Kreze A, Hrnciar J, Dobáková M
Interná klinika A, Nemocnica F.D. Roosevelta, Banská Bystrica.
Vnitr Lek. 1995 Feb;41(2):126-8.
In the submitted paper the authors try to explain the relationship between hyperinsulinism as the cause and the polycystic ovary syndrome as the consequence of hyperinsulinism. This takes place via the insulin like growth factor I, the luteinizing hormone, sex binding hormone globulin, insulin like growth factor I binding protein and growth hormone. By varying interactions of the regulatory hormones gradually the granulosa cells are destroyed and replaced by androstendione producing thecal and stromal cells with impaired folliculogenesis. Chronic hyperestrogenism interferes also with hypothalamic regulation in the nucleus arcuatus. As almost identical changes are found in polycystic ovary syndrome and puberty, genetic and/or environmental factors certainly play a part. Their more detailed specification is a task for the future.
在提交的论文中,作者试图解释高胰岛素血症作为病因与多囊卵巢综合征作为高胰岛素血症后果之间的关系。这一过程通过胰岛素样生长因子I、促黄体生成素、性激素结合球蛋白、胰岛素样生长因子I结合蛋白和生长激素来实现。通过调节激素之间不同的相互作用,颗粒细胞逐渐被破坏,并被产生雄烯二酮的卵泡膜细胞和基质细胞所取代,从而导致卵泡发生受损。慢性高雌激素血症也会干扰弓状核中的下丘脑调节。由于在多囊卵巢综合征和青春期发现了几乎相同的变化,遗传和/或环境因素肯定起到了一定作用。对它们更详细的说明是未来的一项任务。