The Kiss1 system and polycystic ovary syndrome: lessons from physiology and putative pathophysiologic implications.

摘要: Polycystic ovary syndrome (PCOS) is a highly prevalent heterogeneous disease characterized by ovulatory dysfunction, hyperandrogenism, and metabolic alterations. Women with PCOS commonly display dysregulated gonadotropin secretion higher LH pulsatility perturbed LH-FSH ratios, which likely contributes to the ovarian phenotype might be indicative of disrupted GnRH secretory activity. Although involvement altered androgen insulin levels in pathogenesis neuroendocrine alterations has been explored various experimental clinical settings, ultimate mechanisms whereby such neurohormonal perturbations take place remain partially unknown. In recent years, kisspeptins, products Kiss1 gene that operate via surface receptor Gpr54, have emerged as essential elements reproductive brain play an indispensable role control ovulation. addition, neurons are targets transmitters regulatory actions sex steroids cues on axis during early organizing periods adulthood. Furthermore, Kiss1/kisspeptin expression documented species, including humans; yet clear evidence for kisspeptin signaling ovulation, or its alterations, still pending. Based these physiologic features, we discuss putative pathophysiologic implications system generation summarize scarce support role.