Cited by 57Ovarian function and disordersHypothalamic control of reproductive hormonesReproductive Biology and Fertility

Reproductive neuroendocrine dysfunction in polycystic ovary syndrome: Insight from animal models

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Roland, Alison V., Moenter, Suzanne M.·2014·Frontiers in Neuroendocrinology

Abstract

Polycystic ovary syndrome (PCOS) is a common endocrinopathy with elusive origins. A clinically heterogeneous disorder, PCOS is likely to have multiple etiologies comprised of both genetic and environmental factors. Reproductive neuroendocrine dysfunction involving increased frequency and amplitude of gonadotropin-releasing hormone (GnRH) release, as reflected by pulsatile luteinizing hormone (LH) secretion, is an important pathophysiologic component in PCOS. Whether this defect is primary or secondary to other changes in PCOS is unclear, but it contributes significantly to ongoing reproductive dysfunction. This review highlights recent work in animal models, with a particular emphasis on the mouse, demonstrating the ability of pre- and postnatal steroidal and metabolic factors to drive changes in GnRH/LH pulsatility and GnRH neuron function consistent with the observed abnormalities in PCOS. This work has begun to elucidate how a complex interplay of ovarian, metabolic, and neuroendocrine factors culminates in this syndrome.

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Crossref · 10.1016/j.yfrne.2014.04.002

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  • When developing female embryos are exposed to relatively high levels of testosterone, hypothalamic sensitivity to steroid-induced negative feedback is reduced, resulting in increased frequency and amplitude of GnRH and LH pulses with corresponding increases in LH levels.

    “When developing female embryos are exposed to relatively high levels of testosterone—such as in females who develop PCOS—many aspects of HPG activity are affected. Hypothalamic sensitivity to steroid‐induced negative feedback is reduced, resulting in an increased frequency and amplitude of gonadotropin‐releasing hormone (GnRH) and luteinizing hormone (LH) pulses with corresponding increases in LH”

    From Endometriosis and polycystic ovary syndrome are diametric disorders (2021) · cites this paper as Roland & Moenter, 2014

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  • These testosterone-induced alterations to female development are largely consistent across animal models.

    “Importantly, these testosterone‐induced alterations to female development are largely consistent across animal models (Astapova et al., 2019; Roland & Moenter, 2014).”

    From Endometriosis and polycystic ovary syndrome are diametric disorders (2021) · cites this paper as Roland & Moenter, 2014

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References 165 · Cited by 57

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Authors
Roland, A. V., & Moenter, S. M.
Affiliations
University of Michigan (US)
Corresponding author
Moenter, Suzanne M.
Venue
Frontiers in Neuroendocrinology
Publisher
Elsevier BV
Published
2014-10
Volume
35
Issue
4
Pages
494-511
ISSN
0091-3022 (ISSN-L)
OpenAlex
W2037452858
Cited by
57
References
165
Citations by year
2026: 2 · 2025: 2 · 2024: 2 · 2023: 6 · 2022: 2 · 2021: 6 · 2020: 6 · 2019: 3 · 2018: 12 · 2017: 5 · 2016: 3 · 2015: 7 · 2014: 1
FWCI
0.84
Type
journal article
Language
en
Open access
Locations
  • Frontiers in Neuroendocrinology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institute of Diabetes and Digestive and Kidney Diseases (P30DK020572)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (U54HD028934)
Topics
  • Health Sciences › Medicine › Reproductive Medicine › Ovarian function and disorders
  • Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
  • Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Reproductive Biology and Fertility
Keywords
polycystic ovary syndrome, gonadotropin-releasing hormone, GnRH pulsatility, luteinizing hormone secretion, GnRH neurons, metabolic factors, animal models, mouse model, reproductive disorders
MeSH terms
Animals, Female, Humans, Luteinizing Hormone, Gonadotropin-Releasing Hormone, Neurosecretory Systems, Polycystic Ovary Syndrome, Testosterone, Models, Animal

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