Evidence map›Paper›PMID 27367842›Full record

ArticleeLife2016

Glucocorticoid receptor-PPARα axis in fetal mouse liver prepares neonates for milk lipid catabolism.

Gianpaolo Rando, Chek Kun Tan, Nourhène Khaled, Alexandra Montagner, Nicolas Leuenberger, Justine Bertrand-Michel, Eeswari Paramalingam, Hervé Guillou, Walter Wahli

Open access · goldAbstract read
In one paragraph

Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
9.2field-weighted citation impact, top 3% 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

28 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Proteomics identifies the developmental regulation of HKDC1 in liver of pigs and mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Regulation of maternal-fetal metabolic communication.Cellular and molecular life sciences : CMLS · 2021
    Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. The Potential of the FSP1cre-International journal of molecular sciences · 2019
    Article
  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

9 authors at 4 institutions in 3 countries.

Gianpaolo RandoCenter for Integrative Genomics, University of Lausanne, Lausanne, Switzerland.
Chek Kun TanLee Kong Chian School of Medicine, Nanyang Technological University, , Singapore.
Nourhène KhaledCenter for Integrative Genomics, University of Lausanne, Lausanne, Switzerland.
Alexandra MontagnerUMR 1331 ToxAlim Research Centre in Food Toxicology, INRA, Université de Toulouse, Toulouse, France.
Nicolas LeuenbergerCenter for Integrative Genomics, University of Lausanne, Lausanne, Switzerland.
Justine Bertrand-MichelIFR 150 Plateforme Metatoul, Institut Fédératif de Recherche Bio-Médicale de Toulouse INSERM U563, Toulouse, France.
Eeswari ParamalingamLee Kong Chian School of Medicine, Nanyang Technological University, , Singapore.
Hervé GuillouUMR 1331 ToxAlim Research Centre in Food Toxicology, INRA, Université de Toulouse, Toulouse, France.
Walter WahliCenter for Integrative Genomics, University of Lausanne, Lausanne, Switzerland.ORCID 0000-0002-5966-9089
Nanyang Technological University · SGUniversity of Lausanne · CHUniversité Fédérale de Toulouse Midi-Pyrénées · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In mammals, hepatic lipid catabolism is essential for the newborns to efficiently use milk fat as an energy source. However, it is unclear how this critical trait is acquired and regulated. We demonstrate that under the control of PPARα, the genes required for lipid catabolism are transcribed before birth so that the neonatal liver has a prompt capacity to extract energy from milk upon suckling. The mechanism involves a fetal glucocorticoid receptor (GR)-PPARα axis in which GR directly regulates the transcriptional activation of PPARα by binding to its promoter. Certain PPARα target genes such as Fgf21 remain repressed in the fetal liver and become PPARα responsive after birth following an epigenetic switch triggered by β-hydroxybutyrate-mediated inhibition of HDAC3. This study identifies an endocrine developmental axis in which fetal GR primes the activity of PPARα in anticipation of the sudden shifts in postnatal nutrient source and metabolic demands.

Indexed as

Gene Expression Regulation, DevelopmentalLipid MetabolismMetabolismAnimalsEnergy MetabolismLiverMiceMilkPPAR alphaReceptors, GlucocorticoidPPAR alphaReceptors, Glucocorticoiddevelopmental biologyFGF21glucocorticoid receptorHDAC3hepatic steatosisketone bodymousePPARαstem cells

Identifiers

PMID27367842
PMCPMC4963200
OpenAlexW2468337232

What OpenQuestion holds

Textmetadata
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.