Infertility: How can the ovulation function be restored?

October 17, 2012

One of the most frequent is the existence of tumours that induce an over-secretion of this hormone. These women present with chronic infertility due to anovulation. Thanks to the work of the Inserm researchers from unit 693 "Steroid receptors: endocrinian and metabolic physiopathology", the intimate mechanism of the hyperprolactinaemia alterations affecting reproduction in mice has been discovered.

This work has been published in the journal JCI.

Hyperprolactinaemia is a major cause of anovulation and is responsible for menstruation disorders and infertility. However, not much was know in detail of the mechanisms that cause this pathology. All that was known was that an increase in in women disturbed one of the most important hormones affecting reproduction and fertility: GnRH .

Up until now, we had been unable to understand this of prolactin in the GnRH neurons, because most of these neurons did not express the prolactin receptor.

So the researchers put forward another hypothesis: what if it was due to the indirect action of other molecules?

The team led by Jacques Young and Nadine Binart from Inserm unit 693 ": endocrinian and metabolic physiopathology" at the Bicêtre hospital, discovered that prolactin had an indirect effect on GnRH. Using mice as models, they demonstrated that prolactin effectively inhibits the secretion of neurons situated upstream the GnRH neurons and that are essential to their functioning. They secrete a neurohormone known as kisspeptin.

Kisspeptin: the key to infertility?

In mice, hyperprolactinaemia directly inhibits the secretion of kisspeptin and by preventing the of GnRH, effectively blocks ovarian cyclicity. By administering kisspeptin, we can restore the release of GnRH and restart ovarian cyclic functioning and ovulation despite hyperprolactinaemia.

The effect of hyperprolactinaemia on the ovulation cycle (credit: J Young/Inserm)

This is both a physiopathological discovery that for the first time explains the link between and hyperprolactinaemia, and a new approach opening the way to an original therapy. On-going studies are aiming to validate the concept in women, so that we can provide a therapeutic alternative when the subject is resistant to the available medication.

Explore further: Fertility treatment: Safer drug for women leads to same live birth rate

More information: Hyperprolactinaemia-induced ovarian acyclicity is reversed by kisspeptin administration, JCI, 2012.

Related Stories

Recommended for you

Artificial beta cells

December 8, 2016

Researchers led by ETH Professor Martin Fussenegger at the Department of Biosystems Science and Engineering (D-BSSE) in Basel have produced artificial beta cells using a straightforward engineering approach.

Key regulator of bone development identified

December 8, 2016

Loss of a key protein leads to defects in skeletal development including reduced bone density and a shortening of the fingers and toes—a condition known as brachydactyly. The discovery was made by researchers at Penn State ...

Researchers question lifelong immunity to toxoplasmosis

December 8, 2016

Medical students are taught that once infected with Toxoplasma gondii—the "cat parasite"—then you're protected from reinfection for the rest of your life. This dogma should be questioned, argue researchers in an Opinion ...

TET proteins drive early neurogenesis

December 7, 2016

The fate of stem cells is determined by series of choices that sequentially narrow their available options until stem cells' offspring have found their station and purpose in the body. Their decisions are guided in part by ...

0 comments

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.