Limits...
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

Manhattan plots showing the results of epigenome-wide association studies (EWAS) of cord blood DNA methylation in offspring of underweight (n = 24), overweight (n = 94) and obese (n = 32) mothers compared with offspring of normal weight mothers (n = 577). The bottom (blue) line indicates the FDR-adjusted P-value threshold (0.05) and the top (red) line indicates the Bonferroni threshold for genome-wide significance (3.5*10−7, i.e. 0.05/284972 probes).
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4588865&req=5

dyv042-F2: Manhattan plots showing the results of epigenome-wide association studies (EWAS) of cord blood DNA methylation in offspring of underweight (n = 24), overweight (n = 94) and obese (n = 32) mothers compared with offspring of normal weight mothers (n = 577). The bottom (blue) line indicates the FDR-adjusted P-value threshold (0.05) and the top (red) line indicates the Bonferroni threshold for genome-wide significance (3.5*10−7, i.e. 0.05/284972 probes).

Mentions: Compared with offspring of women who were normal weight (n = 577), offspring of women who were obese (n = 32) had 28 sites that were differentially methylated and offspring of women who were underweight (n=24) had a considerably larger number (1621) of sites that were differentially methylated (FDR-corrected P-value < 0.05; Figure 2). Lambdas did not suggest genomic inflation (Figure S2, available as Supplementary data at IJE online: 0.998 for maternal obesity and 0.958 for maternal underweight). There was no overlap in terms of sites associated with maternal obesity and sites associated with maternal underweight. A positive association, where higher methylation is associated with BMI outside the normal range, was seen at 78.6% of the sites associated with obesity and 87.9% of the sites associated with underweight. Table 1 summarizes the top five sites with the largest effect sizes and FDR-adjusted P-values < 0.05. There were no sites that were differentially methylated in offspring of overweight women (n = 94) compared with normal weight women (Figure 2).Figure 2.


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)

Manhattan plots showing the results of epigenome-wide association studies (EWAS) of cord blood DNA methylation in offspring of underweight (n = 24), overweight (n = 94) and obese (n = 32) mothers compared with offspring of normal weight mothers (n = 577). The bottom (blue) line indicates the FDR-adjusted P-value threshold (0.05) and the top (red) line indicates the Bonferroni threshold for genome-wide significance (3.5*10−7, i.e. 0.05/284972 probes).
© Copyright Policy - creative-commons
Related In: Results  -  Collection

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

dyv042-F2: Manhattan plots showing the results of epigenome-wide association studies (EWAS) of cord blood DNA methylation in offspring of underweight (n = 24), overweight (n = 94) and obese (n = 32) mothers compared with offspring of normal weight mothers (n = 577). The bottom (blue) line indicates the FDR-adjusted P-value threshold (0.05) and the top (red) line indicates the Bonferroni threshold for genome-wide significance (3.5*10−7, i.e. 0.05/284972 probes).
Mentions: Compared with offspring of women who were normal weight (n = 577), offspring of women who were obese (n = 32) had 28 sites that were differentially methylated and offspring of women who were underweight (n=24) had a considerably larger number (1621) of sites that were differentially methylated (FDR-corrected P-value < 0.05; Figure 2). Lambdas did not suggest genomic inflation (Figure S2, available as Supplementary data at IJE online: 0.998 for maternal obesity and 0.958 for maternal underweight). There was no overlap in terms of sites associated with maternal obesity and sites associated with maternal underweight. A positive association, where higher methylation is associated with BMI outside the normal range, was seen at 78.6% of the sites associated with obesity and 87.9% of the sites associated with underweight. Table 1 summarizes the top five sites with the largest effect sizes and FDR-adjusted P-values < 0.05. There were no sites that were differentially methylated in offspring of overweight women (n = 94) compared with normal weight women (Figure 2).Figure 2.

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