中文摘要：

通过母体高雄环境建立子代实验性多囊卵巢综合征（PCOS）大鼠模型,并证明此模型大鼠存在卵巢局部胰岛素抵抗。方法是给孕16d的雌鼠皮下注射丙酸睾丸酮,诱导其子代雌鼠发生PCOS,观察子代大鼠体重、动情周期变化、性激素变化及糖代谢变化、卵巢重量和卵巢形态变化、肌肉组织蛋白印迹测定PI-3K和MAPK通路关键蛋白的表达、卵巢免疫组化和蛋白印迹测定PI-3K和MAPK通路关键蛋白的表达确定。结果显示：①动情周期失去规律变化,提示无排卵;②血清17-OHP,A2,T升高;③卵巢组织学检查可镜下看到早期发育的较多的小卵泡、闭锁卵泡,囊状扩张卵泡明显增加,颗粒细胞层数减少,黄体数量明显减少;④OGTT：1h血糖及胰岛素高于对照组,模型组存在着胰岛素抵抗;⑤卵巢局部PI-3K和MAPK途径关键蛋白有表达;⑥卵巢局部蛋白印迹测定PI-3K和MAPK途径关键蛋白IRS-1,P85,GLUT4降低,ERK1升高。由此表明：①此模型大鼠符合PCOS的诊断标准;②此模型大鼠存在卵巢局部胰岛素抵抗。

英文摘要：

This paper studies a rat model for polycystic ovary syndrome （PCOS） and shows that insulin resistance develops in the PCOS models. Female fetuses were exposed to androgen excess in utero in late gestation by subcutaneously injecting pregnant rats with testosterone propionate （TP） for 3 consecutive days. It is shown that （1） A Estrus sees no regular change （suggesting anovulation） （2） There is an increase in baseline serum 17-OHP progesterone, testosterone and androstenedione in model group （3） Ovary histological anatomy shows that there are more atretic follicles and polyfolliculars and less corepus luteums and granular layers in model group than in control group （4） Plasma glucose and insulin at 1 hour of glucose tolerance test is significantly higher in model group than in control group. （5） Key signaling proteins of P1-3K and MAPK path are expressed in local ovary （6） There is a decline in representative Western blots of GLUT4, IRS-1, P85 subunit in PCOS as compared with control group, whereas that of ERK1 is on increase. It is concluded that the PCOS model behaves in accord with diagnostic criteria of PCOS and insulin resistance develops in local oval.