title: Roles of LH and insulin resistance in lean and obese polycystic ovary syndrome.
abstract: OBJECTIVE
  The relationship between insulin resistance and hyperandrogenism led us to study insulin resistance in polycystic ovary syndrome (PCOS) in order to determine its prevalence and pathogenesis.
  
  
  METHODS
  Blood samples were taken on the 8th day after menses commenced.
  
  
  METHODS
  Sixty-one women with PCOS, 30 with normal weight (BMI < 25 kg/m2) (group 1) and 31 with obesity (BMI > 26 kg/m2) (group 2) were studied. They were divided also according to LH level: group A, low or normal LH (n = 23) and group B, high LH (n = 38). Twenty lean control women and 16 obese control women were studied.
  
  
  METHODS
  Serum LH, testosterone, free testosterone, dehydroepiandrosterone, sex-hormone binding globulin, androstenedione, and fasting insulin were measured. Insulin sensitivity was explored by the insulin tolerance test (ITT). ITT was performed by bolus i.v. insulin of 0.1 IU/kg. Blood glucose was measured before (-5,0) and after injection (3, 5, 7, 10, 15 minutes). Insulin sensitivity was given by the ratio of glycaemic variation to initial blood glucose (delta G/G index).
  
  
  RESULTS
  delta G/G was correlated with other insulin resistance parameters, particularly fasting insulin r = 0.40, P < 0.01. The PCOS groups had the following insulin resistances (mean +/- SEM) compared to matched groups: delta G/G lean PCOS vs lead controls: 0.45 +/- 0.02 vs 0.61 +/- 0.01, P < 0.001; delta G/G obese PCOS vs obese controls: 0.32 +/- 0.02 vs 0.40 +/- 0.01, P < 0.02. Insulin resistance was higher in group A than in group B: delta G/G 0.29 +/- 0.02 vs 0.45 +/- 0.02, P < 0.001. The prevalence of insulin resistance was 63% in lean PCOS and 51% in obese PCOS. Positive correlations between delta G/G index and LH were found in group 1 and 2, respectively r = 0.45, P < 0.01 and r = 0.55, P < 0.01.
  
  
  CONCLUSIONS
  PCOS was associated with a significant decrease of insulin sensitivity, independent of obesity. The correlation between LH and insulin sensitivity suggests a complementary action in PCOS.
authors.affiliation: Clinique Médicale B CHU Reims, France.
authors.forename: H
authors.initials: H
authors.lastname: Grulet
authors.forename: A C
authors.initials: AC
authors.lastname: Hecart
authors.forename: B
authors.initials: B
authors.lastname: Delemer
authors.forename: A
authors.initials: A
authors.lastname: Gross
authors.forename: V
authors.initials: V
authors.lastname: Sulmont
authors.forename: M
authors.initials: M
authors.lastname: Leutenegger
authors.forename: J
authors.initials: J
authors.lastname: Caron
mesh_terms: D000293:Adolescent; D000328:Adult; D005260:Female; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology*; D007986:Luteinizing Hormone / Q000097:blood / Q000378:metabolism*; D009765:Obesity / Q000097:blood / Q000150:complications*; D011085:Polycystic Ovary Syndrome / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D015995:Prevalence; D013739:Testosterone / Q000097:blood
chemical_list: D007328:Insulin; D013739:Testosterone; D007986:Luteinizing Hormone