Fetal origins of adult diabetes

According to the fetal origin of adult diseases hypothesis, the intrauterine environment through developmental plasticity may permanently influence long‐term health and disease. Therefore, intrauterine growth restriction (IUGR), due either to maternal, placental, or genetic factors, may permanently alter the endocrine–metabolic status of the fetus, driving an insulin resistance state that can promote survival at the short term but that facilitates the development of type 2 diabetes mellitus and metabolic syndrome in adult life, especially when the intrauterine nutrient restriction is followed by a postnatal obesogenic environment. Furthermore, an energy‐rich environment during fetal programming may also drive the development of excess abdominal fat and type 2 diabetes in later life, demonstrating that both intrauterine nutrient restriction as well as intrauterine nutrient excessive supply may predispose for the development of adult diabetes.