AbstractInsulin deficiency in either the mother or foetus has significant effects on fetal growth and development. In the human, maternal insulin deficiency, or diabetes mellitus, leads to macrosomia and increased adiposity of the foetus, while specific fetal hypo‐insulinaemia is associated with intra‐uterine growth retardation. When maternal diabetes is induced in experimental animals, no consistent increases in fetal bodyweight are observed although the body fat content of the foetus is increased in the majority of species studied. The magnitude of the fetal weight gain during maternal diabetes appears to be determined by the body fat content of the foetus, the severity and duration of the diabetes and by the temporal pattern of maternal hyperglycaemia observed during pregnancy. The latter factors, in particular, influence the level of insulin in the foetus which, in turn, regulates the rate of intra‐uterine growth. By contrast, fetal insulin deficiency has a more uniform effect on fetal growth and leads to impaired growth in both experimental and naturally occurring hypo‐insulinaemic conditions. Fetal insulin deficiency reduces fetal growth by decreasing nutrient uptake and utilization of the fetal tissues and by altering the circulating concentrations of the insulin‐like growth factors. Consequently, deficiencies in either fetal or maternal insulin secretion during pregnancy can alter fetal growth and have important consequences for perinatal survival and postnatal