Fetal, infant, adolescent and adult phenotypes of polycystic ovary syndrome in prenatally androgenized female rhesus monkeys
Open accessAbstract
Old World monkeys provide naturally occurring and experimentally induced phenotypes closely resembling the highly prevalent polycystic ovary syndrome (PCOS) in women. In particular, experimentally induced fetal androgen excess in female rhesus monkeys produces a comprehensive adult PCOS‐like phenotype that includes both reproductive and metabolic dysfunction found in PCOS women. Such a reliable experimental approach enables the use of the prenatally androgenized (PA) female rhesus monkey model to (1) examine fetal, infant and adolescent antecedents of adult pathophysiology, gaining valuable insight into early phenotypic expression of PCOS, and (2) to understand adult pathophysiology from a mechanistic perspective. Elevated circulating luteinizing hormone (LH) levels are the earliest indication of reproductive dysfunction in late gestation nonhuman primate fetuses and infants exposed to androgen excess during early (late first to second trimester) gestation. Such early gestation‐exposed PA infants also are hyperandrogenic, with both LH hypersecretion and hyperandrogenism persisting in early gestation‐exposed PA adults. Similarly, subtle metabolic abnormalities appearing in young nonhuman primate infants and adolescents precede the abdominal adiposity, hyperliplidemia and increased incidence of type 2 diabetes that characterize early gestation‐exposed PA adults. These new insights into the developmental origins of PCOS, and progression of the pathophysiology from infancy to adulthood, provide opportunities for clinical intervention to ameliorate the PCOS phenotype thus providing a preventive health‐care approach to PCOS‐related abnormalities. For example, PCOS‐like traits in PA monkeys, as in PCOS women, can improve with better insulin–glucose homeostasis, suggesting that lifestyle interventions preventing increased adiposity in adolescent daughters of PCOS mothers also may reduce their risk of acquiring many PCOS‐related metabolic abnormalities in adulthood. Am. J. Primatol. 71:776–784, 2009. © 2009 Wiley‐Liss, Inc.
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Prenatal androgen treatment induces HPG changes as well as metabolic alterations including insulin resistance, obesity, and enlarged adipocytes in female rhesus monkeys and mice.
“Prenatal androgen treatment induces HPG changes as well as metabolic alterations including insulin resistance, obesity, and enlarged adipocytes in female rhesus monkeys and mice (Abbott et al., 2009; Roland et al., 2010).”
From Endometriosis and polycystic ovary syndrome are diametric disorders (2021) · cites this paper as Abbott et al., 2009
The fetal and infant phenotype sections report elevated LH in prenatally androgenized female rhesus monkeys, and the metabolic phenotypes section reports insulin resistance in early-gestation-exposed females. The adolescent and infant phenotype sections describe greater weight gain and abdominal adiposity, but do not establish obesity or enlarged adipocytes in these monkeys. The sentence also cites Roland et al. for mice; this verdict assesses Abbott et al. only. Page numbers were not supplied in our copy. (LLM, conf=0.86)
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- Authors
- Abbott, D. H., Tarantal, A. F., & Dumesic, D. A.
- Affiliations
- University of Wisconsin System (US)
- University of California, Davis (US)
- Corresponding author
- Abbott, David H.
- Venue
- American Journal of Primatology
- Publisher
- Wiley
- Published
- 2009-04-14
- Volume
- 71
- Issue
- 9
- Pages
- 776-784
- ISSN
- 0275-2565 (ISSN-L)
- 1098-2345
- PMC
- PMC2916860
- OpenAlex
- W2052785258
- Cited by
- 177
- References
- 88
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 4 · 2023: 11 · 2022: 6 · 2021: 6 · 2020: 7 · 2019: 12 · 2018: 10 · 2017: 15 · 2016: 10 · 2015: 11 · 2014: 16 · 2013: 11 · 2012: 23
- FWCI
- 18.91
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Primatology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (5u01hd044650-05)
- National Center for Research Resources (P51RR000169, R01RR013635, C06RR020141, RR 15459-01, RR-00169, C06RR015459, RR 020141-01, P51RR000167)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (P50HD044405, U01-HD044650)
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Ovarian function and disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Sexual Differentiation and Disorders
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Reproductive Biology and Fertility
- Keywords
- polycystic ovary syndrome, prenatal androgen exposure, rhesus monkeys, hyperandrogenism, developmental origins of health and disease, type 2 diabetes, reproductive disorders, abdominal fat, hyperlipidemia, PCOS prevention
- MeSH terms
- Age Factors, Androgens, Animals, Disease Models, Animal, Female, Luteinizing Hormone, Macaca mulatta, Phenotype, Polycystic Ovary Syndrome, Pregnancy, Prenatal Exposure Delayed Effects
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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