Evidence map›Paper›PMID 31882954›Full record

ArticleScientific reports2019

Fetal androgen exposure is a determinant of adult male metabolic health.

Katarzyna J Siemienowicz, Panagiotis Filis, Sophie Shaw, Alex Douglas, Jennifer Thomas, Sally Mulroy, Forbes Howie, Paul A Fowler, W Colin Duncan, Mick T Rae

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
6.2field-weighted citation impact, top 4% 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

15 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. 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

10 authors at 4 institutions in 1 country.

Katarzyna J SiemienowiczSchool of Applied Science, Edinburgh Napier University, Edinburgh, EH11 4BN, UK.
Panagiotis FilisInstitute of Medical Sciences, School of Medicine, Medical Sciences & Nutrition, University of Aberdeen, Aberdeen, AB25 2ZD, UK.
Sophie ShawInstitute of Medical Sciences, School of Medicine, Medical Sciences & Nutrition, University of Aberdeen, Aberdeen, AB25 2ZD, UK.
Alex DouglasInstitute of Medical Sciences, School of Medicine, Medical Sciences & Nutrition, University of Aberdeen, Aberdeen, AB25 2ZD, UK.
Jennifer ThomasSchool of Applied Science, Edinburgh Napier University, Edinburgh, EH11 4BN, UK.
Sally MulroySchool of Applied Science, Edinburgh Napier University, Edinburgh, EH11 4BN, UK.
Forbes HowieMRC Centre for Reproductive Health, The University of Edinburgh, Edinburgh, EH16 4TJ, UK.
Paul A FowlerInstitute of Medical Sciences, School of Medicine, Medical Sciences & Nutrition, University of Aberdeen, Aberdeen, AB25 2ZD, UK.
W Colin DuncanMRC Centre for Reproductive Health, The University of Edinburgh, Edinburgh, EH16 4TJ, UK.
Mick T RaeSchool of Applied Science, Edinburgh Napier University, Edinburgh, EH11 4BN, UK. m.rae@napier.ac.uk.
Edinburgh Napier University · GBUniversity of Aberdeen · GBMRC Centre for Reproductive Health · GBUniversity of Edinburgh · GB

Funding

Medical Research Council G0500717Medical Research Council G0901807Medical Research Council MR/N022556/1Medical Research Council MR/P011535/1
6 · The paper itself

Abstract

Androgen signalling is a critical driver of male development. Fetal steroid signalling can be dysregulated by a range of environmental insults and clinical conditions. We hypothesised that poor adult male health was partially attributable to aberrant androgen exposure during development. Testosterone was directly administered to developing male ovine fetuses to model excess prenatal androgenic overexposure associated with conditions such as polycystic ovary syndrome (PCOS). Such in utero androgen excess recreated the dyslipidaemia and hormonal profile observed in sons of PCOS patients. 1,084 of 15,134 and 408 of 2,766 quantifiable genes and proteins respectively, were altered in the liver during adolescence, attributable to fetal androgen excess. Furthermore, prenatal androgen excess predisposed to adolescent development of an intrahepatic cholestasis-like condition with attendant hypercholesterolaemia and an emergent pro-fibrotic, pro-oxidative stress gene and protein expression profile evident in both liver and circulation. We conclude that prenatal androgen excess is a previously unrecognised determinant of lifelong male metabolic health.

Indexed as

Maternal ExposurePrenatal Exposure Delayed EffectsAnimalsFemaleInactivation, MetabolicLiverMalePregnancySheepTestosteroneTestosterone

Identifiers

PMID31882954
PMCPMC6934666
OpenAlexW2998634440

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.