title: Polycystic ovaries in non-obese and obese patients: possible pathophysiological mechanism based on new interpretation of facts and findings.
abstract: This study was designed to investigate the basic concentrations of different hormones in obese and non-obese patients with polycystic ovarian disease (PCOD). Eight women with PCOD, of whom four were obese with body mass index (BMI, kg/m2) of > 25 and four were non-obese with BMI < 25, volunteered to participate in this study. Serum samples were taken every 20 min over an 8 h period, starting at 2300 h, on day 5 of a spontaneous or gestagen-induced cycle. Basic insulin concentration was found to be significantly higher in the obese women compared with their non-obese counterparts (P < 0.0001). Serum concentrations of insulin-like growth factor binding protein (IGFBP-I) and sex hormone binding globulin (SHBG) were found to be significantly lower (P < 0.001 for both hormones) in the obese compared with the non-obese women. Serum concentrations of insulin-like growth factor I (IGF-I) did not differ between the two groups. The non-obese women had significantly higher serum concentrations of luteinizing hormone (LH) (P < 0.001) and of growth hormone (GH) (P < 0.002) than their obese counterparts. Based on these results, two models of the development of PCOD were suggested. In obese women, hyperinsulinaemia causes an excessive production of androgens through the enhancement of IGF-I receptors which, in synergism with LH, causes increased activity of cytochrome P-450c 17a. In non-obese patients, relative increase of GH concentration stimulates excessive ovarian IGF-I production. At this point synergism with LH results in excessive production of androgens by the same mechanism as in obese patients.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Obstetrics and Gynaecology, Kaplan Hospital, Rehovot, Israel.
authors.forename: V
authors.initials: V
authors.lastname: Insler
authors.forename: Z
authors.initials: Z
authors.lastname: Shoham
authors.forename: A
authors.initials: A
authors.lastname: Barash
authors.forename: R
authors.initials: R
authors.lastname: Koistinen
authors.forename: M
authors.initials: M
authors.lastname: Seppälä
authors.forename: M
authors.initials: M
authors.lastname: Hen
authors.forename: B
authors.initials: B
authors.lastname: Lunenfeld
authors.forename: Z
authors.initials: Z
authors.lastname: Zadik
mesh_terms: D000328:Adult; D002352:Carrier Proteins / Q000097:blood; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D013006:Growth Hormone / Q000097:blood; D006801:Humans; D007328:Insulin / Q000097:blood; D018970:Insulin-Like Growth Factor Binding Protein 1; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D007986:Luteinizing Hormone / Q000097:blood; D009765:Obesity / Q000150:complications* / Q000503:physiopathology; D011085:Polycystic Ovary Syndrome / Q000150:complications* / Q000503:physiopathology*; D012738:Sex Hormone-Binding Globulin / Q000378:metabolism
chemical_list: D002352:Carrier Proteins; D007328:Insulin; D018970:Insulin-Like Growth Factor Binding Protein 1; D012738:Sex Hormone-Binding Globulin; D007334:Insulin-Like Growth Factor I; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D013006:Growth Hormone