Evidence map›Paper›PMID 28333238›Full record

ArticleHuman reproduction (Oxford, England)2017

Clustering of PCOS-like traits in naturally hyperandrogenic female rhesus monkeys.

D H Abbott, B H Rayome, D A Dumesic, K C Lewis, A K Edwards, K Wallen, M E Wilson, S E Appt, J E Levine

Open access · bronzeAbstract read
In one paragraph

Article in Human reproduction (Oxford, England), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
8.5field-weighted citation impact, top 2% 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

39 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Prediction of CD8Scientific reports · 2025
    Article
  3. Review
  4. Testosterone mediates life-history trade-offs in female mammals.Biological reviews of the Cambridge Philosophical Society · 2025
    Review
  5. Review
  6. Non-human primate: the new frontier model of female reproductive engineering.Frontiers in bioengineering and biotechnology · 2025
    Review
  7. Review
  8. Roles of estrogen and its receptors in polycystic ovary syndrome.Frontiers in cell and developmental biology · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Polycystic Ovary Syndrome: An Evolutionary Adaptation to Lifestyle and the Environment.International journal of environmental research and public health · 2022
    Review
  17. Review
  18. IsPathogens (Basel, Switzerland) · 2021
    Article
  19. 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 1 country.

D H AbbottDepartment of Obstetrics and Gynecology, University of Wisconsin, Madison, WI, USA.
B H RayomeWisconsin National Primate Research Center, University of Wisconsin, Madison, WI, USA.
D A DumesicDepartment of Obstetrics and Gynecology, University of California, Los Angeles, CA, USA.
K C LewisOpAns, LLC, Durham, NC, USA.
A K EdwardsWisconsin National Primate Research Center, University of Wisconsin, Madison, WI, USA.
K WallenDivision of Developmental & Cognitive Neuroscience, Yerkes National Primate Research Center, USA.
M E WilsonDivision of Developmental & Cognitive Neuroscience, Yerkes National Primate Research Center, USA.
S E ApptDepartment of Pathology, Wake Forest School of Medicine, Winston Salem, NC, USA.
J E LevineWisconsin National Primate Research Center, University of Wisconsin, Madison, WI, USA.
University of Wisconsin–Madison · USEmory National Primate Research CenterUniversity of California, Los Angeles · USWake Forest University · 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
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 HD044405NIH HHS P51 OD011106
6 · The paper itself

Abstract

Study question: Do naturally occurring, hyperandrogenic (≥1 SD of population mean testosterone, T) female rhesus monkeys exhibit traits typical of women with polycystic ovary syndrome (PCOS)? Summary answer: Hyperandrogenic female monkeys exhibited significantly increased serum levels of androstenedione (A4), 17-hydroxyprogesterone (17-OHP), estradiol (E2), LH, antimullerian hormone (AMH), cortisol, 11-deoxycortisol and corticosterone, as well as increased uterine endometrial thickness and evidence of reduced fertility, all traits associated with PCOS. What is known already: Progress in treating women with PCOS is limited by incomplete knowledge of its pathogenesis and the absence of naturally occurring PCOS in animal models. A female macaque monkey, however, with naturally occurring hyperandrogenism, anovulation and polyfollicular ovaries, accompanied by insulin resistance, increased adiposity and endometrial hyperplasia, suggests naturally occurring origins for PCOS in nonhuman primates. Study design, size, duration: As part of a larger study, circulating serum concentrations of selected pituitary, ovarian and adrenal hormones, together with fasted insulin and glucose levels, were determined in a single, morning blood sample obtained from 120 apparently healthy, ovary-intact, adult female rhesus monkeys (Macaca mulatta) while not pregnant or nursing. The monkeys were then sedated for somatometric and ultrasonographic measurements. Participants/materials, setting, methods: Female monkeys were of prime reproductive age (7.2 ± 0.1 years, mean ± SEM) and represented a typical spectrum of adult body weight (7.4 ± 0.2 kg; maximum 12.5, minimum 4.6 kg). Females were defined as having normal (n = 99) or high T levels (n = 21; ≥1 SD above the overall mean, 0.31 ng/ml). Electronic health records provided menstrual and fecundity histories. Steroid hormones were determined by tandem LC-MS-MS; AMH was measured by enzymeimmunoassay; LH, FSH and insulin were determined by radioimmunoassay; and glucose was read by glucose meter. Most analyses were limited to 80 females (60 normal T, 20 high T) in the follicular phase of a menstrual cycle or anovulatory period (serum progesterone <1 ng/ml). Main results and the role of chance: Of 80 monkeys, 15% (n = 12) exhibited classifiable PCOS-like phenotypes. High T females demonstrated elevations in serum levels of LH (P < 0.036), AMH (P < 0.021), A4 (P < 0.0001), 17-OHP (P < 0.008), E2 (P < 0.023), glucocorticoids (P < 0.02-0.0001), the serum T/E2 ratio (P < 0.03) and uterine endometrial thickness (P < 0.014) compared to normal T females. Within the high T group alone, anogenital distance, a biomarker for fetal T exposure, positively correlated (P < 0.015) with serum A4 levels, while clitoral volume, a biomarker for prior T exposure, positively correlated (P < 0.002) with postnatal age. Only high T females demonstrated positive correlations between serum LH, and both T and A4. Five of six (83%) high T females with serum T ≥2 SD above T mean (0.41 ng/ml) did not produce live offspring. Large scale data: N/A. Limitations, reasons for caution: This is an initial study of a single laboratory population in a single nonhuman primate species. While two biomarkers suggest lifelong hyperandrogenism, phenotypic expression during gestation, prepuberty, adolescence, mid-to-late reproductive years and postmenopause has yet to be determined. Wider implications of the findings: Characterizing adult female monkeys with naturally occurring hyperandrogenism has identified individuals with high LH and AMH combined with infertility, suggesting developmental linkage among traits with endemic origins beyond humans. PCOS may thus be an ancient phenotype, as previously proposed, with a definable pathogenic mechanism(s). Study funding/competing interest(s): Funded by competitive supplement to P51 OD011106 (PI: Mallick), by P50 HD028934 (PI: Marshall) and by P50 HD044405 (PI: Dunaif). The authors have no potential conflicts of interest.

Indexed as

AndrostenedioneAnimalsAnti-Mullerian HormoneCorticosteroneCortodoxoneEndometriumEstradiolFemaleFertilityHydrocortisoneHydroxyprogesteronesHyperandrogenismMacaca mulattaPhenotypePolycystic Ovary SyndromeAndrostenedioneAnti-Mullerian HormoneCorticosteroneCortodoxoneEstradiolHydrocortisoneHydroxyprogesteronesdevelopmental programmingenlarged uterine endotheliumhigh AMHhypergonadotropichypersteroidogenicinfertility

Identifiers

PMID28333238
PMCPMC6251677
OpenAlexW2589734243

What OpenQuestion holds

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Registered trials

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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.