected glucose intolerance, and eliminated accelerated T1D in VDR-deficient NOD mice. These findings suggest that calcium and/or vitamin D supplementation may improve disease outcomes in some T1D-prone individuals that are calcium deficient.

Indexed as

AnimalsCalciumCalcium, DietaryDiabetes Mellitus, Type 1FemaleHypocalcemiaInsulin-Secreting CellsMaleMiceMice, Inbred NODReceptors, CalcitriolVitamin DCalciumCalcium, DietaryReceptors, CalcitriolVitamin D

Identifiers

PMID21952242
PMCPMC3230053
OpenAlexW2012179814

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.