Abstract
Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women and a major cause of anovulatory infertility. A diagnosis of PCOS is established based the presence of two out of three clinical symptoms, which are criteria accepted by the ESHRE/ASRM (European Society of Human Reproduction and Embryology/American Society for Reproductive Medicine). Gonadotropin-releasing hormone (GnRH) is responsible for the release of luteinizing hormone, and follicle stimulating hormone from the pituitary and contributes a leading role in controlling reproductive function in humans. The goal of this review is to present the current knowledge on neuroendocrine determinations of PCOS. The role of such neurohormones as GnRH, and neuropeptides kisspeptin, neurokinin B, phoenixin-14, and galanin is discussed in this aspect. Additionally, different neurotransmitters (gamma-aminobutyric acid (GABA), glutamate, serotonin, dopamine, and acetylcholine) can also be involved in neuroendocrine etiopathogenesis of PCOS. Studies have shown a persistent rapid GnRH pulse frequency in women with PCOS present during the whole ovulatory cycle. Other studies have proved that patients with PCOS are characterized by higher serum kisspeptin levels. The observations of elevated serum kisspeptin levels in PCOS correspond with the hypothesis that overactivity in the kisspeptin system is responsible for hypothalamic-pituitary-gonadal axis overactivity. In turn, this causes menstrual disorders, hyperandrogenemia and hyperandrogenism. Moreover, abnormal regulation of Neurokinin B (NKB) is also suspected of contributing to PCOS development, while NKB antagonists are used in the treatment of PCOS leading to reduction in Luteinizing hormone (LH) concentration and total testosterone concentration. GnRH secretion is regulated not only by kisspeptin and neurokinin B, but also by other neurohormones, such as phoenixin-14, galanin, and Glucagon-like peptide-1 (GLP-1), that have favorable effects in counteracting the progress of PCOS. A similar process is associated with the neurotransmitters such as GABA, glutamate, serotonin, dopamine, and acetylcholine, as well as the opioid system, which may interfere with secretion of GnRH, and therefore, influence the development and severity of symptoms in PCOS patients. Additional studies are required to explain entire, real mechanisms responsible for PCOS neuroendocrine background.
Highlights
Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women and a major cause of anovulatory infertility [1].A diagnosis of PCOS is established based on criteria accepted by the ESHRE/ASRM in Rotterdam in 2003
We focus on KNDy neurons, a group which express Kisspeptin, Neurokinin B, and Dynorphin A, produced in the hypothalamus
Authors investigated the available data from clinical studies, review articles, and meta-analyses following Medical Subject Headings (MeSH) terms, alone or in combination: PCOS, Polycystic ovary syndrome, gonadotropin-releasing hormone (GnRH), Gonadotropin-releasing hormone, Phoenixin, Galanin, Kisspeptin, Neurokinin B, Dynorphin A, KNDy neurons, and neurohormones
Summary
Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women and a major cause of anovulatory infertility [1]. Exposure to advanced glycation end-products (AGEs), often found in thermally processed foods, as well as diets high in protein and low in carbohydrates, stimulate insulin resistance. Increased levels of circulating insulin play a crucial role in the development of PCOS [7]. Excess insulin, acting synergistically with LH, stimulates ovarian theca cells to increase androgen production, and this excess of androgens inhibits the production of hepatic sex hormone binding globulin. A vicious cascade of events arises; excess insulin stimulates further androgen production in the ovaries and a reduction in the production of sex hormone binding globulin (SHBG) in the liver. Patients with PCOS demonstrate an increased level of circulation luteinizing hormone, which stimulates androgen secretion by ovarian theca cells [8,9]. The resulting chronic anovulation is due to the relatively low level of Follicle-stimulating hormone (FSH) that occurs secondary to the altered GnRH release pattern. KNDy play a key role in regulating pulsatile secretion of GnRH and as mediators of steroid hormone negative feedback
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