The placenta is the main determinant of fetal growth and development in utero. It supplies all the nutrients and oxygen required for fetal growth and secretes hormones that facilitate maternal allocation of nutrients to the fetus. Abnormalities in placental development and function can lead to pregnancy complications and abnormal fetal growth. In addition poor placental development and abnormal birth weight can increase the risk of developing degenerative diseases such as hypertension, obesity, type 2 diabetes and the metabolic syndrome in later life (1). The processes by which adverse intrauterine conditions permanently alter fetal tissue development and function are known as developmental programming (2). However, compared to fetal tissues, little is known about programming of the placenta by adverse gestational environments. In this presentation I will describe our findings of the environmental regulation of placental phenotype with particular emphasis on the impact of maternal nutritional challenges and oxygen scarcity in mice. I will provide evidence that shows the placenta is not just a passive organ for the materno-fetal transfer of nutrients and oxygen; indeed the placenta can adapt morphologically and functionally to optimise fetal substrate supply under adverse intrauterine conditions. While these adaptations help meet the fetal drive for growth, they alter the amount and relative proportions of specific metabolic substrates supplied to the fetus during development. This will have consequences for the developmental programming of offspring health in later life. Current work in the lab is focussed on identifying the molecular mechanisms by which the placenta adapts. This information will aid in the discovery of therapeutic strategies for improving pregnancy outcome and long-term adult health.