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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

Associations between cord blood DNA methylation and offspring adiposity. The heatmaps are built using effect sizes. Positive associations appear more red and negative associations appear more blue. CpG sites were selected based on their association with maternal underweight or obesity, the effect size for which is indicated in the far right-hand panel. Stars indicate associations with a P-value < 0.05 (before correction for multiple testing).
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dyv042-F5: Associations between cord blood DNA methylation and offspring adiposity. The heatmaps are built using effect sizes. Positive associations appear more red and negative associations appear more blue. CpG sites were selected based on their association with maternal underweight or obesity, the effect size for which is indicated in the far right-hand panel. Stars indicate associations with a P-value < 0.05 (before correction for multiple testing).

Mentions: Figure 5 shows effect sizes for associations between methylation at birth and various measures of offspring adiposity (results are shown for the top 25 CpG sites with the largest effect sizes and an FDR-adjusted P-value < 0.05 for the association between maternal underweight/obesity and cord blood methylation). In general, sites that were hypermethylated in association with maternal obesity or hypomethylated in association with maternal underweight tended to be positively associated with offspring adiposity, and sites hypomethylated in association with maternal obesity or hypermethylated in association with maternal underweight tended to be inversely associated with offspring adiposity. This trend is strongest for birthweight and largely consistent over different measures of offspring adiposity recorded at different times (Table S6, available as Supplementary data at IJE online). It should be noted that associations between offspring adiposity and cord blood methylation at individual sites did not survive correction for multiple testing.Figure 5.


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)

Associations between cord blood DNA methylation and offspring adiposity. The heatmaps are built using effect sizes. Positive associations appear more red and negative associations appear more blue. CpG sites were selected based on their association with maternal underweight or obesity, the effect size for which is indicated in the far right-hand panel. Stars indicate associations with a P-value < 0.05 (before correction for multiple testing).
© Copyright Policy - creative-commons
Related In: Results  -  Collection

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

dyv042-F5: Associations between cord blood DNA methylation and offspring adiposity. The heatmaps are built using effect sizes. Positive associations appear more red and negative associations appear more blue. CpG sites were selected based on their association with maternal underweight or obesity, the effect size for which is indicated in the far right-hand panel. Stars indicate associations with a P-value < 0.05 (before correction for multiple testing).
Mentions: Figure 5 shows effect sizes for associations between methylation at birth and various measures of offspring adiposity (results are shown for the top 25 CpG sites with the largest effect sizes and an FDR-adjusted P-value < 0.05 for the association between maternal underweight/obesity and cord blood methylation). In general, sites that were hypermethylated in association with maternal obesity or hypomethylated in association with maternal underweight tended to be positively associated with offspring adiposity, and sites hypomethylated in association with maternal obesity or hypermethylated in association with maternal underweight tended to be inversely associated with offspring adiposity. This trend is strongest for birthweight and largely consistent over different measures of offspring adiposity recorded at different times (Table S6, available as Supplementary data at IJE online). It should be noted that associations between offspring adiposity and cord blood methylation at individual sites did not survive correction for multiple testing.Figure 5.

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