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【2】

一只筱蝶 (一只筱蝶) 路人甲
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发表于:2014-03-02 23:21 [只看楼主] [划词开启]

Introduction

   With the worldwide epidemic of metabolic syndrome, the proportion of women that are overweight or obese and with GDM during pregnancy has increased. The resulting abnormal placenta environment may have deleterious effects on fetal metabolic programming and lead to the increased adverse perinatal outcomes, not only perinatal mortality, macrosomia, shoulder dystocia , but also preeclampsia . GDM and obesity in pregnancy often increase the risk for the baby to develop metabolic syndrome later in life .Placenta plays an important role in this scenario, but basis research is leg behind in this area. Only a few studies with rodent models were designed to address the consequences of maternal obesity to understand the metabolic reprogramming in offspring, but no close attention has been paid to the state changes of placental vascular structure. When capillarization increases rapidly, this tree delivers blood to an extensive and expanding capillary network with a large surface area for exchange and is vital for fetal growth and survival. Nevertheless, the factors that control the normal growth and development of the fetoplacental vasculature in the late gestational are still unknown.

介绍

      随着代谢综合征(MS)在世界范围内的流行,超重或肥胖已经妊娠期糖尿病(GDM)妇女的比例不断增加。由此产生的胎盘异常环境可能对胎儿的代谢过程造成有害影响,增加围产儿不良妊娠结局。不仅是围产儿死亡,巨大儿,肩难产,也包括子痫前期。GDM和孕期肥胖往往会增加胎儿在以后的生活中发展为代谢综合征的风险。胎盘在这个环节中起着重要作用,但关于这方面的基础研究比较缺乏。只有少数以啮齿类动物模型的研究旨在解决产妇肥胖的后果,了解后代代谢程序,但没有密切关注胎盘血管结构的状态变化。当毛细血管迅速增加,胎盘提供血液丰富和交换面积扩大的毛细血管网,对胎儿生长和生存至关重要。然而,在妊娠后期控制胎儿胎盘血管正常生长和发展的因素仍未知。



    Since murine and human placenta exhibit many same characteristics , in the present work, we found that high-fat mouse models are accompanied with increased maternal adiposity, fast glucose and insulin, impaired glucose and insulin tolerance, which is very similar to human GDM symptoms. Because placental function increases dramatically in the last half of gestation to supply enough oxygen and nutrients for exponential fetal growth, maternal hypertension and other complications start and accelerates during the last half of gestation, it is requisite to monitor the pathological events of the placenta in this period. Therefore, based on this GDM animal model, we then took GD 18.5 as a dam time to investigate the changes in placental vascular structure of exchange area and placental environment in this late gestation period.

  由于大鼠胎盘和人类胎盘有许多共同点,在目前的工作中,我们发现,高脂肪饮食的大鼠模型,都伴随着增加产妇肥胖,空腹血糖和胰岛素,糖耐量和胰岛素耐受性,这与人类妊娠期糖尿病的症状非常相似在妊娠后半期,由于胎盘功能的急剧增加,为胎儿生长提供足够的氧气和营养。妊娠后半期,母体高血压和其他并发症开始出现并加剧。因此在这一时期检测胎盘的病理改变显得尤为重要。因此,在此基础上的GDM动物模型,将妊娠第18.5天作为妊娠后半期,对胎盘环境和血管结构变化进行研究。

Our findings show that high fat diet induces more maternal weight gain and fetus weight, with changed maternal circulating metabolic and inflammation factors, and disordered placental vascular environment and development.


   我们的研究结果显示,高脂饮食诱导的孕期孕妇体重增加和胎儿的重量增加更加明显,与改变产妇循环代谢和炎症因子和无序的胎盘血管环境及发展相关。

分类: 英语

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