In eutherian mammals, the successful outcome of pregnancy depends on balancing the genetically-determined fetal drive for growth with the maternal nutrient requirements to support the pregnancy and the subsequent lactation. Failure to achieve the right balance of nutrient allocation can lead to pregnancy complications for the mother and abnormal development of the fetus with long-term consequences for both maternal and infant health. The placenta, which forms the functional interface between the mother and fetus is thought to be central to the allocation of nutrients during pregnancy; it controls materno-fetal nutrient exchange and secretes hormones with metabolic impacts1. My talk will focus on our findings using environmental and genetic manipulations of the insulin-like growth factor-2-phosphoinositide-3 kinase (IGF2-PI3K) system in mice which explore the regulation of materno-fetal nutrient allocation by the placenta during pregnancy. I will present data demonstrating that the placenta is able to respond to both maternal signals of resource availability, as well as, to fetal signals of nutrient demand, by adapting its transport phenotype. I will also demonstrate that maternal nutrient allocation to the fetus can be additionally modified by the endocrine actions of the placenta on maternal physiology. By studying the placenta and materno-fetal nutrient allocation, our work aims to understand the aetiology of pregnancy complications, developmental mechanisms and origins of health and disease.