Toscano V, Bianchi P, Balducci R, Guglielmi R, Mangiantini A, Lubrano C, Sciarra F
Istituto di V Clinica Medica, Endocrinologia III, Università La Sapienza, Rome, Italy.
Clin Endocrinol (Oxf). 1992 Feb;36(2):197-202. doi: 10.1111/j.1365-2265.1992.tb00958.x.
Because of continued debate about the role of insulin in the development of hirsutism and in the induction of the polycystic ovary syndrome, we have evaluated the hormonal pattern in a group of hirsute patients.
Fifty-four hirsute patients (age range 18-39 years) of whom 26 patients were obese (O) (BMI 28-53 kg/m2 and W/H greater than 0.85), 12 with ultrasonographic evidence of polycystic ovaries (O PCO) and 14 with normal ovaries. Twenty-eight patients were within normal weight range, and, of these, 14 presented ultrasonographic evidence of polycystic ovaries and 14 had normal ovaries. Two groups of age-matched subjects (obese and normal weight), normally menstruating, without hirsutism or history of endocrinopathies or ultrasonographic evidence of polycystic ovaries, served as controls.
Androstenedione and testosterone were evaluated in all patients by RIA, following ether extraction, DHEAS, LH, FSH and insulin were evaluated directly by RIA. SHBG was evaluated by the concanavalin method. Free testosterone (FT%) was calculated according to the formula FT = 4.038-1.607 log SHBG. Integrated areas under the response curve were calculated for LH and insulin respectively following i.v. administration of GnRH (100 micrograms) or oral administration of glucose (75 g).
Results (mean +/- standard deviation) showed comparable values of androstenedione in all groups of obese patients and in obese controls (7.3 +/- 2.6 in patients with polycystic ovaries, 7.1 +/- 2.9 in non-polycystic ovary patients and 7.4 +/- 2.6 nmol/l in obese controls, respectively), regardless of baseline and area insulin, the presence or absence of polycystic ovaries, or hirsutism. SHBG levels showed a similar pattern (24 +/- 10, 23.8 +/- 7.9 and 36 +/- 19 nmol/l) as did the percentage of free testosterone, regardless of the presence or absence of hirsutism. Regression analysis of the insulin and LH values (baseline and area) against the androgens and SHBG plasma levels showed that only LH area correlated positively with testosterone (r = 0.36, P less than 0.03), androstenedione (r = 0.44, P less than 0.02), % free testosterone (r = 0.53, P less than 0.001), testosterone/SHBG ratio (r = 0.39, P less than 0.03) and inversely with SHBG (r = -0.57, P less than 0.001).
These results showed (1) no linear relationship between high levels of insulin, ovarian androgen production or free hormone availability, and (2) make it very doubtful that insulin plays a primary role in polycystic ovarian syndrome or hirsutism.
由于关于胰岛素在多毛症发展及多囊卵巢综合征诱导过程中的作用一直存在争议,我们对一组多毛症患者的激素模式进行了评估。
54例多毛症患者(年龄范围18 - 39岁),其中26例肥胖(O)(体重指数28 - 53kg/m²且腰臀比大于0.85),12例有多囊卵巢超声证据(O PCO),14例卵巢正常。28例患者体重在正常范围内,其中14例有多囊卵巢超声证据,14例卵巢正常。两组年龄匹配的受试者(肥胖和正常体重),月经正常,无多毛症或内分泌疾病史或多囊卵巢超声证据,作为对照。
所有患者经乙醚提取后采用放射免疫分析法(RIA)评估雄烯二酮和睾酮,直接采用RIA评估硫酸脱氢表雄酮(DHEAS)、促黄体生成素(LH)、促卵泡生成素(FSH)和胰岛素。采用伴刀豆球蛋白法评估性激素结合球蛋白(SHBG)。游离睾酮(FT%)根据公式FT = 4.038 - 1.607 log SHBG计算。静脉注射促性腺激素释放激素(GnRH,100微克)或口服葡萄糖(75克)后,分别计算LH和胰岛素反应曲线下的积分面积。
结果(均值±标准差)显示,所有肥胖患者组和肥胖对照组的雄烯二酮值相当(多囊卵巢患者为7.3±2.6,非多囊卵巢患者为7.1±2.9,肥胖对照组为7.4±2.6 nmol/l),无论基础胰岛素和胰岛素面积、多囊卵巢的有无或多毛症情况如何。SHBG水平呈现相似模式(分别为24±10、23.8±7.9和36±19 nmol/l),游离睾酮百分比也是如此,与多毛症的有无无关。胰岛素和LH值(基础值和面积)与雄激素及SHBG血浆水平的回归分析显示,仅LH面积与睾酮(r = 0.36,P < 0.03)、雄烯二酮(r = 0.44,P < 0.02)、游离睾酮%(r = 0.53,P < 0.001)、睾酮/SHBG比值(r = 0.39,P < 0.03)呈正相关,与SHBG呈负相关(r = -0.57,P < 0.001)。
这些结果表明(1)高水平胰岛素、卵巢雄激素产生或游离激素可用性之间不存在线性关系,(2)使得胰岛素在多囊卵巢综合征或多毛症中起主要作用这一点非常可疑。