Fetal growth patterns as early markers of fetal programming

Abstract

The Barker hypothesis1 postulates that some organs and functions undergo programming during fetal life, setting in motion adaptative responses with delayed effects into adulthood. Although there is mounting evidence on the association between fetal exposure to some insults and permanent changes in postnatal life, the underlying mechanisms are not well understood, but could include epigenetic mechanisms involving gene imprinting. Imprinted genes have a role in placental development, regulating fetal demand, and the placental supply of maternal nutrients.