Seifer D B, Collins R L
Yale University School of Medicine, New Haven, Connecticut.
Fertil Steril. 1990 Nov;54(5):757-71. doi: 10.1016/s0015-0282(16)53928-4.
beta-Endorphin has a role in the regulation of the normal menstrual cycle and possibly in the onset of puberty. We have reviewed the evidence pointing to an alteration in this neuropeptide that may contribute to the pathogenesis of various reproductive dysfunctions. Elevated or high levels of beta-endorphin have been associated with exercise-associated amenorrhea, stress-associated amenorrhea, and polycystic ovarian syndrome. Depressed or low levels of beta-endorphin have been associated with PMS and menopause. Alterations in the levels of beta-endorphin may change the pulsatile release of GnRH via noradrenergic and/or dopaminergic pathways. We have primarily focused on beta-endorphin as representative of the endogenous opioid peptides, but other opioid peptides may also contribute to the pathogenesis of various types of reproductive dysfunction. Perhaps it will become possible to characterize and hone our understanding of the function of beta-endorphin and the other substances composing the endogenous opioid peptides. A better understanding of their role in physiological as well as pathophysiological processes may allow for the development of rational approaches to the treatment of specific disorders pertaining to reproduction. Many questions remain unanswered. Among the most relevant are: what is the precise mechanism of action by which beta-endorphin exerts its influence on pulsatile GnRH release? Is there a functional relationship between CNS and peripheral (serum) levels of beta-endorphin? Are the detected changes in beta-endorphin levels merely associated, or are they a cause of a particular disorder? Since it took almost 40 years between the time prostaglandins were first discovered and eventual realization of their clinical application, it may take some time before the beta-endorphin story is complete.
β-内啡肽在正常月经周期的调节中发挥作用，并且可能与青春期的开始有关。我们回顾了指向这种神经肽改变的证据，这种改变可能促成各种生殖功能障碍的发病机制。β-内啡肽水平升高或过高与运动性闭经、应激性闭经和多囊卵巢综合征有关。β-内啡肽水平降低或过低与经前综合征和更年期有关。β-内啡肽水平的改变可能通过去甲肾上腺素能和/或多巴胺能途径改变促性腺激素释放激素（GnRH）的脉冲式释放。我们主要关注β-内啡肽作为内源性阿片肽的代表，但其他阿片肽也可能促成各种类型生殖功能障碍的发病机制。也许将有可能明确并加深我们对β-内啡肽以及构成内源性阿片肽的其他物质功能的理解。更好地了解它们在生理以及病理生理过程中的作用，可能有助于开发针对特定生殖疾病的合理治疗方法。许多问题仍未得到解答。其中最相关的问题包括：β-内啡肽对GnRH脉冲式释放施加影响的精确作用机制是什么？β-内啡肽的中枢神经系统（CNS）水平与外周（血清）水平之间是否存在功能关系？检测到的β-内啡肽水平变化仅仅是相关联的，还是它们是特定疾病的原因？由于从前列腺素首次被发现到最终实现其临床应用花了近40年时间，β-内啡肽的故事可能还需要一些时间才能完整。
