Mechanisms of homocysteine transport by human placenta:Relationship to placental vascular distensibility and birthweight

低出生体重儿（LBW）比正常出生体重儿在童年后期发生发育迟缓和脑瘫的风险更大。成年后，LBW可能易患心血管疾病。这可能与较高浓度的一种称为同型半胱氨酸的氨基酸有关，这种氨基酸会损害血管壁。在怀孕期间，亚最佳叶酸或维生素B12状态可能会导致母体血浆中同型半胱氨酸浓度升高，并降低胎儿生长。胎盘如何转运同型半胱氨酸尚不清楚。同型半胱氨酸诱导的胎盘血管损伤可能是胎盘功能受损和LBW之间的因果关系。我们的项目将确定运输系统，携带同型半胱氨酸在正常妊娠胎盘和调查是否这些转运是由维生素叶酸和B12，在同型半胱氨酸的代谢转化的重要微量营养素调制。我们计划探讨脐带血中同型半胱氨酸浓度之间的关系，正常的变化，在出生时婴儿的大小，和胎盘动脉血管的扩张性能作为一个模型，胎儿血管的血管功能，可以检查。我们希望，我们的工作将导致新的举措，以及持续的护理，以改善胎儿的生长和新生儿的健康。

Low birthweight (LBW) infants are at greater risk of developmental delay and cerebral palsy in later childhood than those of normal birthweight. In adult life, LBW may predispose to cardiovascular disease. This may be linked to a higher concentration of an amino acid called homocysteine which damages blood vessel walls. In pregnancy, sub-optimal folate or vitamin B12 status may contribute to raised homocysteine concentrations in maternal plasma and reduced fetal growth. How homocysteine is transported by the placenta is unknown. It is possible that homocysteine-induced damage to placental blood vessels provides a causative link between impaired placental function and LBW. Our project will identify transport systems that carry homocysteine across the placenta in normal pregnancies and investigate whether these transporters are modulated by the vitamins folate and B12, micronutrients important in the metabolic conversion of homocysteine. We plan to explore relationships between homocysteine concentrations in cord blood, normal variations in infant size at birth, and the distensible properties of placental arterial vessels as a model of fetal vessels in which vascular function can be examined. We hope that our work will lead to new initiatives together with a continuum of care to improve fetal growth and health of newborn infants.