Fetal growth is largely controlled by the interaction of the genome with the availability of oxygen and glucose and by endocrine responses to variations in their supply. Insulin-like growth factor II (IGF-II), and probably IGF-I, modulate fetal growth. Insulin and thyroid hormones are controlled by the supply of glucose and oxygen, respectively, and they influence fetal growth, partly via IGF-I. Circulating IGF-I and -II are controlled acutely and chronically by glucose availability to the fetus. The transfer of substrates from the mother to the fetus is determined by placental transfer capacity and by placental utilization of those substrates. The fetus controls the latter via its blood concentrations of oxygen and glucose and possibly IGF-I. In the mother, placental hormones and proteins, such as progesterone, placental lactogen, placental growth hormone and proteases, increase circulating IGFs and alter the stability and concentrations of IGF binding proteins. These changes may direct the metabolic and growth adaptation of the mother to pregnancy, which ensures an adequate flow of substrates to the developing fetus.