Abstract
BackgroundNeonatal adiposity is a risk factor for childhood obesity. Investigating contributors to neonatal adiposity is important for understanding early life obesity risk. Epigenetic changes of metabolic genes in cord blood may contribute to excessive neonatal adiposity and subsequent childhood obesity. This study aims to evaluate the association of cord blood DNA methylation patterns with anthropometric measures and cord blood leptin, a biomarker of neonatal adiposity.MethodsA cross-sectional study was performed on a multiethnic cohort of 114 full term neonates born to mothers without gestational diabetes at a university hospital. Cord blood was assayed for leptin and for epigenome-wide DNA methylation profiles via the Illumina 450K platform. Neonatal body composition was measured by air displacement plethysmography. Multivariable linear regression was used to analyze associations between individual CpG sites as well as differentially methylated regions in cord blood DNA with measures of newborn adiposity including anthropometrics (birth weight, fat mass and percent body fat) and cord blood leptin. False discovery rate was estimated to account for multiple comparisons.Results247 CpG sites as well as 18 differentially methylated gene regions were associated with cord blood leptin but no epigenetic changes were associated with birth weight, fat mass or percent body fat. Genes of interest identified in this study are DNAJA4, TFR2, SMAD3, PLAG1, FGF1, and HNF4A.ConclusionEpigenetic changes in cord blood DNA are associated with cord blood leptin levels, a measure of neonatal adiposity.
Highlights
Adiposity at birth may be a predictor of obesity in childhood and adulthood.[1]
247 CpG sites as well as 18 differentially methylated gene regions were associated with cord blood leptin but no epigenetic changes were associated with birth weight, fat mass or percent body fat
Genes of interest identified in this study are DNAJA4, Transferrin receptor 2 (TFR2), SMAD3, PLAG1, FGF1, and HNF4A
Summary
Adiposity at birth may be a predictor of obesity in childhood and adulthood.[1]. Obesity has a current estimated prevalence of 17% among children aged 2–19 and has become increasingly challenging to treat once present.[2]. Epigenetics, the study of modifications to DNA that alter gene expression without changing gene sequence, is one mechanism contributing to the early life development of excess adiposity and future risk of an adverse metabolic phenotype.[7] Aberrant methylation of CpG dinucleotides in DNA is a type of epigenetic modification that can be both heritable and modifiable by one’s environment. Maternal pregnancy characteristics, and the intrauterine milieu can alter susceptibility of neonatal DNA to methylation, leading to changes in the child’s gene expression, gene regulation, and metabolic risk.[8, 9] Prior studies have demonstrated associations between maternal phenotypes and offspring DNA methylation, supporting the hypothesis that the intrauterine environment impacts fetal epigenetics.[10,11,12] Methylation patterns present at birth which are associated with newborn adiposity or later childhood obesity suggest that epigenetics may be partially responsible for the perinatal origins of obesity risk and predict future obesity. This study aims to evaluate the association of cord blood DNA methylation patterns with anthropometric measures and cord blood leptin, a biomarker of neonatal adiposity
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
