{"title":"胰岛素样生长因子结合蛋白:它们在多囊卵巢综合征中起作用吗?","authors":"N A Cataldo","doi":"10.1055/s-2007-1016295","DOIUrl":null,"url":null,"abstract":"<p><p>Insulin-like growth factor (IGF) binding proteins are produced by ovarian follicular cells and can oppose the effects of the IGFs and gonadotropins on these cells. Since polycystic ovarian syndrome (PCOS) is characterized by disordered follicular development, with the accumulation of antral follicles within the ovary which fail to respond appropriately to endogenous FSH, it has been hypothesized that one or more IGFBPs, which can act as FSH antagonists in vitro, could play a role in inhibiting follicular development in this syndrome. Follicular fluid IGFBP levels, however, do not differ between PCOS follicles and the androgenic, presumably atretic follicles of cycling women without PCOS. Serum IGFBP-1 levels are lower in PCOS, likely because of hyperinsulinemia, and serum free IGF-1 levels are raised. This alternation may drive the excess thecal androgen production characteristic of PCOS follicles. Alterations in IGFBPs may sustain the anovulatory steady state in PCOS but are unlikely to initiate development of the syndrome.</p>","PeriodicalId":79457,"journal":{"name":"Seminars in reproductive endocrinology","volume":"15 2","pages":"123-36"},"PeriodicalIF":0.0000,"publicationDate":"1997-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-2007-1016295","citationCount":"36","resultStr":"{\"title\":\"Insulin-like growth factor binding proteins: do they play a role in polycystic ovary syndrome?\",\"authors\":\"N A Cataldo\",\"doi\":\"10.1055/s-2007-1016295\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Insulin-like growth factor (IGF) binding proteins are produced by ovarian follicular cells and can oppose the effects of the IGFs and gonadotropins on these cells. Since polycystic ovarian syndrome (PCOS) is characterized by disordered follicular development, with the accumulation of antral follicles within the ovary which fail to respond appropriately to endogenous FSH, it has been hypothesized that one or more IGFBPs, which can act as FSH antagonists in vitro, could play a role in inhibiting follicular development in this syndrome. Follicular fluid IGFBP levels, however, do not differ between PCOS follicles and the androgenic, presumably atretic follicles of cycling women without PCOS. Serum IGFBP-1 levels are lower in PCOS, likely because of hyperinsulinemia, and serum free IGF-1 levels are raised. This alternation may drive the excess thecal androgen production characteristic of PCOS follicles. Alterations in IGFBPs may sustain the anovulatory steady state in PCOS but are unlikely to initiate development of the syndrome.</p>\",\"PeriodicalId\":79457,\"journal\":{\"name\":\"Seminars in reproductive endocrinology\",\"volume\":\"15 2\",\"pages\":\"123-36\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1997-05-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1055/s-2007-1016295\",\"citationCount\":\"36\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Seminars in reproductive endocrinology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1055/s-2007-1016295\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Seminars in reproductive endocrinology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1055/s-2007-1016295","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Insulin-like growth factor binding proteins: do they play a role in polycystic ovary syndrome?
Insulin-like growth factor (IGF) binding proteins are produced by ovarian follicular cells and can oppose the effects of the IGFs and gonadotropins on these cells. Since polycystic ovarian syndrome (PCOS) is characterized by disordered follicular development, with the accumulation of antral follicles within the ovary which fail to respond appropriately to endogenous FSH, it has been hypothesized that one or more IGFBPs, which can act as FSH antagonists in vitro, could play a role in inhibiting follicular development in this syndrome. Follicular fluid IGFBP levels, however, do not differ between PCOS follicles and the androgenic, presumably atretic follicles of cycling women without PCOS. Serum IGFBP-1 levels are lower in PCOS, likely because of hyperinsulinemia, and serum free IGF-1 levels are raised. This alternation may drive the excess thecal androgen production characteristic of PCOS follicles. Alterations in IGFBPs may sustain the anovulatory steady state in PCOS but are unlikely to initiate development of the syndrome.