title: The influence of luteinizing hormone and insulin on sex steroids and sex hormone-binding globulin in the polycystic ovarian syndrome.
abstract: OBJECTIVE
  To examine the relationship between hyperinsulinemia, sex hormone-binding globulin (SHBG), and body mass index (BMI) on LH-induced hyperandrogenemia in patients with polycystic ovarian syndrome (PCOS).
  
  
  METHODS
  Insulin responses during an oral glucose tolerance test (OGTT) were assessed in 25 consecutive women with PCOS and 20 control women matched for BMI. Insulin responses and sensitivity (SI) were also determined using a frequently sampled intravenous glucose tolerance test (IVGTT).
  
  
  METHODS
  The clinical research center at a university medical center.
  
  
  METHODS
  Serum LH, SI, and basal, peak, and area under the curve (AUC-insulin responses) were determined and correlated with SHBG, androstenedione (A), T, and free T concentrations.
  
  
  RESULTS
  Compared with controls, the AUC-insulin response during OGTT was greater in PCOS, with an average increase of 44%. During IVGTT, AUC-insulin response was also significantly higher in PCOS versus controls, with an average increase of 53%. In addition, SI was reduced in PCOS versus controls with an average decrease of 53%. The average differences in oral- and intravenous-glucose-induced hyperinsulinemia and in insulin sensitivity between PCOS and controls were relatively constant across the entire physiological range of BMI. In PCOS, baseline LH showed strong positive correlations with baseline A and T. However, there were no significant correlations between either basal, peak, or AUC-insulin response during OGTT and IVGTT with basal T or A concentrations or between insulin and androgen levels measured at 30-minute intervals throughout the OGTT. However, basal, peak, and AUC-insulin responses during OGTT were strongly correlated with fasting SHBG binding capacity.
  
  
  CONCLUSIONS
  These data are consistent with the hypothesis that hyperinsulinemia in PCOS influences the biologically active component of T by lowering SHBG concentrations while having little apparent impact on LH-induced secretion of androgens in vivo.
authors.affiliation: Department of Obstetrics and Gynecology, University of California Los Angeles (UCLA).
authors.forename: R P
authors.initials: RP
authors.lastname: Buyalos
authors.forename: M E
authors.initials: ME
authors.lastname: Geffner
authors.forename: R M
authors.initials: RM
authors.lastname: Watanabe
authors.forename: R N
authors.initials: RN
authors.lastname: Bergman
authors.forename: J A
authors.initials: JA
authors.lastname: Gornbein
authors.forename: H L
authors.initials: HL
authors.lastname: Judd
mesh_terms: D000284:Administration, Oral; D000328:Adult; D001786:Blood Glucose / Q000032:analysis; D015992:Body Mass Index; D005260:Female; D005951:Glucose Tolerance Test; D012739:Gonadal Steroid Hormones / Q000097:blood*; D006801:Humans; D007275:Injections, Intravenous; D007328:Insulin / Q000097:blood / Q000494:pharmacology*; D007986:Luteinizing Hormone / Q000494:pharmacology*; D011085:Polycystic Ovary Syndrome / Q000097:blood* / Q000473:pathology; D012738:Sex Hormone-Binding Globulin / Q000032:analysis*
chemical_list: D001786:Blood Glucose; D012739:Gonadal Steroid Hormones; D007328:Insulin; D012738:Sex Hormone-Binding Globulin; D007986:Luteinizing Hormone