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Tissue-specific Leptin promoter DNA methylation is associated with maternal and infant perinatal factors

Lesseur, Corina, Armstrong, David A., Paquette, Alison G., Koestler, Devin C., Padbury, James F., Marsit, Carmen J.
Molecular and Cellular Endocrinology 2013 v.381 pp. 160-167
DNA methylation, blood, epigenetics, gender, gene expression, genotype, humans, infant growth, infants, leptin, mothers, obesity, pregnancy outcome, single nucleotide polymorphism, small for gestational age, women
Leptin a regulator of body weight is involved in reproductive and developmental functions. Leptin promoter DNA methylation (LEP) regulates gene expression in a tissue-specific manner and has been linked to adverse pregnancy outcomes. In non-pathologic human pregnancies, we assessed LEP methylation, genotyped the single nucleotide polymorphism (SNP) rs2167270 in placental (n=81), maternal and cord blood samples (n=60), and examined the association between methylation, genotype, and perinatal factors. Maternal blood LEP methylation was lower in pre-pregnancy obese women (P=0.01). Cord blood LEP methylation was higher in small for gestational age (SGA) (P=4.6×10−3) and A/A genotype (P=1.6×10−4), lower (−1.47, P=0.03) in infants born to pre-pregnancy obese mothers and correlated (P=0.01) with maternal blood LEP. Gender was associated with placental LEP methylation (P=0.05). These results suggest that LEP epigenetic control may be influenced by perinatal factors including: maternal obesity, infant growth, genotype and gender in a tissue-specific manner and may have multigenerational implications.