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.

journal_name

Ann N Y Acad Sci

authors

Kanaka-Gantenbein C

doi

10.1111/j.1749-6632.2010.05683.x

subject

Has Abstract

pub_date

2010-09-01 00:00:00

pages

99-105

eissn

0077-8923

issn

1749-6632

journal_volume

1205

pub_type

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