Maternal and Fetal Health Research Centre, St Mary's Hospital, Oxford Road, Manchester, UK.
Am J Physiol Endocrinol Metab. 2012 Jan 15;302(2):E233-42. doi: 10.1152/ajpendo.00192.2011. Epub 2011 Oct 25.
Teenagers have an increased risk of delivering small-for-gestational-age (SGA) infants. Young maternal age and continued skeletal growth have been implicated as causal factors. In growing adolescent sheep, impaired placental development and nutrient transfer cause reduced birth weight. In human pregnancies, SGA is associated with reduced placental amino acid transport. Maternal growth has no effect on placental morphology or cell turnover, but growing teenagers have higher birth weight:placental weight ratios than nongrowing teenagers. We hypothesized that placental nutrient transporter activity would be affected by maternal age and/or growth status. Placentas from teenagers and adults were collected. Teenagers were defined as growing or nongrowing based on knee height measurements. System A amino acid transporter activity was quantified as sodium-dependent uptake of [(14)C]methylaminoisobutyric acid into placental fragments. Teenagers had lower placental system A activity than adults (P < 0.05). In adults, placental system A activity was lower in SGA infants than appropriate-for-gestational-age (AGA) infants (P < 0.05). In teenagers, AGA and SGA infants had lower placental system A activity than AGA infants born to adults (P < 0.05). Placental system A activity was higher in growing teenagers than in nongrowing teenagers (P < 0.001). Placental mRNA expression of system A transporter isoforms SLC38A1 and -2 was lower in teenagers than in adults (P < 0.05) but did not differ between growing and nongrowing teenagers. There was no difference in transporter protein expression/localization between cohorts. Teenagers have inherently reduced placental transport, which may underlie their susceptibility to delivering SGA infants. Growing teenagers appear to overcome this susceptibility by stimulating the activity, but not expression, of system A transporters.
青少年生育小于胎龄儿(SGA)的风险增加。年轻的母亲年龄和持续的骨骼生长被认为是因果因素。在生长中的青春期绵羊中,胎盘发育和营养物质转移受损会导致出生体重降低。在人类妊娠中,SGA 与胎盘氨基酸转运减少有关。母体生长对胎盘形态或细胞更替没有影响,但生长中的青少年的出生体重与胎盘重量比高于非生长中的青少年。我们假设胎盘营养转运体的活性会受到母亲年龄和/或生长状态的影响。收集了青少年和成年人的胎盘。根据膝关节高度测量,将青少年定义为生长或非生长。通过胎盘片段对 [(14)C]甲基氨基异丁酸的钠依赖性摄取来量化系统 A 氨基酸转运体的活性。青少年的胎盘系统 A 活性低于成年人(P < 0.05)。在成年人中,SGA 婴儿的胎盘系统 A 活性低于适当胎龄(AGA)婴儿(P < 0.05)。在青少年中,AGA 和 SGA 婴儿的胎盘系统 A 活性低于出生于成年人的 AGA 婴儿(P < 0.05)。生长中的青少年的胎盘系统 A 活性高于非生长中的青少年(P < 0.001)。青少年的胎盘系统 A 转运体同工型 SLC38A1 和 -2 的 mRNA 表达低于成年人(P < 0.05),但在生长和非生长的青少年之间没有差异。转运体蛋白表达/定位在队列之间没有差异。青少年的胎盘转运固有减少,这可能是他们易发生 SGA 婴儿的原因。生长中的青少年似乎通过刺激系统 A 转运体的活性(而非表达)来克服这种易感性。