While prolactin (PRL) is known as the pituitary hormone of lactation, accumulating evidence shows that PRL acts on many tissues and in many pathophysiological conditions. The major isoform, 23 kDa PRL, acts via a membrane receptor, the prolactin receptor (PRL-R), a member of the hematopoietic cytokine superfamily, and for which the mechanism of activation has been elucidated. The aim of this symposium is to present and discuss data supporting actions of PRL in hyperprolactinemia in the context of gonadotropic deficiency. High levels of PRL in humans may interfere with reproductive function mainly by actions at the hypothalamus. Our data suggest that Kisspeptin neurons appear to be the missing link between hyperprolactinemia and GnRH deficiency. Otherwise, germline PRLR mutations have been suspected to be a specific genetic cause of prolactinoma in humans. This will be discussed in light of our recent results.
20 May 2017 - 23 May 2017