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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.