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Maternal pre-pregnancy BMI and gestational weight gain, offspring DNA methylation and later offspring adiposity: findings from the Avon Longitudinal Study of Parents and Children.

Sharp GC, Lawlor DA, Richmond RC, Fraser A, Simpkin A, Suderman M, Shihab HA, Lyttleton O, McArdle W, Ring SM, Gaunt TR, Davey Smith G, Relton CL - Int J Epidemiol (2015)

Bottom Line: There were no consistent associations of gestational weight gain with offspring DNA methylation.Our data suggest that both maternal obesity and, to a larger degree, underweight affect the neonatal epigenome via an intrauterine mechanism, but weight gain during pregnancy has little effect.We found some evidence that associations of maternal underweight with lower offspring adiposity and maternal obesity with greater offspring adiposity may be mediated via increased DNA methylation.

View Article: PubMed Central - PubMed

Affiliation: MRC Integrative Epidemiology Unit at the University of Bristol, Bristol, UK, School of Social and Community Medicine, University of Bristol, Bristol, UK and gemma.sharp@bristol.ac.uk.

No MeSH data available.


Related in: MedlinePlus

A conceptual framework showing the relationships of interest. GWG and maternal BMI are hypothesized to affect offspring adiposity via offspring DNA methylation. Specific hypotheses are: (i) maternal pre-pregnancy BMI and/or GWG is associated with differential methylation at CpG sites in offspring cord blood; (ii) methylation at these sites is also associated with offspring adiposity (we would also expect consistency between different measures of adiposity and age at measurement); and (iii) maternal adiposity is persistently associated with differential methylation in offspring at time points beyond birth.
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dyv042-F1: A conceptual framework showing the relationships of interest. GWG and maternal BMI are hypothesized to affect offspring adiposity via offspring DNA methylation. Specific hypotheses are: (i) maternal pre-pregnancy BMI and/or GWG is associated with differential methylation at CpG sites in offspring cord blood; (ii) methylation at these sites is also associated with offspring adiposity (we would also expect consistency between different measures of adiposity and age at measurement); and (iii) maternal adiposity is persistently associated with differential methylation in offspring at time points beyond birth.

Mentions: In this paper, our primary aim is to identify differential methylation in offspring at birth that is associated with both maternal adiposity in pregnancy and offspring adiposity from birth to adolescence. Figure 1 shows the conceptual framework and hypothesized relationships. We hypothesize that: (i) maternal pre-pregnancy BMI and/or GWG are associated with differential methylation at CpG sites in offspring cord blood; (ii) methylation at these sites is also associated with offspring adiposity (we would also expect consistency between different measures of adiposity and age at measurement); and (iii) maternal adiposity is persistently associated with differential methylation in offspring at time points beyond birth. We addressed some previous limitations in human studies by: (i) testing non-linear associations of maternal pre-pregnancy BMI or GWG with DNA methylation; (ii) examining associations of maternal exposures with offspring methylation at different ages and then examining whether identified differentially methylated sites are related to subsequent offspring adiposity; and (iii) using a negative control (paternal BMI)26 to explore causation.27Figure 1.


Maternal pre-pregnancy BMI and gestational weight gain, offspring DNA methylation and later offspring adiposity: findings from the Avon Longitudinal Study of Parents and Children.

Sharp GC, Lawlor DA, Richmond RC, Fraser A, Simpkin A, Suderman M, Shihab HA, Lyttleton O, McArdle W, Ring SM, Gaunt TR, Davey Smith G, Relton CL - Int J Epidemiol (2015)

A conceptual framework showing the relationships of interest. GWG and maternal BMI are hypothesized to affect offspring adiposity via offspring DNA methylation. Specific hypotheses are: (i) maternal pre-pregnancy BMI and/or GWG is associated with differential methylation at CpG sites in offspring cord blood; (ii) methylation at these sites is also associated with offspring adiposity (we would also expect consistency between different measures of adiposity and age at measurement); and (iii) maternal adiposity is persistently associated with differential methylation in offspring at time points beyond birth.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4588865&req=5

dyv042-F1: A conceptual framework showing the relationships of interest. GWG and maternal BMI are hypothesized to affect offspring adiposity via offspring DNA methylation. Specific hypotheses are: (i) maternal pre-pregnancy BMI and/or GWG is associated with differential methylation at CpG sites in offspring cord blood; (ii) methylation at these sites is also associated with offspring adiposity (we would also expect consistency between different measures of adiposity and age at measurement); and (iii) maternal adiposity is persistently associated with differential methylation in offspring at time points beyond birth.
Mentions: In this paper, our primary aim is to identify differential methylation in offspring at birth that is associated with both maternal adiposity in pregnancy and offspring adiposity from birth to adolescence. Figure 1 shows the conceptual framework and hypothesized relationships. We hypothesize that: (i) maternal pre-pregnancy BMI and/or GWG are associated with differential methylation at CpG sites in offspring cord blood; (ii) methylation at these sites is also associated with offspring adiposity (we would also expect consistency between different measures of adiposity and age at measurement); and (iii) maternal adiposity is persistently associated with differential methylation in offspring at time points beyond birth. We addressed some previous limitations in human studies by: (i) testing non-linear associations of maternal pre-pregnancy BMI or GWG with DNA methylation; (ii) examining associations of maternal exposures with offspring methylation at different ages and then examining whether identified differentially methylated sites are related to subsequent offspring adiposity; and (iii) using a negative control (paternal BMI)26 to explore causation.27Figure 1.

Bottom Line: There were no consistent associations of gestational weight gain with offspring DNA methylation.Our data suggest that both maternal obesity and, to a larger degree, underweight affect the neonatal epigenome via an intrauterine mechanism, but weight gain during pregnancy has little effect.We found some evidence that associations of maternal underweight with lower offspring adiposity and maternal obesity with greater offspring adiposity may be mediated via increased DNA methylation.

View Article: PubMed Central - PubMed

Affiliation: MRC Integrative Epidemiology Unit at the University of Bristol, Bristol, UK, School of Social and Community Medicine, University of Bristol, Bristol, UK and gemma.sharp@bristol.ac.uk.

No MeSH data available.


Related in: MedlinePlus