Lager Susanne, Powell Theresa L
Department of Obstetrics and Gynecology, Center for Pregnancy and Newborn Research, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, Mail Code 7836, San Antonio, TX 78229-3900, USA.
J Pregnancy. 2012;2012:179827. doi: 10.1155/2012/179827. Epub 2012 Dec 10.
Abnormal fetal growth, both growth restriction and overgrowth, is associated with perinatal complications and an increased risk of metabolic and cardiovascular disease later in life. Fetal growth is dependent on nutrient availability, which in turn is related to the capacity of the placenta to transport these nutrients. The activity of a range of nutrient transporters has been reported to be decreased in placentas of growth restricted fetuses, whereas at least some studies indicate that placental nutrient transport is upregulated in fetal overgrowth. These findings suggest that changes in placental nutrient transport may directly contribute to the development of abnormal fetal growth. Detailed information on the mechanisms by which placental nutrient transporters are regulated will therefore help us to better understand how important pregnancy complications develop and may provide a foundation for designing novel intervention strategies. In this paper we will focus on recent studies of regulatory mechanisms that modulate placental transport of amino acids, fatty acids, and glucose.
胎儿生长异常，包括生长受限和生长过速，均与围产期并发症以及日后发生代谢和心血管疾病的风险增加相关。胎儿生长取决于营养物质的供应，而营养物质的供应又与胎盘转运这些营养物质的能力有关。据报道，生长受限胎儿的胎盘内一系列营养转运蛋白的活性降低，而至少一些研究表明，胎儿生长过速时胎盘营养转运上调。这些发现提示，胎盘营养转运的改变可能直接导致胎儿生长异常的发生。因此，关于胎盘营养转运蛋白调控机制的详细信息将有助于我们更好地理解妊娠并发症是如何发生的，并可能为设计新的干预策略提供基础。在本文中，我们将重点关注调节胎盘氨基酸、脂肪酸和葡萄糖转运的调控机制的最新研究。
