2014.03.29【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【3】

一只筱蝶 (一只筱蝶) 路人甲
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发表于:2014-03-29 16:45 [只看楼主] [划词开启]
Discussion

In GDM, there are strong gene-environment interactions that trigger the pathogenetic process. 

Thus, despite their different genetic predisposition, environmental factors, mainly lifestyle-related factors

 such as high-saturated-fat diet, may enhance glucose intolerance and promote insulin resistance and

 obesity during pregnancy. In this study, we have developed an attractive model to further study the

 physiologic and molecular abnormalities in GDM. Mice model was fed with a moderately high fat diet for

 a long time before pregnancy ,as increased maternal adiposity, fast glucose and insulin, impaired

 glucose and insulin tolerance, which were very similar to the common metabolic abnormalities of human

 GDM, and Liang et  fed high fat food to female C57BL/6J mouse for 8 weeks before mating and

 considered them as GDM model, changes in fetus and placentas with these metabolic impairments also

 may be applied to GDM woman. In our study, we found that maternal and litter’s weight gain in HF

 group was more than that in CF group, placental weight also increased, which promoted an increase level

 in exchange nutrient function in HF group, but placenta weight did not show a parallel growth in litter

 weight.


在妊娠期糖尿病的发病过程中,有很强的基因-环境相互作用。因此,尽管它们有不同的遗传倾向,环境因素,主要是与生活方式有关的因素,如高饱和脂肪的饮食,可提高葡萄糖耐受不良,在孕期促进胰岛素抗性和肥胖。在这项研究中,我们已经开发了一个具有吸引力的模型,用来研究GDM的生理和分子异常。孕前,大鼠模型给予很长一段时间的适当的高脂肪饮食,以增加母亲肥胖,空腹血糖和胰岛素,糖耐量和胰岛素耐受性,这于人类妊娠期糖尿病常见的代谢异常非常类似。Liang等的研究中,对C57BL/6J雌鼠交配前8周,高脂肪食物喂养,并认为是GDM模型。在胎儿和胎盘的这些代谢障碍的变化,也可以应用到GDM的妇女中来。在我们的研究中,我们发现,孕产妇和幼崽的体重增加,HF组明显多于CF组,胎盘重量也增加,促进了HF组交换营养物质的功能的水平,但胎盘的重量和幼崽体重并不平行生长。


A physiological state of insulin resistance is required to preferentially direct the maternal nutrients toward

 the fetoplacental unit, allowing adequate growth of the fetus. When women develop GDM, insulin

 resistance is more severe and disrupts the intrauterine milieu, which resulting in accelerated fetal

 development with increased risk of macrosomia. Jones et found high fat diet before and during pregnancy could cause marked up-regulation of placental nutrient transport and fetal overgrowth in mice,

 in which glucose transporter 1 (GLUT1) and sodium-coupled neutral amino acid transporter (SNAT) 2

 were elevated. They suggested that up regulation of specific placental nutrient transporter isoforms

 constituted a mechanism linking maternal high fat diet and obesity to fetal overgrowth. It coincided with

 our results on this point in placenta.

   胰岛素抵抗的生理状态,要求母体直接向胎儿胎盘单元提供营养素,从而保证胎儿的适当生长。当女性发生GDM,胰岛素抵抗更加严重,破坏了子宫内环境,从而导致胎儿的发育加速,巨大儿的风险增加。Jones等学者发现孕前和孕期高脂肪饮食会显著上调大鼠胎盘输送养分,导致胎鼠过度生长。其中葡萄糖转运蛋白1 ( GLUT1 )和钠结合中性氨基酸转运体2( SNAT )均升高。他们提出胎盘养分转运体亚型调控构成连接母体高脂饮食及肥胖和胎儿过度生长的机制。这正好与我们在胎盘这一点的研究结果相同。





分类: 英语

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