Current Concepts in the Polycystic Ovary Syndrome
- 1 February 2001
- journal article
- review article
- Published by Annual Reviews in Annual Review of Medicine
- Vol. 52 (1), 401-419
- https://doi.org/10.1146/annurev.med.52.1.401
Abstract
▪ Abstract Over the past 20 years, it has been clearly documented that the polycystic ovary syndrome (PCOS) has major metabolic sequelae related to insulin resistance and that insulin resistance plays an important role in the pathogenesis of the reproductive disturbances of the disorder. Family studies have indicated a genetic susceptibility to PCOS. Polycystic ovaries and hyperandrogenemia are present in ∼50% of sisters of affected women. Increased androgen secretion and insulin resistance persist in cultured theca cells and skin fibroblasts, respectively, from women with PCOS; this finding suggests that these are intrinsic, presumably genetic, defects. Insulin resistance and elevated low-density lipoprotein (LDL) levels also cluster in the sisters of women with PCOS, consistent with genetic traits. Moreover, the brothers of women with PCOS have insulin resistance and elevated dehydroepiandrosterone sulfate (DHEAS) levels, which supports a genetic basis for these findings. Family-based studies of linkage...Keywords
This publication has 80 references indexed in Scilit:
- Ovulatory and Metabolic Effects of d-Chiro-Inositol in the Polycystic Ovary SyndromeNew England Journal of Medicine, 1999
- Insulin Stimulates Testosterone Biosynthesis by Human Thecal Cells from Women with Polycystic Ovary Syndrome by Activating Its Own Receptor and Using Inositolglycan Mediators as the Signal Transduction SystemJournal of Clinical Endocrinology & Metabolism, 1998
- Cellular Insulin Resistance in Adipocytes from Obese Polycystic Ovary Syndrome Subjects Involves Adenosine Modulation of Insulin SensitivityJournal of Clinical Endocrinology & Metabolism, 1997
- Decreases in Ovarian Cytochrome P450c17α Activity and Serum Free Testosterone after Reduction of Insulin Secretion in Polycystic Ovary SyndromeNew England Journal of Medicine, 1996
- Excessive insulin receptor serine phosphorylation in cultured fibroblasts and in skeletal muscle. A potential mechanism for insulin resistance in the polycystic ovary syndrome.Journal of Clinical Investigation, 1995
- Insulin secretory defects in polycystic ovary syndrome. Relationship to insulin sensitivity and family history of non-insulin-dependent diabetes mellitus.Journal of Clinical Investigation, 1995
- Insulin receptor phosphorylation, insulin receptor substrate-1 phosphorylation, and phosphatidylinositol 3-kinase activity are decreased in intact skeletal muscle strips from obese subjects.Journal of Clinical Investigation, 1995
- Defects in beta-cell function in functional ovarian hyperandrogenismJournal of Clinical Endocrinology & Metabolism, 1993
- Evidence for distinctive and intrinsic defects in insulin action in polycystic ovary syndromeDiabetes, 1992
- A Chronobiologic Abnormality in Luteinizing Hormone Secretion in Teenage Girls with the Polycystic-Ovary SyndromeNew England Journal of Medicine, 1983