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Ann N Y Acad Sci. 2010 Sep;1205:99-105. doi: 10.1111/j.1749-6632.2010.05683.x.

Fetal origins of adult diabetes.

Author information

1
Division of Endocrinology, Diabetes and Metabolism, First Department of Pediatrics, University of Athens, Agia Sophia Children's Hospital, Athens, Greece. ganten@hol.gr

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.

[Indexed for MEDLINE]

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