title: Fetal origins of adult diabetes.
abstract: 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.
authors.affiliation: Division of Endocrinology, Diabetes and Metabolism, First Department of Pediatrics, University of Athens, Agia Sophia Children's Hospital, Athens, Greece. ganten@hol.gr
authors.forename: Christina
authors.initials: C
authors.lastname: Kanaka-Gantenbein
mesh_terms: D000328:Adult; D000818:Animals; D003920:Diabetes Mellitus / Q000209:etiology* / Q000235:genetics; D044127:Epigenesis, Genetic / Q000502:physiology; D005260:Female; D047109:Fetal Development / Q000235:genetics / Q000502:physiology*; D006801:Humans; D008954:Models, Biological; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000209:etiology* / Q000235:genetics; D012307:Risk Factors