title: The significance of polycystic-appearing ovaries versus normal-appearing ovaries in patients with polycystic ovary syndrome.
abstract: OBJECTIVE
  To evaluate what hormonal or biochemical parameters are most highly associated with the finding of polycystic-appearing ovaries as compared with normal-appearing ovaries in women with polycystic ovary syndrome (PCOS).
  
  
  METHODS
  Prospective randomized study.
  
  
  METHODS
  Academic medical center.
  
  
  METHODS
  Ten women with PCOS-five with normal-appearing ovaries and five with polycystic-appearing ovaries-were matched for age and body mass index. All had serum T levels between 80 and 150 ng/dL (conversion factor to SI unit, 3.467).
  
  
  METHODS
  Insulin infusion for the purpose of performing insulin tolerance testing to evaluate insulin resistance or sensitivity.
  
  
  METHODS
  We measured serum T, DHEAS, androstenedione, sex-hormone binding globulin, 5 alpha-androstane-3 alpha-17 beta-androstenediol glucuronide, FSH, LH, insulin-like growth factor-I, insulin-like growth factor binding protein-1, and insulin-like growth factor binding protein-3. Insulin resistance, measured by insulin tolerance testing, also was done on the same day after the patient had fasted for at least 8 hours.
  
  
  RESULTS
  Serum androgens and binding proteins were not significantly different in both groups. Insulin tolerance testing demonstrated a slower glucose disappearance in the polycystic appearing ovary group (Kitt glucose was 4.58% +/- 1.4%/min in the normal-appearing ovaries group versus 2.07% +/- 1.07%/min in the polycystic-appearing ovaries group).
  
  
  CONCLUSIONS
  Women with PCOS and polycystic-appearing ovaries do not demonstrate any definitive serum hormonal differences compared with women with PCOS and normal-appearing ovaries. The presence of polycystic-appearing ovaries correlates significantly with the presence of insulin resistance.
authors.affiliation: Department of Obstetrics and Gynecology, University of Southern California School of Medicine, Los Angeles, USA.
authors.forename: S
authors.initials: S
authors.lastname: Najmabadi
authors.forename: J G
authors.initials: JG
authors.lastname: Wilcox
authors.forename: B D
authors.initials: BD
authors.lastname: Acacio
authors.forename: M H
authors.initials: MH
authors.lastname: Thornton
authors.forename: B A
authors.initials: BA
authors.lastname: Kolb
authors.forename: R J
authors.initials: RJ
authors.lastname: Paulson
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D002352:Carrier Proteins / Q000097:blood; D015331:Cohort Studies; D005260:Female; D012739:Gonadal Steroid Hormones / Q000097:blood; D006065:Gonadotropins, Pituitary / Q000097:blood; D006801:Humans; D007004:Hypoglycemic Agents / Q000008:administration & dosage / Q000494:pharmacology; D007328:Insulin / Q000008:administration & dosage / Q000494:pharmacology; D007333:Insulin Resistance / Q000502:physiology*; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D010053:Ovary; D011085:Polycystic Ovary Syndrome / Q000097:blood / Q000503:physiopathology*; D011446:Prospective Studies
chemical_list: D001786:Blood Glucose; D002352:Carrier Proteins; D012739:Gonadal Steroid Hormones; D006065:Gonadotropins, Pituitary; D007004:Hypoglycemic Agents; D007328:Insulin; D007334:Insulin-Like Growth Factor I