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作 者:许倩 刘斌 王道娟 王勇[1] XU Qian;LIU Bin;WANG Dao-juan;WANG Yong(State Key Laboratory of Analytacal Chemistry for Life Science&Jiangsu Key Laboratory of Molecular Medicine,Medical School,Nanjing University,Nanjing 210093,China)
机构地区:[1]南京大学医学院生命分析化学国家重点实验室,江苏省医学分子技术重点实验室,210093
出 处:《国际妇产科学杂志》2021年第2期203-208,共6页Journal of International Obstetrics and Gynecology
基 金:国家自然科学基金(81771539)。
摘 要:多囊卵巢综合征是一种育龄女性常见的内分泌紊乱疾病,以雄激素过多和胰岛素抵抗为主要特征,病理生理突出表现为卵泡发育不良。其发病原因至今尚不明确,现多认为雄激素在其发病中起重要作用。在胚胎早期发育过程中,过量雄激素暴露影响卵巢外神经内分泌系统,类固醇激素负反馈途径缺陷与促性腺激素释放激素神经元活性异常引起下丘脑-垂体-性腺轴损害,最终导致下游靶器官的形态功能异常而产生相应临床改变。这一过程中的主要微观机制主要涉及弓状核中的kisspeptin-神经激肽B-强啡肽神经元以及GABA能神经元的电生理和分泌活动的改变等。综述胚胎发育早期雄激素过量引起的神经内分泌改变及其导致多囊卵巢综合征的主要证据与可能机制,并对胚胎发育期高雄激素诱导神经内分泌紊乱的临床应用作出展望。Characterized by excess androgen and insulin resistance,polycystic ovary syndrome(PCOS)is a common endocrine disorder with follicular atresia and stasis.Though the etiology and pathogenesis of PCOS remains unclear,androgen is now thought to play an important role in the onset of PCOS.Early in embryonic development,neuroendocrine dysfunction induced by excess androgen affects the hypothalamic-pituitary-ovary axis owing to defects of steroid hormone negative feedback pathway and abnormal activity of gonadotropin releasing hormone neurons,resulting in the downstream consequence in target organs.The key mechanism probably is the abnormal steroid hormone feedback and the increased activity of gonadotropin-releasing hormone neurons.This review discusses the major evidence and conceivable mechanisms by which neuroendocrine dysfunction induced by excess androgen at early developmental points originates PCOS,and prospects the potential clinical applications for preventing and intervening PCOS.
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