Grulet H, Hecart A C, Delemer B, Gross A, Sulmont V, Leutenegger M, Caron J
Clinique Médicale B CHU Reims, France.
Clin Endocrinol (Oxf). 1993 Jun;38(6):621-6. doi: 10.1111/j.1365-2265.1993.tb02144.x.
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.
Blood samples were taken on the 8th day after menses commenced.
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.
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).
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.
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.
胰岛素抵抗与高雄激素血症之间的关系促使我们研究多囊卵巢综合征（PCOS）中的胰岛素抵抗，以确定其患病率和发病机制。
在月经开始后的第8天采集血样。
研究了61例PCOS女性，其中30例体重正常（BMI<25kg/m²）（第1组），31例肥胖（BMI>26kg/m²）（第2组）。她们还根据促黄体生成素（LH）水平进行了分组：A组，LH水平低或正常（n=23）；B组，LH水平高（n=38）。研究了20例体重正常的对照女性和16例肥胖的对照女性。
测定血清LH、睾酮、游离睾酮、脱氢表雄酮、性激素结合球蛋白、雄烯二酮和空腹胰岛素。通过胰岛素耐量试验（ITT）评估胰岛素敏感性。ITT通过静脉推注0.1IU/kg胰岛素进行。在注射前（-5、0分钟）和注射后（3、5、7、10、15分钟）测量血糖。胰岛素敏感性通过血糖变化与初始血糖的比值（ΔG/G指数）表示。
ΔG/G与其他胰岛素抵抗参数相关，尤其是空腹胰岛素，r=0.40，P<0.01。与匹配组相比，PCOS组具有以下胰岛素抵抗（均值±标准误）：瘦型PCOS组与瘦型对照组的ΔG/G：0.45±0.02对0.61±0.01，P<0.001；肥胖型PCOS组与肥胖型对照组的ΔG/G：0.32±0.02对0.40±0.01，P<0.02。A组的胰岛素抵抗高于B组：ΔG/G为0.29±0.02对0.45±0.02，P<0.001。瘦型PCOS中胰岛素抵抗的患病率为63%，肥胖型PCOS中为51%。在第1组和第2组中分别发现ΔG/G指数与LH之间存在正相关，r=0.45，P<0.01和r=0.55，P<0.01。
PCOS与胰岛素敏感性显著降低相关，与肥胖无关。LH与胰岛素敏感性之间的相关性表明在PCOS中存在互补作用。
