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母体营养不良影响胎盘形态和转运体表达:导致后代生长不良的根源。

Maternal malnutrition impacts placental morphology and transporter expression: an origin for poor offspring growth.

机构信息

Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada; Health Sciences, Carleton University, Ottawa, Ontario, Canada.

Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.

出版信息

J Nutr Biochem. 2020 Apr;78:108329. doi: 10.1016/j.jnutbio.2019.108329. Epub 2020 Jan 8.

DOI:10.1016/j.jnutbio.2019.108329
PMID:32004932
Abstract

The placenta promotes fetal growth through nutrient transfer and selective barrier systems. An optimally developed placenta can adapt to changes in the pregnancy environment, buffering the fetus from adverse exposures. We hypothesized that the placenta adapts differently to suboptimal maternal diets, evidenced by changes in placental morphology, developmental markers and key transport systems. Mice were fed a control diet (CON) during pregnancy, undernourished (UN) by 30% of control intake from gestational day (GD) 5.5-18.5 or fed 60% high-fat diet (HF) 8 weeks before and during pregnancy. At GD18.5, placental morphometry, development and transport were assessed. Junctional and labyrinthine areas of UN and HF placentae were smaller than CON by >10%. Fetal blood space area and fetal blood space:fetal weight ratios were reduced in HF vs. CON and UN. Trophoblast giant cell marker Ctsq mRNA expression was lower in UN vs. HF, and expression of glycogen cell markers Cx31.1 and Pcdh12 was lower in HF vs. UN. Efflux transporter Abcb1a mRNA expression was lower in HF vs. UN, and Abcg2 expression was lower in UN vs. HF. mRNA expression of fatty acid binding protein Fabp was higher in UN vs. CON and HF. mRNA and protein levels of the lipid transporter FAT/CD36 were lower in UN, and FATP4 protein levels were lower in HF vs. UN. UN placentae appear less mature with aberrant transport, whereas HF placentae adapt to excessive nutrient supply. Understanding placental adaptations to common nutritional adversities may reveal mechanisms underlying the developmental origins of later disease.

摘要

胎盘通过营养物质转移和选择性屏障系统促进胎儿生长。一个发育良好的胎盘可以适应妊娠环境的变化,缓冲胎儿免受不利因素的影响。我们假设胎盘对不良的母体饮食有不同的适应方式,这表现在胎盘形态、发育标志物和关键转运系统的变化上。在妊娠期间,小鼠被喂食对照饮食(CON),从妊娠第 5.5-18.5 天开始,饮食中 30%的营养摄入不足(UN),或者在妊娠前 8 周和妊娠期间喂食 60%的高脂肪饮食(HF)。在妊娠第 18.5 天,评估胎盘形态、发育和转运。UN 和 HF 胎盘的连接区和迷路区比 CON 小>10%。HF 与 CON 和 UN 相比,胎儿血腔面积和胎儿血腔:胎儿体重比降低。UN 与 HF 相比,滋养层巨细胞标志物 Ctsq mRNA 表达降低,HF 与 UN 相比,糖原细胞标志物 Cx31.1 和 Pcdh12 的表达降低。外排转运体 Abcb1a mRNA 表达在 HF 比 UN 降低,Abcg2 表达在 UN 比 HF 降低。UN 比 CON 和 HF 中脂肪酸结合蛋白 Fabp 的 mRNA 表达更高。UN 中脂质转运蛋白 FAT/CD36 的 mRNA 和蛋白水平降低,HF 中 FATP4 蛋白水平比 UN 降低。UN 胎盘似乎成熟度较低,转运异常,而 HF 胎盘适应过多的营养供应。了解胎盘对常见营养逆境的适应机制可能揭示发育起源与后期疾病之间的关系。

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