Weber R F, Pache T D, Jacobs M L, Docter R, Loriaux D L, Fauser B C, Birkenhäger J C
Department of Internal Medicine III and Clinical Endocrinology, Erasmus University Rotterdam, The Netherlands.
Clin Endocrinol (Oxf). 1993 Mar;38(3):295-300. doi: 10.1111/j.1365-2265.1993.tb01009.x.
Hyperandrogenism in patients with polycystic ovary syndrome has been shown to correlate with hyperinsulinaemia of insulin resistance. We have investigated if basal levels of insulin and the response to the intravenous administration of glucagon can reveal insulin resistance in patients with polycystic ovary syndrome.
Nine obese (BMI > 25 kg/m2) and nine non-obese (BMI 19-25 kg/m2) women with PCOS, chosen from a population of 91 women attending the infertility clinic, and 19 normally cycling women (seven obese, 12 non-obese) were studied. Oligo or amenorrhoea, hirsutism, and 12 or more follicles in a given ovary were selection criteria.
Glucagon, 1 mg, was given intravenously to 18 of the 91 women and to the control subjects. Blood was taken at -5, 0, 5, 10 and 15 minutes for measurements of integrated areas under the response curve for insulin, C-peptide and glucose, respectively. Basal blood samples were drawn for fasting insulin, C-peptide, glucose, testosterone, sex hormone-binding globulin (SHBG), free fatty acids and IGF-I measurements. The free androgen index was calculated according to the formula FAI = testosterone x 100/SHBG.
There were no significant differences in maximal increment and area under the response curve for glucose, C-peptide and insulin. FAI was significantly higher in all patients with features of polycystic ovary syndrome. However, fasting insulin levels were significantly higher only in obese patients when compared with obese control subjects and lean patients.
The administration of 1 mg glucagon i.v. did not distinguish patients with polycystic ovary syndrome from control subjects. The mild insulin resistance of polycystic ovary syndrome is related only to obesity and is therefore unlikely to play an important role in the hyperandrogenism associated with the syndrome.
多囊卵巢综合征患者的高雄激素血症已被证明与胰岛素抵抗的高胰岛素血症相关。我们研究了胰岛素基础水平以及对静脉注射胰高血糖素的反应是否能揭示多囊卵巢综合征患者的胰岛素抵抗。
从91名到不孕不育门诊就诊的女性中选取了9名肥胖(体重指数>25kg/m²)和9名非肥胖(体重指数19 - 25kg/m²)的多囊卵巢综合征女性,以及19名月经周期正常的女性(7名肥胖,12名非肥胖)进行研究。入选标准为月经稀发或闭经、多毛,以及一侧卵巢有12个或更多卵泡。
对91名女性中的18名以及对照受试者静脉注射1mg胰高血糖素。在注射前5分钟、0分钟、5分钟、10分钟和15分钟采集血液,分别测量胰岛素、C肽和葡萄糖反应曲线下的积分面积。采集基础血样用于检测空腹胰岛素、C肽、葡萄糖、睾酮、性激素结合球蛋白(SHBG)、游离脂肪酸和胰岛素样生长因子-I。根据公式FAI = 睾酮×100/SHBG计算游离雄激素指数。
葡萄糖、C肽和胰岛素的最大增加值及反应曲线下面积无显著差异。所有有多囊卵巢综合征特征的患者的游离雄激素指数均显著更高。然而,与肥胖对照受试者和瘦患者相比,仅肥胖患者的空腹胰岛素水平显著更高。
静脉注射1mg胰高血糖素无法区分多囊卵巢综合征患者和对照受试者。多囊卵巢综合征的轻度胰岛素抵抗仅与肥胖有关,因此不太可能在与该综合征相关的高雄激素血症中起重要作用。