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

低出生体重（LBW）婴儿比正常出生体重的婴儿在儿童后期发育迟缓和脑瘫的风险更大。成年后，体重过低可能易患心血管疾病。这可能与一种叫做同型半胱氨酸的氨基酸浓度较高有关，这种氨基酸会损害血管壁。在怀孕期间，叶酸或维生素B12水平低于理想水平可能导致母体血浆中同型半胱氨酸浓度升高和胎儿生长减慢。同型半胱氨酸如何通过胎盘运输尚不清楚。可能同型半胱氨酸引起的胎盘血管损伤在胎盘功能受损和低体重之间提供了因果联系。我们的项目将确定在正常妊娠中携带同型半胱氨酸通过胎盘的运输系统，并研究这些运输系统是否受到维生素叶酸和B12的调节，这两种微量营养素对同型半胱氨酸的代谢转化很重要。我们计划探索脐带血中同型半胱氨酸浓度、出生时婴儿大小的正常变化和胎盘动脉血管的可扩张特性之间的关系，作为胎儿血管的模型，可以检查血管功能。我们希望我们的工作将导致新的举措与连续的护理，以改善胎儿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.