Purpose of review: Placental nutrient uptake and transfer may have a unique role, as changes in trophoblast nutrient-sensing signaling pathways regulate cell metabolism and may affect the fetal growth and health programming in the offspring.
Recent findings: The functionality of the placenta could affect the neonatal adiposity and the fetal levels of key nutrients such as long-chain polyunsaturated fatty acids. Insulin, oxygen and amino acid concentrations may regulate the mammalian target of rapamycin (mTOR) nutrient sensor in the human placenta affecting trophoblast metabolism and nutrient delivery.
Summary: The mechanisms involved in both placental uptake and transfer of macronutrients are reviewed. Fatty acid, cholesterol and amino acid transport across the placenta involves a complex system to ensure nutrient delivery to the growing fetus. The placental glucose transfer is important for fetal macrosomia, but lipid disturbances in both maternal and placental compartments may contribute to neonatal fat accretion. Maternal insulin has little effect on the avidity of glucose transport by the placenta, but may interfere in placental metabolism via mTOR nutrient sensor. mTOR is a positive regulator of the amino acid carriers and constitutes a critical link between maternal nutrient availability and fetal growth, thereby influencing the long-term health of the fetus.