The fetus requires amino acids for the processes of protein synthesis, carbon accretion, oxidative metabolism, and biosynthesis, which ultimately determine growth rate in utero. The fetal supply of amino acids is critically dependent on the transport capacity of the placenta. System A amino acid transporters in the syncytiotrophoblast microvillous plasma membrane, directed toward maternal blood, actively accumulate amino acids, while system L exchangers mediate uptake of essential amino acids from the maternal circulation. The functional capacity and protein abundance of these transporters in the placenta are related to fetal growth in both humans and experimental animals. Maternal nutritional and endocrine signals including insulin, insulin-like growth factors, adipokines, and steroid hormones regulate placental amino acid transport, against the background of growth signals originating from the fetus. Anabolic signals of abundant maternal resource availability stimulate placental amino acid transport to optimize offspring fitness, whereas catabolic signals reduce placental amino acid transport in an attempt to ensure survival and long-term reproductive capacity of the mother when resources are scarce. These signals regulate placental amino acid transport by controlling transcription, translation, plasma membrane trafficking, and degradation of transporters. Adaptations in placental amino acid transport capacity may underlie either under- or overgrowth of the fetus when maternal nutrient and hormone levels are altered as a result of altered maternal nutrition or metabolic disease. Strategies to modulate placental amino acid transport may prove effective to normalize fetal growth in intrauterine growth restriction and fetal overgrowth.