Wallace J M, Luther J S, Milne J S, Aitken R P, Redmer D A, Reynolds L P, Hay W W
Development, Growth and Function Division, Rowett Research Institute, Greenburn Road, Bucksburn, Aberdeen, AB21 9SB, UK.
Placenta. 2006 Apr;27 Suppl A:S61-8. doi: 10.1016/j.placenta.2005.12.002. Epub 2006 Jan 25.
The risks of miscarriage, prematurity and low birth weight are particularly acute in adolescent girls who are still growing at the time of conception. The role of maternal nutrition in mediating pregnancy outcome in this vulnerable group has been examined in sheep models. When singleton bearing adolescent dams are overnourished to promote rapid maternal growth throughout pregnancy, growth of both the placenta and fetus is impaired, and birth occurs prematurely relative to control adolescents of equivalent age. Studies at mid-gestation, prior to alterations in placental mass, suggest that reduced proliferation of the fetal trophectoderm, impaired angiogenesis, and attenuated uteroplacental blood flows are early defects in placental development. By late pregnancy, relative placental mass is reduced by 45% but uteroplacental metabolism and placental glucose transfer capacity remain normal when expressed on a placental weight specific basis. The asymmetrically growth-restricted fetuses are hypoxic, hypoglycemic and have reduced insulin and IGF-1 concentrations. Absolute umbilical nutrient uptakes are attenuated but fetal utilisation of glucose, oxygen and amino acids remains normal on a fetal weight basis. This suggests altered sensitivities to metabolic signals and may have implications for subsequent metabolic health. At the other end of the nutritional spectrum, many girls who become pregnant have inadequate or marginal nutritional status during pregnancy. This situation is replicated in a second model whereby dams are prevented from growing during pregnancy by relatively underfeeding. Limiting maternal intake in this way gradually depletes maternal body reserves leading to a lower transplacental glucose gradient and a modest slowing of fetal growth in late pregnancy. These changes appear to be independent of alterations in placental growth per se. Thus, while the underlying mechanisms differ, maternal intake at both ends of the nutritional spectrum is a powerful determinant of fetal growth in pregnant adolescents.
对于怀孕时仍处于生长阶段的青春期女孩来说,流产、早产和低出生体重的风险尤为突出。在绵羊模型中研究了母体营养在调节这一弱势群体妊娠结局中的作用。当怀有单胎的青春期母羊在整个孕期过度营养以促进母体快速生长时,胎盘和胎儿的生长都会受到损害,并且相对于同龄的对照青春期母羊,会早产。在胎盘质量改变之前的妊娠中期研究表明,胎儿滋养外胚层增殖减少、血管生成受损以及子宫胎盘血流减弱是胎盘发育的早期缺陷。到妊娠晚期,相对胎盘质量减少了45%,但以胎盘重量为特定基础表示时,子宫胎盘代谢和胎盘葡萄糖转运能力仍保持正常。生长受限不对称的胎儿会出现缺氧、低血糖,胰岛素和IGF - 1浓度降低。脐部绝对营养物质摄取减少,但以胎儿体重为基础,胎儿对葡萄糖、氧气和氨基酸的利用仍保持正常。这表明对代谢信号的敏感性发生了改变,可能对后续的代谢健康产生影响。在营养范围的另一端,许多怀孕的女孩在孕期营养状况不足或处于边缘状态。在第二个模型中也出现了这种情况,即通过相对不足喂养使母羊在孕期无法生长。以这种方式限制母体摄入量会逐渐耗尽母体身体储备,导致胎盘葡萄糖梯度降低,妊娠晚期胎儿生长适度减缓。这些变化似乎与胎盘生长本身的改变无关。因此,虽然潜在机制不同,但营养范围两端的母体摄入量都是怀孕青少年胎儿生长的有力决定因素。