INSULIN RESISTANCE IN NON-OBESE PATIENTS WITH POLYCYSTIC OVARIAN DISEASE
INSULIN RESISTANCE IN NON-OBESE PATIENTS WITH POLYCYSTIC OVARIAN DISEASE
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DOI：
10.1210/jcem-57-2-356
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发表时间：
1983-01-01
影响因子：
5.8
通讯作者：
KAPLAN, SA
中科院分区：
文献类型：
--
作者：
CHANG, RJ;NAKAMURA, RM;KAPLAN, SA
为了确定在没有肥胖和黑棘皮病的情况下多囊卵巢病（PCO）是否发生胰岛素抵抗，在10名没有黑棘皮病的非肥胖PCO患者和10名体重和身高匹配的正常女性中测定了口服葡萄糖后的循环胰岛素水平。与对照组相比，PCO患者的平均血清睾酮（T）、雄烯二酮（A）、脱氢表雄酮（D）、D硫酸盐和LH [黄体生成素]水平显著升高。在PCO患者中，平均值±。SE基础胰岛素水平（18.7 ±. 2.9μ U/ml）和响应于葡萄糖的胰岛素水平的总和（674 ± 0.001 μ U/ml）。119 μ U/ml）显著高于对照组（11.0 ± 0.001 μ U/ml）。0.8μ U/ml和248 ± 0.001 μ U/ml。29 μ U/ml）。在所有受试者中，血清T和A水平与基础胰岛素水平和胰岛素总和显著相关，而D和D硫酸盐水平与基础胰岛素水平和胰岛素总和不显著相关。两组的血清皮质醇、GH [生长激素]和PRL [催乳素]水平相似。在PCO中，存在显著程度的胰岛素抵抗，这显然与肥胖无关。本研究中血清T和A水平与循环胰岛素水平呈正相关，提示PCO中的胰岛素抵抗可能部分是高雄激素血症的结果。
To determine whether insulin resistance occurs in polycystic ovarian disease (PCO) in the absence of obesity and acanthosis nigricans, circulating levels of insulin in response to oral glucose administration were measured in 10 nonobese PCO patients without acanthosis nigricans and in 10 normal women matched for weight and height. Mean serum testosterone (T), androstenedione (A), dehydroepiandrostrone (D), D sulfate and LH [luteinizing hormone] levels were significantly elevated in the PCO patients compared to those in control subjects. In PCO patients, the mean .+-. SE basal insulin levels (18.7 .+-. 2.9 .mu.U/ml) and the sum of the insulin levels in response to glucose (674 .+-. 119 .mu.U/ml) were significantly greater than those in the control group (11.0 .+-. 0.8 .mu.U/ml and 248 .+-. 29 .mu.U/ml, respectively). In all subjects, serum levels of T and A, but not D and D sulfate, were significantly correlated to basal insulin levels and insulin sums. Serum cortisol, GH [growth hormone], and PRL [prolactin] levels were similar in both groups. In PCO, a significant degree of insulin resistance exists, which clearly is not related to obesity. The positive correlation of serum T and A levels to circulating insulin levels in this study suggests that the insulin resistance in PCO may be, in part, a consequence of hyperandrogenism.