Olszanecka-Glinianowicz Magdalena, Banaś Michał, Zahorska-Markiewicz Barbara, Kuglin Dorota, Mokrzycka Joanna, Mentel Alicja
Department of Pathophysiology, Medical University of Silesia, Poland.
Endokrynol Pol. 2005 Nov-Dec;56(6):921-6.
of the present study was to evaluate serum concentrations of adrenal and ovarian androgens and sex hormone-binding globulin in obese women without additional diseases and in obese women with polycystic ovary syndrome with and without insulin resistance.
The study group involved 73 obese women (39 with PCOS--A and 34 obese without additional diseases--B). The serum concentration of glucose and insulin were measured and the study group was divided on the basis of HOMA index into two subgroups: A I-PCO without insulin resistance (n=18, mean age 27.2+/-5.9 yr; BMI 33.2+/-3.5 kg/m2); AII-PCO with insulin resistance (n=21, mean age 27.5+/-7.1 yr; BMI 37.6+/-6.5 kg/m2); B I-obese without insulin resistance (n=8, age 33.5+/-7.5 yr; BMI 35.2+/-4.8 kg/m2); B II-obese with insulin resistance (n=24, age 30.3+/-5.2 yr; BMI 36.4+/-5.8 kg/m2). Body mass and height were measured and body mass index was calculated with formula. Body composition was measured using bioimpedance method. The serum concentrations of FSH, LH, total and free testosterone, androstendione, DHEAS, SHBG and insulin were determined by RIA method and glucose was determined by enzymatic procedure.
We observed significantly higher body mass, fat mass and BMI in AII subgroup when compared to AI, BI and BII subgroups. Only serum concentration of free testosterone was significantly higher in AII subgroup when compared to AI subgroup. We observed a positive correlation between serum concentrations of insulin and free testosterone in both groups A and B, moreover we observed positive correlations between serum concentrations of insulin and both DHEAS and LH in group B.
It seems that insulin resistance plays a key role in the development of hyperandrogenism in obese women. However mechanisms leading to hyperandrogenism in PCOS are still unrevealed and seem to be more complex.
本研究的目的是评估无其他疾病的肥胖女性以及患有和未患有胰岛素抵抗的多囊卵巢综合征肥胖女性的肾上腺和卵巢雄激素及性激素结合球蛋白的血清浓度。
研究组包括73名肥胖女性(39名患有多囊卵巢综合征——A组,34名无其他疾病的肥胖女性——B组)。测量血清葡萄糖和胰岛素浓度,并根据稳态模型评估法(HOMA)指数将研究组分为两个亚组:AI——无胰岛素抵抗的多囊卵巢综合征(n = 18,平均年龄27.2±5.9岁;体重指数33.2±3.5kg/m²);AII——有胰岛素抵抗的多囊卵巢综合征(n = 21,平均年龄27.5±7.1岁;体重指数37.6±6.5kg/m²);BI——无胰岛素抵抗的肥胖者(n = 8,年龄33.5±7.5岁;体重指数35.2±4.8kg/m²);BII——有胰岛素抵抗的肥胖者(n = 24,年龄30.3±5.2岁;体重指数36.4±5.8kg/m²)。测量体重和身高,并用公式计算体重指数。采用生物电阻抗法测量身体成分。采用放射免疫分析法(RIA)测定血清促卵泡生成素(FSH)、促黄体生成素(LH)、总睾酮和游离睾酮、雄烯二酮、硫酸脱氢表雄酮(DHEAS)、性激素结合球蛋白(SHBG)和胰岛素的浓度,采用酶法测定葡萄糖浓度。
我们观察到,与AI、BI和BII亚组相比,AII亚组的体重、脂肪量和体重指数显著更高。与AI亚组相比,仅AII亚组的游离睾酮血清浓度显著更高。我们观察到A组和B组中胰岛素血清浓度与游离睾酮之间均呈正相关,此外,我们还观察到B组中胰岛素血清浓度与DHEAS和LH均呈正相关。
胰岛素抵抗似乎在肥胖女性高雄激素血症的发生中起关键作用。然而,多囊卵巢综合征中导致高雄激素血症的机制仍未明确,似乎更为复杂。