The placenta is a transient multifunctional organ that prevents direct contact between maternal and fetal blood. In order to sustain appropriate fetal development, the mother must provide glucose, amino acids, and fatty acids, which must be transported to the fetus across the placenta. Thus, fetal growth directly depends on maternal nutrient availability and the placenta’s ability to flux nutrients from maternal circulation to the fetus. There are specific nutrient transporters that help transport nutrients from maternal circulation to the fetus. Changes in the expression and activity of these transporters affect nutrient-transport ability and consequently lead to restricted and excessive fetal growth. These growth-affected babies typically have poor neonatal outcomes and tend to develop diseases later in life. Therefore, information on the molecular mechanisms responsible for alterations in placental nutrient transporters is critical to understanding the mechanisms underlying altered fetal growth and fetal programming.

In the recent study, we show that elevated maternal testosterone levels, similar to those observed in IUGR women, increase placental FABP4 expression via transcriptional upregulation that preferentially routes long-chain polyunsaturated fatty acids (LCPUFA) toward cellular storage in the placenta, leading to offspring lipid deficiency.