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. DESIGN: Blood samples were taken on the 8th day after menses commenced. PATIENTS: 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. MEASUREMENTS: 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. CONCLUSION: 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.
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. DESIGN: Blood samples were taken on the 8th day after menses commenced. PATIENTS: 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. MEASUREMENTS: 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. CONCLUSION: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.