Kwan Sze Ting Cecilia, King Julia H, Yan Jian, Wang Zhen, Jiang Xinyin, Hutzler Jason S, Klein Hallie R, Brenna J Thomas, Roberson Mark S, Caudill Marie A
Division of Nutritional Sciences, and.
Departments of Food Science and.
J Nutr. 2017 Nov;147(11):2083-2092. doi: 10.3945/jn.117.256107. Epub 2017 Sep 20.
Fetal growth is dependent on placental nutrient supply, which is influenced by placental perfusion and transporter abundance. Previous research indicates that adequate choline nutrition during pregnancy improves placental vascular development, supporting the hypothesis that choline may affect placental nutrient transport. The present study sought to determine the impact of maternal choline supplementation (MCS) on placental nutrient transporter abundance and nutrient metabolism during late gestation. Female non-Swiss albino mice were randomly assigned to the 1×, 2×, or 4× choline diet (1.4, 2.8, and 5.6 g choline chloride/kg diet, respectively) 5 d before mating ( = 16 dams/group). The placentas and fetuses were harvested on gestational day (E) 15.5 and E18.5. The placental abundance of macronutrient, choline, and acetylcholine transporters and glycogen metabolic enzymes, and the placental concentration of glycogen were quantified. Choline metabolites and docosahexaenoic acid (DHA) concentrations were measured in the placentas and/or fetal brains. Data were stratified by gestational day and fetal sex and were analyzed by using mixed linear models. At E15.5, MCS downregulated the placental transcript and protein abundance of glucose transporter 1 (GLUT1) (-40% to -73%, < 0.05) and the placental transcript abundance of glycogen-synthesizing enzymes (-24% to -50%, ≤ 0.05). At E18.5, MCS upregulated GLUT3 protein abundance (+55%, = 0.016) and the transcript abundance of glycogen-synthesizing enzymes only in the female placentas (+36% to +60%, < 0.05), resulting in a doubling ( = 0.01) of the glycogen concentration. A higher placental transcript abundance of the transporters for DHA, choline, and acetylcholine was also detected in response to MCS, consequently altering their concentrations in the placentas or fetal brains ( ≤ 0.05). These data suggest that MCS modulates placental nutrient transporter abundance and nutrient metabolism in late gestation of mouse pregnancy, with subsequent effects on nutrient supply for the developing fetus.
胎儿生长依赖于胎盘的营养供应，而胎盘营养供应受胎盘灌注和转运蛋白丰度的影响。先前的研究表明，孕期充足的胆碱营养可改善胎盘血管发育，支持胆碱可能影响胎盘营养转运的假说。本研究旨在确定孕期母体补充胆碱（MCS）对妊娠晚期胎盘营养转运蛋白丰度和营养代谢的影响。在交配前5天，将雌性非瑞士白化小鼠随机分为1倍、2倍或4倍胆碱饮食组（分别为1.4、2.8和5.6 g氯化胆碱/千克饮食，每组16只母鼠）。在妊娠第（E）15.5天和E18.5天收集胎盘和胎儿。对常量营养素、胆碱和乙酰胆碱转运蛋白以及糖原代谢酶的胎盘丰度，以及胎盘糖原浓度进行定量。在胎盘和/或胎儿脑中测量胆碱代谢物和二十二碳六烯酸（DHA）浓度。数据按妊娠天数和胎儿性别分层，并使用混合线性模型进行分析。在E15.5时，MCS下调了葡萄糖转运蛋白1（GLUT1）的胎盘转录本和蛋白丰度（-40%至-73%，P<0.05）以及糖原合成酶的胎盘转录本丰度（-24%至-50%，P≤0.05）。在E18.5时，MCS上调了GLUT3蛋白丰度（+55%，P = 0.016），并且仅在雌性胎盘上调了糖原合成酶的转录本丰度（+36%至+60%，P<0.05），导致糖原浓度加倍（P = 0.01）。还检测到，作为对MCS的反应，DHA、胆碱和乙酰胆碱转运蛋白的胎盘转录本丰度更高，从而改变了它们在胎盘或胎儿脑中的浓度（P≤0.05）。这些数据表明，MCS在小鼠妊娠晚期调节胎盘营养转运蛋白丰度和营养代谢，随后影响发育中胎儿的营养供应。
