Hyperprolactinemia-induced ovarian acyclicity is reversed by kisspeptin administration
Open accessAbstract
Hyperprolactinemia is the most common cause of hypogonadotropic anovulation and is one of the leading causes of infertility in women aged 25-34. Hyperprolactinemia has been proposed to block ovulation through inhibition of GnRH release. Kisspeptin neurons, which express prolactin receptors, were recently identified as major regulators of GnRH neurons. To mimic the human pathology of anovulation, we continuously infused female mice with prolactin. Our studies demonstrated that hyperprolactinemia in mice induced anovulation, reduced GnRH and gonadotropin secretion, and diminished kisspeptin expression. Kisspeptin administration restored gonadotropin secretion and ovarian cyclicity, suggesting that kisspeptin neurons play a major role in hyperprolactinemic anovulation. Our studies indicate that administration of kisspeptin may serve as an alternative therapeutic approach to restore the fertility of hyperprolactinemic women who are resistant or intolerant to dopamine agonists.
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PRL infusions reduce kisspeptin and GnRH expression, resulting in anovulation.
“In support of this hypothesis, PRL infusions have been shown to reduce the kisspeptin and GnRH expression, resulting in anovulation (27).”
From Kisspeptin Overcomes GnRH Neuronal Suppression Secondary to Hyperprolactinemia in Humans (2022) · cites this paper as [27]
The Results and Discussion report that PRL treatment decreased hypothalamic Kiss1 expression and was accompanied by anovulation. They also report inhibited GnRH release, but explicitly state that hypothalamic Gnrh gene expression was not altered. The claim therefore conflates reduced GnRH release with reduced GnRH expression. (LLM, conf=0.91)
Experimental — accuracy not yet measuredIn female mice with hyperprolactinemia, kisspeptin administration restores GnRH and gonadotropin secretion and ovarian cyclicity.
“In female mice with hyperprolactinemia, kisspeptin administration was shown to restore GnRH and gonadotropin secretion and ovarian cyclicity (27).”
From Kisspeptin Overcomes GnRH Neuronal Suppression Secondary to Hyperprolactinemia in Humans (2022) · cites this paper as [27]
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- Authors
- Sonigo, C., Bouilly, J., Carré, N., Tolle, V., Caraty, A., Tello, J., Simony-Conesa, F.-J., Millar, R., Young, J., & Binart, N.
- Affiliations
- Université Paris-Sud (FR)
- Inserm (FR)
- Centre National de la Recherche Scientifique (FR)
- University of Edinburgh (GB)
- University of Cape Town (ZA)
- Corresponding author
- Binart, Nadine
- Venue
- Journal of Clinical Investigation
- Published
- 2012-10-01
- Volume
- 122
- Issue
- 10
- Pages
- 3791-3795
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC3461919
- OpenAlex
- W2161243079
- Cited by
- 197
- References
- 24
- Citations by year
- 2026: 8 · 2025: 14 · 2024: 19 · 2023: 15 · 2022: 21 · 2021: 10 · 2020: 15 · 2019: 20 · 2018: 15 · 2017: 17 · 2016: 10 · 2015: 8 · 2014: 8 · 2013: 13 · 2012: 2
- FWCI
- 11.55
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, other-oa)
- UpSpace Institutional Repository (University of Pretoria) (submittedVersion)
- Funders
- University of Pretoria
- Fondation pour la Recherche Médicale
- Medical Research Council
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Reproductive Biology and Fertility
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- hyperprolactinemia, kisspeptin, anovulation, GnRH neurons, prolactin receptor, gonadotropin secretion, female infertility, dopamine agonist resistance, kisspeptin neurons
- MeSH terms
- Animals, Anovulation, Disease Models, Animal, Drug Evaluation, Preclinical, Female, Gene Expression Regulation, Gonadotropins, Pituitary, Hyperprolactinemia, Hypothalamo-Hypophyseal System, Hypothalamus, Gonadotropin-Releasing Hormone, Male, Prolactin, Pulsatile Flow, RNA, Messenger, Infusion Pumps, Implantable, Estrous Cycle, Mice, Kisspeptins
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