Evidence map›Paper›PMID 24715510›Full record

ReviewSeminars in reproductive medicine2014

Intrauterine environment and polycystic ovary syndrome.

Daniel A Dumesic, Mark O Goodarzi, Gregorio D Chazenbalk, David H Abbott

Open access · bronzeAbstract readReview
In one paragraph

Review in Seminars in reproductive medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
11.6field-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

48 citing papers in PubMed, 87 citations in OpenAlex.

  1. Trial
  2. Review
  3. Observational
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  9. Review
  10. Article
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  15. Article
  16. Article
  17. Review
  18. Polycystic Ovary Syndrome: the Epigenetics Behind the Disease.Reproductive sciences (Thousand Oaks, Calif.) · 2022
    Review
  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

4 authors at 3 institutions in 1 country.

Daniel A DumesicDepartment of Obstetrics and Gynecology, David Geffen School of Medicine at UCLA, Los Angeles, California.
Mark O GoodarziDivision of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California.
Gregorio D ChazenbalkDepartment of Obstetrics and Gynecology, David Geffen School of Medicine at UCLA, Los Angeles, California.
David H AbbottWisconsin National Primate Research Center, Madison, Wisconsin.
University of California, Los Angeles · USCedars-Sinai Medical Center · USUniversity of Wisconsin–Madison · US

Funding

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
PROJECT 4: ANDROGEN EXCESS IN ADIPOGENIC DYSFUNCTION IN PCOS WOMENU54HD071836 · NICHD · OREGON HEALTH & SCIENCE UNIVERSITY · PI STOUFFER, RICHARD L · 2013 to 2013
$1.9M
NICHD NIH HHS P50 HD044405NICHD NIH HHS P50 HD071836NICHD NIH HHS U54 HD071836
6 · The paper itself

Abstract

The maternal-fetal environment plays an important role in developmental programming of adult disease. Metabolic and hormonal dysfunction during human fetal development accompanies gestational diabetes as a common occurrence in mothers with polycystic ovary syndrome (PCOS), while human fetal androgen excess from congenital adrenal hyperplasia or virilizing tumors precedes PCOS-like symptoms after birth. To date, clinical studies of infant blood levels at term have yet to confirm that human fetal androgen excess promotes PCOS development after birth. Earlier in development, however, circulating androgen levels in the second trimester female human fetus can normally rise into the male range. Furthermore, midgestational amniotic testosterone levels are elevated in female fetuses of PCOS compared with normal mothers and might influence fetal development because experimentally induced fetal androgen excess in animals produces a PCOS-like phenotype with reproductive and metabolic dysfunction. Such alterations in the maternal-fetal environment likely program adult PCOS by epigenetic modifications of genetic susceptibility of the fetus to PCOS after birth. Understanding this phenomenon requires advanced fetal surveillance technologies and postnatal assessment of midgestational androgen exposure for new clinical strategies to improve reproduction in PCOS women, optimize long-term health of their offspring, and minimize susceptibility to acquiring PCOS in future generations.

Indexed as

FemaleHumansMaternal-Fetal ExchangePolycystic Ovary SyndromePregnancyUterus

Identifiers

PMID24715510
PMCPMC4800983
OpenAlexW2409203647

What OpenQuestion 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 OpenQuestion graph.