Prenatal androgen excess is considered one of the main causes of the development of polycystic ovary syndrome. In this study, we investigated the effect of prenatal hyperandrogenization (PH) on the physiology of the adult uterine tissue using a murine model of fetal programming caused by androgen excess in adult female rats. Pregnant rats were hyperandrogenized with testosterone and female offspring were studied when adult. Our results showed that PH leads to hyperglycemia and hyperinsulinemia. Consequently, PH developed insulin resistance and a systemic inflammatory state reflected by increased C-reactive protein. In the uterine tissue, levels of PPAR gamma—an important metabolic sensor in the endometrium—were found to be impaired. Moreover, PH induced a pro-inflammatory and an unbalanced oxidative state in the uterus reflected by increased COX-2, lipid peroxidation, and NF-κB. In summary, our results revealed that PH leads to a compromised metabolic state likely consequence of fetal reprogramming.

产前雄激素过多被认为是多囊卵巢综合征发生的主要原因之一。在这项研究中，我们使用成年雌性大鼠雄激素过多引起的胎儿编程小鼠模型，研究了产前雄激素过多（PH）对成年子宫组织生理学的影响。用睾酮使怀孕的大鼠雄激素过多，并在成年后对雌性后代进行研究。我们的结果表明，PH 会导致高血糖和高胰岛素血症。因此，PH 出现胰岛素抵抗和 C 反应蛋白增加所反映的全身炎症状态。在子宫组织中，PPAR γ（子宫内膜中重要的代谢传感器）的水平被发现受损。此外，PH 会诱导子宫内促炎和不平衡的氧化状态，具体表现为 COX-2、脂质过氧化和 NF-κB 的增加。总之，我们的结果表明，PH 会导致代谢状态受损，这可能是胎儿重新编程的结果。