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

Corina Lesseur; David A. Armstrong; Alison G. Paquette; Devin C. Koestler; James F. Padbury; Carmen J. Marsit

doi:10.1016/j.mce.2013.07.024

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

Corina Lesseur
, David A. Armstrong
, Alison G. Paquette
, Devin C. Koestler
, James F. Padbury
, Carmen J. Marsit

Research output: Contribution to journal › Article › peer-review

84 Scopus citations

Abstract

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.

Original language	English
Pages (from-to)	160-167
Number of pages	8
Journal	Molecular and Cellular Endocrinology
Volume	381
Issue number	1-2
DOIs	https://doi.org/10.1016/j.mce.2013.07.024
State	Published - 5 Dec 2013
Externally published	Yes

Keywords

DNA methylation
Epigenetics
Leptin
Maternal obesity
Pregnancy
Rs2167270

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10.1016/j.mce.2013.07.024

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title = "Tissue-specific Leptin promoter DNA methylation is associated with maternal and infant perinatal factors",

abstract = "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.",

keywords = "DNA methylation, Epigenetics, Leptin, Maternal obesity, Pregnancy, Rs2167270",

author = "Corina Lesseur and Armstrong, \{David A.\} and Paquette, \{Alison G.\} and Koestler, \{Devin C.\} and Padbury, \{James F.\} and Marsit, \{Carmen J.\}",

note = "Funding Information: Thanks to Joyce Lee for her hard work in recruitment of subjects into this study and the support of the staff of the Brown Center for the Study of Children at Risk for their efforts. This work was funded by the National Institute of Health (NIH) through the following Grants: R01MH094609 (NIH-NIMH), P20GM103537 (NIH-NIGMS) and P30CA23108 (NIH-NCI). Its contents are the responsibility of the authors and do not necessarily represent the official views of the funding institutions. ",

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AU - Paquette, Alison G.

AU - Koestler, Devin C.

AU - Padbury, James F.

AU - Marsit, Carmen J.

N1 - Funding Information: Thanks to Joyce Lee for her hard work in recruitment of subjects into this study and the support of the staff of the Brown Center for the Study of Children at Risk for their efforts. This work was funded by the National Institute of Health (NIH) through the following Grants: R01MH094609 (NIH-NIMH), P20GM103537 (NIH-NIGMS) and P30CA23108 (NIH-NCI). Its contents are the responsibility of the authors and do not necessarily represent the official views of the funding institutions.

PY - 2013/12/5

Y1 - 2013/12/5

N2 - 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.

AB - 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.

KW - DNA methylation

KW - Epigenetics

KW - Leptin

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KW - Pregnancy

KW - Rs2167270

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JO - Molecular and Cellular Endocrinology

JF - Molecular and Cellular Endocrinology

IS - 1-2

ER -

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

Abstract

Keywords

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