Abstract
Polycystic ovary syndrome (PCOS) is the most common form of anovulatory infertility, characterized by an increase of androgen levels, impaired steroid feedback into the brain, and often a metabolic phenotype, including weight gain and insulin resistance.
The neuropeptide kisspeptin is a master regulator of reproductive hormone secretion, and kisspeptin neurons express androgen receptors so are potential mediators of hyperandrogenemia. We hypothesised that the excessive secretion of reproductive hormones observed during PCOS is due to an impaired androgen signalling in kisspeptin neurons, leading to an over-activation of the kisspeptin system.