Persistence of insulin resistance in polycystic ovarian disease after inhibition of ovarian steroid secretion.
Six nonobese women with polycystic ovarian disease (PCOD) showed significant hyperinsulinemia, compared with controls after oral glucose (P less than 0.05). As an indicator of insulin sensitivity, in vitro proliferation of erythrocyte progenitor cells of PCOD subjects exposed to physiologic concentrations of insulin was significantly blunted (P less than 0.001). Monocyte insulin receptor binding was not impaired in the PCOD subjects. Three of the PCOD patients were treated with a long-acting gonadotropin-releasing hormone agonist for 6 months, which resulted in marked suppression of ovarian androgen secretion but no demonstrable changes in in vivo or in vitro indicators of insulin resistance. Thus insulin resistance in PCOD subjects appears to be unrelated to ovarian hyperandrogenism (or acanthosis or obesity). Although certain tissues are insulin-resistant in PCOD patients, the ovary may remain sensitive and overproduce androgens in response to high circulating insulin levels.
D000328:Adult; D001835:Body Weight; D005260:Female; D005951:Glucose Tolerance Test; D007987:Gonadotropin-Releasing Hormone / Q000031:analogs & derivatives / Q000627:therapeutic use; D006412:Hematopoietic Stem Cells / Q000187:drug effects; D006728:Hormones / Q000627:therapeutic use; D006801:Humans; D006946:Hyperinsulinism / Q000209:etiology* / Q000378:metabolism; D007328:Insulin / Q000494:pharmacology; D007333:Insulin Resistance; D009000:Monocytes / Q000378:metabolism; D011085:Polycystic Ovary Syndrome / Q000150:complications* / Q000188:drug therapy / Q000378:metabolism; D011972:Receptor, Insulin / Q000378:metabolism
D006728:Hormones; D007328:Insulin; D007987:Gonadotropin-Releasing Hormone; C010661:surfagon; D011972:Receptor, Insulin