Читать книгу Genetic Disorders and the Fetus - Группа авторов - Страница 146

Fetal growth is dependent on efficient nutrient delivery to the fetus. This is determined by maternal availability, maternal blood flow to the placenta, the amount of placental surface in contact with maternal blood, and the efficiency of placental transport.^{22, 23} Transport of substances across the placenta can occur by (i) passive transport (simple or facilitated diffusion); (ii) active transport; and (iii) vesicular transport, by which large molecules are captured by microvesicles. A well‐functioning placenta can be extremely efficient at extracting nutrients for the fetus even when maternal supplies are low. For example, there is a threefold increase in folate concentration in the placenta compared with maternal blood;²⁴ this is accomplished via several folate receptors highly expressed in the human placenta, including folate receptor 1 (FOLR1), proton‐coupled high‐affinity folate transporter (PCFT), and reduced folate carrier (RFC).²⁵ As the fetus grows and requires more nutrients, the placenta alters gene expression to increase nutrient supply to the fetus;²⁶ for example, upregulation of System A transporters can increase delivery of amino acids.^{3, 27} There is also an increase in iron transport proteins, which absorb iron from maternal blood,²⁸ and of placental CRH, which increases the production of maternal glucose needed to support the growing fetal brain.²⁹ One pathway by which increased cortisol can lead to growth restriction is by interfering with CRH‐driven glucose production.²⁹