Disturbances in fetal insulin secretion are associated with abnormalities in fetal growth in a variety of species: excessive insulin secretion can lead to fetal macrosomia while fetal hypoinsulinaemia invariably causes fetal growth retardation. Fetal insulin deficiency caused by pancreatectomy (PX) of the sheep fetus leads to reduced body weight, crown-rump length and limb lengths at delivery near term. The growth rate in utero fell by 40-50% after PX and could be restored to normal values by insulin replacement treatment. These changes in growth were accompanied by reductions of 30-40% in the rates of umbilical uptake, utilization and oxidation of glucose by the sheep fetus. Insulin is therefore a physiological regulator of fetal growth and acts in part by stimulating the cellular uptake of glucose and its preferential use for oxidative metabolism in the fetal tissues.