Placental iron transport and maternal absorption

Abstract

The iron need in pregnancy is significantly higher in comparison to that in the nonpregnant state. The iron absorbed during pregnancy is used for expansion of the maternal erythrocyte mass, to fulfill the fetus's iron needs, to create placenta, and to cope with blood loss at delivery. Term neonates have a total body store of about 1 g of iron, all derived from the mother. Despite the overall increase in nutritional requirements, biochemical, metabolic, and physiological adjustments of the maternal organism happen in order to meet the extra demands and to support the homeostasis of iron. In all healthy pregnant women with sufficient iron stores, the increased iron absorption is coupled with the mobilization of iron stores. Unfortunately, iron deficiency during pregnancy is alarmingly common. The function of placental transport determines the composition of umbilical cord blood providing nutrients and oxygen to the fetus to ensure appropriate fetal growth. Iron in the developing fetus is accumulated against a concentration gradient and, in the case of maternal iron deficiency, the placenta can protect the fetus significantly through the increased expression of placental transferrin receptor together with a rise in divalent metal transporter 1 (DMT1). Despite the resistance of the fetus to maternal deficiency, any stress that alters placental development or function may have consequences for the developing fetus. Despite its central importance in fetal development, little is known about the mechanism of iron transfer across the placenta. Consequently, it is crucial to understand the molecular basis of placental iron transport in order to optimize the iron intake recommendation, reducing adverse pregnancy outcomes for both the mother and her child.