2014.03.02【英译中】妊娠糖尿病诱发慢性缺氧应激和小鼠胎盘过度炎症反应

一只筱蝶 (一只筱蝶) 路人甲
101 0 0
发表于:2014-03-02 22:40 [只看楼主] [划词开启]

Gestational diabetes induces chronic hypoxia stress and excessive inflammatory response in murine placenta

Abstract



Metabolic impairments in maternal obesity and gestational diabetes mellitus (GDM) induce an abnormal environment in peripheral blood and cause vascular structure alterations which affect the placental development and function. A GDM model was developed using C57BL/6J female mice fed with high fat food (HF) (40% energy from fat) and a control group with control food (CF) (14% energy from fat) for 14 weeks before mating and throughout the gestation period. A subset of dams was sacrificed at gestational day (GD) 18.5 to evaluate the fetal and placental development. HF-fed dams exhibited significant increase in the maternal weight gain and homeostasis model assessment for insulin resistance index (HOMA-IR), impaired insulin secretion of glucose stimulus and glucose clearance of insulin stimulus before pregnancy; in addition, they also had the increase in the fetal and placental weight. HF-fed dams at GD 18.5 showed the high level of circulating maternal inflammation factors and were associated with increased oxidative stress and hypoxia in the labyrinth, abnormal vascular development with a high level of hypoxia inducible factor-1α (HIF-1α) and VEGF-A expression, but without a parallel increase in CD31 level; were induced an exaggerated inflammatory response in placental vascular endothelial cell. Our findings show that GDM induces more maternal weight gain and fetus weight, with abnormal maternal circulating metabolic and inflammation factors, and forms a placental hypoxia environment and impacts the placental vascular development. Our findings indicate that gestational diabetes induce excessive chronic hypoxia stress and inflammatory response in placentas which may contribute mechanisms to the high risks of perinatal complications of obesity and GDM mothers.

摘要




产妇肥胖和妊娠期糖尿病(GDM)代谢障碍引起的外周血中异常的环境而导致的血管结构改变影响胎盘的发育和功能。GDM模型使用C57BL/6J雌性小鼠,交配前14周和整个怀孕期喂高脂肪食品的雌鼠(HF)(40%的能量来自脂肪),对照组(CF)控制饮食(14%的能量来自脂肪)。妊娠第18.5天,对符合条件的孕鼠进行解剖,获取胎鼠和胎盘,进行研究。高脂饮食喂养的孕鼠,体重增加和胰岛素抵抗指数的稳态模型评估指数显著增加( HOMA-IR),葡萄糖刺激受损的胰岛素分泌和胰岛素刺激的葡萄糖清除率叫孕前增加。此外,胎儿和胎盘的重量均增加。高脂饮食组大鼠妊娠第18.5天,母体循环系统炎症因子处于高水平,可能与宫内缺氧和氧化应激增加相关。异常血管的生成与缺氧诱导因子-1α(HIF-1α)和血管内皮生长因子-A表达增加有关,但CD 31水平没有平行增加,诱导血管内皮细胞过度的炎症反应。我们的研究结果显示,妊娠期糖尿病引起孕妇体重增加和胎儿体重增加,异常的产妇循环代谢和炎症因子,并形成胎盘缺氧的环境,影响胎盘血管发育。我们的研究结果表明,妊娠期糖尿病诱发胎盘过度的慢性缺氧应激,可能导致肥胖和妊娠期糖尿病产妇围产期并发症炎症反应的高风险。






分类: 英语

  • 0

    点赞

  • 收藏

  • 扫一扫分享朋友圈

    二维码

  • 分享

课程推荐

需要先加入社团哦

编辑标签

最多可添加10个标签,不同标签用英文逗号分开

保存

编辑官方标签

最多可添加10个官方标签,不同标签用英文逗号分开

保存
知道了

复制到我的社团