Evidence map›Paper›PMID 31499494›Full record

ReviewFrontiers of hormone research2019

In utero Androgen Excess: A Developmental Commonality Preceding Polycystic Ovary Syndrome?

David H Abbott, Marissa Kraynak, Daniel A Dumesic, Jon E Levine

Abstract readReview
In one paragraph

Review in Frontiers of hormone research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
63.5field-weighted citation impact, top 1% 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

27 citing papers in PubMed, 38 citations in OpenAlex.

  1. Trial
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  3. Review
  4. Article
  5. Article
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  7. Review
  8. Article
  9. Review
  10. Review
  11. Androgen signalling in the ovaries and endometrium.Molecular human reproduction · 2023
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Polycystic Ovary Syndrome: An Evolutionary Adaptation to Lifestyle and the Environment.International journal of environmental research and public health · 2022
    Review
  19. Review
  20. 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 2 institutions in 1 country.

David H AbbottWisconsin National Primate Research Center, University of Wisconsin, Madison, Wisconsin, USA, abbott@primate.wisc.edu.
Marissa KraynakWisconsin National Primate Research Center, University of Wisconsin, Madison, Wisconsin, USA.
Daniel A DumesicDepartment of Obstetrics and Gynecology, David Geffen School of Medicine, University of California, Los Angeles, California, USA.
Jon E LevineWisconsin National Primate Research Center, University of Wisconsin, Madison, Wisconsin, USA.
University of Wisconsin–Madison · USUniversity of California, Los Angeles · US

Funding

WNPRC Supplemental Request for Nonhuman Primate Enclosures to Equip HIV/AIDS-Related Research FacilitiesP51OD011106 · OD · UNIVERSITY OF WISCONSIN-MADISON · PI Dorota A. Grejner-Brzezinska · 2012 to 2026
$150.7M
Role of Androgen Excess in Provoking Oxidative Stress in FemalesP50HD044405 · NICHD · NORTHWESTERN UNIVERSITY AT CHICAGO · PI DUNAIF, ANDREA E · 2002 to 2017
$17.2M
PROJECT 4: ANDROGEN EXCESS IN ADIPOGENIC DYSFUNCTION IN PCOS WOMENP50HD071836 · NICHD · OREGON HEALTH & SCIENCE UNIVERSITY · PI HENNEBOLD, JON D · 2014 to 2021
$14.7M
Testosterone-GnRH Frequency and the Evolution of PCOS in AdolescenceP50HD028934 · NICHD · UNIVERSITY OF VIRGINIA · PI HAISENLEDER, DANIEL J. · 2014 to 2018
$8.6M
NICHD NIH HHS P50 HD028934NICHD NIH HHS P50 HD044405NICHD NIH HHS P50 HD071836NIH HHS P51 OD011106
6 · The paper itself

Abstract

In utero androgen excess reliably induces polycystic ovary syndrome (PCOS)-like reproductive and metabolic traits in female monkeys, sheep, rats, and mice. In humans, however, substantial technical and ethical constraints on fetal sampling have curtailed safe, pathogenic exploration during gestation. Evidence consistent with in utero origins for PCOS in humans has thus been slow to amass, but the balance now leans toward developmental fetal origins. Given that PCOS is familial and highly heritable, difficulties encountered in discerning genetic contributions to PCOS pathogenesis are puzzling and, to date, accounts for <10% of PCOS presentations. Unaccounted heritability notwithstanding, molecular commonality in pathogenic mechanisms is emerging, suggested by co-occurrence at the same gene loci of (1) PCOS genetic variants (PCOS women), (2) epigenetic alterations in DNA methylation (PCOS women), and (3) bioinformatics, gene networks-identified, epigenetic alterations in DNA methylation (female rhesus monkeys exposed to testosterone (T) in utero). In addition, naturally occurring hyperandrogenism in female monkeys singles out individuals with PCOS-like reproductive and metabolic traits accompanied by somatic biomarkers of in utero T exposure. Such phenotypic and molecular convergence between highly related species suggests not only dual genetic and epigenetic contributions to a developmental origin of PCOS but also common molecular pathogenesis extending beyond humans.

Indexed as

HyperandrogenismPolycystic Ovary SyndromePrenatal Exposure Delayed EffectsAndrogensAnimalsFemaleHumansPregnancyAndrogens

Identifiers

PMID31499494
PMCPMC6954824
OpenAlexW2972730817

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.