Placental regulation of fetal nutrient supply

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.