Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 381, Issue 1-2, Pages 160-167Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2013.07.024
Keywords
Leptin; Epigenetics; DNA methylation; rs2167270; Pregnancy; Maternal obesity
Categories
Funding
- National Institute of Health (NIH) [R01MH094609 (NIH-NIMH), P20GM103537 (NIH-NIGMS), P30CA23108 (NIH-NCI)]
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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 x 10(-3)) and A/A genotype (P = 1.6 x 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. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
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