Evidence map›Paper›PMID 28426756›Full record

ArticlePloS one2017

Excessive dietary intake of vitamin A reduces skull bone thickness in mice.

Thomas Lind, Caroline Öhman, Gabriela Calounova, Annica Rasmusson, Göran Andersson, Gunnar Pejler, Håkan Melhus

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

12 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Role of vitamins beyond vitamin DInternational journal of molecular medicine · 2024
    Review
  5. Review
  6. Article
  7. Cranium growth, patterning and homeostasis.Development (Cambridge, England) · 2022
    Article
  8. Article
  9. Review
  10. Vitamin A decreases the anabolic bone response to mechanical loading by suppressing bone formation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  11. Article
  12. 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

7 authors at 2 institutions in 1 country.

Thomas LindDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden.ORCID http://orcid.org/0000-0003-2791-688X
Caroline ÖhmanDepartment of Engineering Sciences, Division of Applied Materials Science, The Ångström Laboratory, Uppsala University, Uppsala, Sweden.
Gabriela CalounovaDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden.
Annica RasmussonDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden.
Göran AnderssonDepartment of Laboratory Medicine, Division of Pathology, Karolinska University Hospital Huddinge, Karolinska Institute, Stockholm, Sweden.
Gunnar PejlerDepartment of Medical Biochemistry and Microbiology, Uppsala University, Uppsala, Sweden.
Håkan MelhusDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden.
Uppsala University · SEKarolinska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calvarial thinning and skull bone defects have been reported in infants with hypervitaminosis A. These findings have also been described in humans, mice and zebrafish with loss-of-function mutations in the enzyme CYP26B1 that degrades retinoic acid (RA), the active metabolite of vitamin A, indicating that these effects are indeed caused by too high levels of vitamin A and that evolutionary conserved mechanisms are involved. To explore these mechanisms, we have fed young mice excessive doses of vitamin A for one week and then analyzed the skull bones using micro computed tomography, histomorphometry, histology and immunohistochemistry. In addition, we have examined the effect of RA on gene expression in osteoblasts in vitro. Compared to a standard diet, a high dietary intake of vitamin A resulted in a rapid and significant reduction in calvarial bone density and suture diastasis. The bone formation rate was almost halved. There was also increased staining of tartrate resistant acid phosphatase in osteocytes and an increased perilacunar matrix area, indicating osteocytic osteolysis. Consistent with this, RA induced genes associated with bone degradation in osteoblasts in vitro. Moreover, and in contrast to other known bone resorption stimulators, vitamin A induced osteoclastic bone resorption on the endocranial surfaces.

Indexed as

AnimalsIntercellular Adhesion Molecule-1MiceOsteocytesSkullVitamin AX-Ray MicrotomographyIntercellular Adhesion Molecule-1Vitamin A

Identifiers

PMID28426756
PMCPMC5398668
OpenAlexW2606159727

What OpenQuestion holds

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LicenceCC BY
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.