OBJECTIVE The relationship between insulin resistance and hyperandroge
nism led us to study insulin resistance in polycystic ovary syndrome (
PCOS) in order to determine its prevalence and pathogenesis. DESIGN Bl
ood samples were taken on the 8th day after menses commenced. PATIENTS
Sixty-one women with PCOS, 30 with normal weight (BMI < 25 kg/m2) (gr
oup 1) and 31 with obesity (BMI > 26 kg/m2) (group 2) were studied. Th
ey 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, testostero
ne, free testosterone, dehydroepiandrosterone, sex-hormone binding glo
bulin, androstenedione, and fasting insulin were measured. Insulin sen
sitivity was explored by the insulin tolerance test (ITT). ITT was per
formed 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 b
lood glucose (DELTAG/G index). RESULTS DELTAG/G was correlated with ot
her 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: AG/G lean PCOS vs lead contr
ols: 0.45 +/- 0.02 vs 0.61 +/- 0.01, P < 0.001; AG/G obese PCOS vs obe
se controls: 0.32 +/- 0.02 vs 0.40 +/- 0.01, P < 0.02. Insulin resista
nce was higher in group A than in group B: DELTAG/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 DEL
TAG/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 compleme
ntary action in PCOS.