Evidence map›Paper›PMID 15193143›Full record

ArticleThe Biochemical journal2004

Opposing actions of cellular retinol-binding protein and alcohol dehydrogenase control the balance between retinol storage and degradation.

Andrei Molotkov, Norbert B Ghyselinck, Pierre Chambon, Gregg Duester

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

24 citing papers in PubMed, 44 citations in OpenAlex.

  1. Vitamin A supplementation downregulatesAnimal nutrition (Zhongguo xu mu shou yi xue hui) · 2022
    Article
  2. Article
  3. New insights and changing paradigms in the regulation of vitamin A metabolism in development.Wiley interdisciplinary reviews. Developmental biology · 2017
    Review
  4. Comparative genomics reveals convergent evolution between the bamboo-eating giant and red pandas.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. The key role of vitamin A in spermatogenesis.The Journal of clinical investigation · 2010
    Review
  18. Review
  19. Article
  20. Retinoic acid regulation of the somitogenesis clock.Birth defects research. Part C, Embryo today : reviews · 2007
    Review
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

4 authors at 1 institution in 1 country.

Andrei MolotkovOncoDevelopmental Biology Program, Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.
Norbert B Ghyselinck
Pierre Chambon
Gregg Duester
Collège de France · FR

Funding

GENETIC DISSECTION OF ALCOHOL/RETINOL METABOLIC PATHWAYSR01AA009731 · NIAAA · BURNHAM INSTITUTE FOR MEDICAL RESEARCH · PI DUESTER, GREGG L · 1995 to 2002
$1.1M
NIAAA NIH HHS AA09731
6 · The paper itself

Abstract

Vitamin A homoeostasis requires the gene encoding cellular retinol-binding protein-1 (Crbp1) which stimulates conversion of retinol into retinyl esters that serve as a storage form of vitamin A. The gene encoding alcohol dehydrogenase-1 (Adh1) greatly facilitates degradative metabolism of excess retinol into retinoic acid to protect against toxic effects of high dietary vitamin A. Crbp1-/-/Adh1-/- double mutant mice were generated to explore whether the stimulatory effect of CRBP1 on retinyl ester formation is due to limitation of retinol oxidation by ADH1, and whether ADH1 limits retinyl ester formation by opposing CRBP1. Compared with wild-type mice, liver retinyl ester levels were greatly reduced in Crbp1-/- mice, but Adh1-/- mice exhibited a significant increase in liver retinyl esters. Importantly, relatively normal liver retinyl ester levels were restored in Crbp1-/-/Adh1-/- mice. During vitamin A deficiency, the additional loss of Adh1 completely prevented the excessive loss of liver retinyl esters observed in Crbp1-/- mice for the first 5 weeks of deficiency and greatly minimized this loss for up to 13 weeks. Crbp1-/- mice also exhibited increased metabolism of a dose of retinol into retinoic acid, and this increased metabolism was not observed in Crbp1-/-/Adh1-/- mice. Our findings suggest that opposing actions of CRBP1 and ADH1 enable a large fraction of liver retinol to remain esterified due to CRBP1 action, while continuously allowing some retinol to be oxidized to retinoic acid by ADH1 for degradative retinoid turnover under any dietary vitamin A conditions.

Indexed as

Alcohol DehydrogenaseAnimalsDietEsterificationGenotypeHomeostasisLiverMiceMice, KnockoutRetinol-Binding ProteinsRetinol-Binding Proteins, CellularTime FactorsVitamin AVitamin A DeficiencyAlcohol DehydrogenaseRetinol-Binding ProteinsRetinol-Binding Proteins, CellularVitamin A

Identifiers

PMID15193143
PMCPMC1134070
OpenAlexW1990895444

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.