Celik Onder, Aydin Suleyman, Celik Nilufer, Ugur Kader, Yavuzkir Seyda, Hatirnaz Safak, Yardim Meltem, Celik Sude
Private Clinic, Obstetrics and Gynecology, Usak, Turkey.
Department of Medical Biochemistry, Firat University, School of Medicine, Elazig, Turkey.
Cell Mol Biol (Noisy-le-grand). 2019 Mar 31;65(3):32-40.
Obesity and hyperandrogenemia are known to have adverse effects on both developing follicle and endometrium receptivity in polycystic ovarian syndrome (PCOS). Insulin resistance also contributes to this dilemma as a cause or a consequence and leads to worsening of the clinical picture. The difficulty in obtaining pregnancy despite the presence of a large number of oocyte has concentrated our attention on oocyte quality and development. However, the occurence of subfertility has also caused us to investigate the presence of different etiologic agents in non-obese PCOS women with normal androgen and insulin levels. In this context peptides have become the most accused and investigated molecules in cases of impaired fertility due to PCOS. Most of the studies investigating the relationship between PCOS and peptide did not support each other. The difficulties in measuring peptide levels as well as the individual variations in peptide synthesis and release are possible causes of this incongruity. For all these reasons, the incorporation of studies investigating the relationship between PCOS, peptide and subfertility in an article has become critical to pioneering future work. Understanding the association between peptides and subfertility will help us to understand the effects of peptides on failed fertility in PCOS. Moreover, updating our knowledge about peptides may allow us designing new drugs to to treat subfertility in PCOS. This review provides a general summary of the mechanisms of action of neuroendocrine peptides in regulating reproductive events. Since it is not usual to discuss all peptides in this context, only the effects of key central and peripheral peptides on fertility in PCOS have been extensively addressed.
众所周知，肥胖和高雄激素血症对多囊卵巢综合征（PCOS）中发育中的卵泡和子宫内膜容受性均有不良影响。胰岛素抵抗作为一个原因或结果也促成了这一困境，并导致临床症状恶化。尽管存在大量卵母细胞，但受孕困难使我们将注意力集中在卵母细胞质量和发育上。然而，生育力低下的发生也促使我们研究雄激素和胰岛素水平正常的非肥胖PCOS女性中不同病因的存在情况。在这种情况下，肽已成为PCOS导致生育力受损病例中最受指责和研究的分子。大多数研究PCOS与肽之间关系的研究结果并不相互支持。测量肽水平的困难以及肽合成和释放的个体差异可能是造成这种不一致的原因。出于所有这些原因，在一篇文章中纳入研究PCOS、肽与生育力低下之间关系的研究对于开创未来工作至关重要。了解肽与生育力低下之间的关联将有助于我们理解肽对PCOS中生育失败的影响。此外，更新我们对肽的认识可能使我们能够设计新药物来治疗PCOS中的生育力低下。本综述提供了神经内分泌肽调节生殖事件作用机制的一般概述。由于在此背景下讨论所有肽并不常见，因此仅广泛探讨了关键的中枢和外周肽对PCOS生育力的影响。
