Evidence map›Paper›PMID 23906633›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2013

Cell-autonomous regulation of brown fat identity gene UCP1 by unliganded vitamin D receptor.

Peter J Malloy, Brian J Feldman

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Article
  3. NFIA determines theiScience · 2022
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Beyond the bone: Bone morphogenetic protein signaling in adipose tissue.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2019
    Review
  9. Article
  10. Small molecules for fat combustion: targeting obesity.Acta pharmaceutica Sinica. B · 2019
    Review
  11. Review
  12. Article
  13. Adipose-specific Vdr deletion alters body fat and enhances mammary epithelial density.The Journal of steroid biochemistry and molecular biology · 2016
    Article
  14. Extraskeletal actions of vitamin D.Annals of the New York Academy of Sciences · 2016
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

2 authors at 1 institution in 1 country.

Peter J MalloyLokey Stem Cell Research Building, 265 Campus Drive, Stanford, California 94305-5457. Feldman@stanford.edu.
Brian J Feldman
Stanford University · US

Funding

Using Components of the Circadian Clock to Regulate Stem Cell Fate DecisionsDP2OD006740 · OD · STANFORD UNIVERSITY · PI FELDMAN, BRIAN J · 2010 to 2010
$2.4M
NIH HHS DP2 OD006740
6 · The paper itself

Abstract

White adipose tissue stores energy in the form of lipids, and brown adipose tissue expends energy via uncoupled fatty acid oxidation, which leads to the generation of heat. Obesity reflects an imbalance between energy storage and energy expenditure and is strongly associated with metabolic and cardiovascular disease. Therefore, there are important medical and biological implications for elucidating the mechanisms that promote energy expenditure in humans. Animal models with altered vitamin D receptor (VDR) expression have changes in energy expenditure. However, the specific mechanism for this effect has not been elucidated and the relevance for humans is unclear. Here we show, using human patient samples from individuals with hereditary vitamin D resistant rickets, that the VDR directly inhibits the expression of uncoupling protein-1 (UCP1), the critical protein for uncoupling fatty acid oxidation in brown fat and burning energy. The inhibition is enforced by VDR occupancy of a negative response element in the promoter proximal region of the UCP1 gene. Deletion of VDR increases UCP1 expression and results in a "browning" of adipocytes. Importantly, we found that this process occurs cell autonomously and is independent of the physiologic VDR hormone ligand, 1,25-dihydroxyvitamin D. These results identify a mechanism for modulating energy balance in humans.

Indexed as

Gene SilencingAdipose Tissue, BrownBase SequenceCell DifferentiationCells, CulturedChromatin ImmunoprecipitationFamilial Hypophosphatemic RicketsFibroblastsHumansIon ChannelsLigandsMitochondrial ProteinsProtein BindingReceptors, CalcitriolUncoupling Protein 1Vitamin D Response ElementIon ChannelsLigandsMitochondrial ProteinsReceptors, CalcitriolUCP1 protein, humanUncoupling Protein 1

Identifiers

PMID23906633
PMCPMC3787131
OpenAlexW2106718278

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.