Abstract
A large number of epidemiological studies have revealed that there is a relationship between early growth restriction and the subsequent development of type 2 diabetes or the metabolic syndrome. The mechanistic basis of this relationship and the relative roles played by genes and the environment remains the subject of much current debate. Animal models of early growth restriction have been developed in an attempt to understand its relationship with adult disease and to provide insight into the underlying molecular mechanisms. These models show many features of the metabolic syndrome. In the maternal protein restriction model, insulin resistance and hypertension is observed. The uterine artery ligation model shows obesity in adulthood. This provides strong evidence that alterations in the fetal environment can lead to diabetes in adult life.