多囊卵巢综合征（PCOS）中卵巢类固醇生成及其他组织胰岛素信号通路的缺陷。
Defects in insulin signaling pathways in ovarian steroidogenesis and other tissues in polycystic ovary syndrome (PCOS).
作者信息
Diamanti-Kandarakis Evanthia, Argyrakopoulou Georgia, Economou Frangiskos, Kandaraki Eleni, Koutsilieris Michael
机构信息
Endocrine Section, First Department of Internal Medicine, University of Athens Medical School, 17 Ag. Thoma, Goudi 11527, Athens, Greece.
出版信息
J Steroid Biochem Mol Biol. 2008 Apr;109(3-5):242-6. doi: 10.1016/j.jsbmb.2008.03.014. Epub 2008 Mar 12.
The polycystic ovary syndrome (PCOS) is the most common endocrinopathy in women of reproductive age today. Women with PCOS often demonstrate defective ovarian steroid biosynthesis and present with hyperandrogenemia. Moreover, 50-70% of PCOS women are insulin resistant and hyperinsulinemic. Insulin acts on the ovary via its own receptor and interacts with gonadotrophins, modulating steroidogenesis. The precise role of insulin and the molecular mechanisms that take place are not yet completely explicated. This review will be focused on insulin's action on the ovary and other target tissues, describing the intracellular signaling pathways implicated in steroidogenesis and their defects in women with PCOS.
多囊卵巢综合征（PCOS）是当今育龄女性中最常见的内分泌疾病。患有PCOS的女性通常表现出卵巢类固醇生物合成缺陷，并伴有高雄激素血症。此外，50%-70%的PCOS女性存在胰岛素抵抗和高胰岛素血症。胰岛素通过自身受体作用于卵巢，并与促性腺激素相互作用，调节类固醇生成。胰岛素的确切作用以及所发生的分子机制尚未完全阐明。本综述将聚焦于胰岛素对卵巢和其他靶组织的作用，描述与类固醇生成相关的细胞内信号通路及其在PCOS女性中的缺陷。
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