TY - JOUR
T1 - DNA methylation of IGF2, GNASAS, INSIGF and LEP and being born small for gestational age
AU - Tobi, Elmar W.
AU - Heijmans, Bastiaan T.
AU - Kremer, Dennis
AU - Putter, Hein
AU - Delemarre-van de Waal, Henriette A.
AU - Finken, Martijn J. J.
AU - Wit, Jan M.
AU - Slagboom, P. Eline
PY - 2011
Y1 - 2011
N2 - Being born small for gestational age (SGA), a proxy for intrauterine growth restriction (IUGR) and prenatal famine exposure are both associated with a greater risk of metabolic disease. Both associations have been hypothesized to involve epigenetic mechanisms. We investigated whether prenatal growth restriction early in pregnancy was associated with changes in DNA methylation at loci that were previously shown to be sensitive to early gestational famine exposure. We compared 38 individuals born preterm (<32 weeks) and with a birth weight too low for their gestational age (less than -1SDS; SGA) with 75 individuals born preterm but with a birth weight appropriate for their gestational age (greater than -1SDS) and a normal postnatal growth (greater than -1SDS at three months post term; AGA). The SGA individuals were not only lighter at birth, but also had a smaller length (p = 3.3 × 10-13) and head circumference at birth (p = 4.1 × 10-13). The DNA methylation levels of IGF2, GNASAS, INSIGF and LEP were 48.5, 47.5, 79.4 and 25.7% respectively. This was not significantly different between SGA and AGA individuals. Risk factors for being born SGA, including preeclampsia and maternal smoking, were also not associated with DNA methylation at these loci. Growth restriction early in development is not associated with DNA methylation at loci shown to be affected by prenatal famine exposure. Our and previous results by others indicate that prenatal growth restriction and famine exposure may be associated with different epigenetic changes or non-epigenetic mechanisms that may lead to similar later health outcomes. © 2011 Landes Bioscience.
AB - Being born small for gestational age (SGA), a proxy for intrauterine growth restriction (IUGR) and prenatal famine exposure are both associated with a greater risk of metabolic disease. Both associations have been hypothesized to involve epigenetic mechanisms. We investigated whether prenatal growth restriction early in pregnancy was associated with changes in DNA methylation at loci that were previously shown to be sensitive to early gestational famine exposure. We compared 38 individuals born preterm (<32 weeks) and with a birth weight too low for their gestational age (less than -1SDS; SGA) with 75 individuals born preterm but with a birth weight appropriate for their gestational age (greater than -1SDS) and a normal postnatal growth (greater than -1SDS at three months post term; AGA). The SGA individuals were not only lighter at birth, but also had a smaller length (p = 3.3 × 10-13) and head circumference at birth (p = 4.1 × 10-13). The DNA methylation levels of IGF2, GNASAS, INSIGF and LEP were 48.5, 47.5, 79.4 and 25.7% respectively. This was not significantly different between SGA and AGA individuals. Risk factors for being born SGA, including preeclampsia and maternal smoking, were also not associated with DNA methylation at these loci. Growth restriction early in development is not associated with DNA methylation at loci shown to be affected by prenatal famine exposure. Our and previous results by others indicate that prenatal growth restriction and famine exposure may be associated with different epigenetic changes or non-epigenetic mechanisms that may lead to similar later health outcomes. © 2011 Landes Bioscience.
UR - https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=79951486887&origin=inward
UR - https://www.ncbi.nlm.nih.gov/pubmed/20930547
U2 - https://doi.org/10.4161/epi.6.2.13516
DO - https://doi.org/10.4161/epi.6.2.13516
M3 - Article
C2 - 20930547
SN - 1559-2294
VL - 6
SP - 171
EP - 176
JO - EPIGENETICS
JF - EPIGENETICS
IS - 2
ER -