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Hyperprolactinemia-induced ovarian acyclicity is reversed by kisspeptin administration

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Author(s)

Charlotte Sonigo, Justine Bouilly, Nadege Carre, Virginie Tolle, Alain Caraty, Javier Tello, Fabian-Jesus Simony-Conesa, Robert Millar, Jacques Young, Nadine Binart

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Abstract

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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Details

Original languageEnglish
Pages (from-to)3791-3795
Number of pages5
JournalThe Journal of Clinical Investigation
Volume122
Issue number10
DOIs
Publication statusPublished - 1 Oct 2012

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