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Abstract. Epigenetic marks at birth predict childhood body composition at age 9 years

Abstract. Epigenetic marks at birth predict childhood body composition at age 9 years
Abstract. Epigenetic marks at birth predict childhood body composition at age 9 years
Objective: While genomic variation explains only a modest proportion of the risk of cardiovascular and metabolic disease, animal models demonstrate that maternal environmental influences alter epigenetic processes in the offspring, with important effects on their later body composition and cardiometabolic function. Whether such processes operate in humans has not been examined.

Methods: Using DNA extracted from stored umbilical cord tissue from healthy neonates who were subsequently extensively phenotyped, we related the DNA methylation status of specific CpGs 5’ from candidate genes to body composition measured by DXA scanning at age 9 years. Appropriate institutional ethics committee clearance and participants’ informed consent were obtained.

Results: Methylation, measured by the Sequenom MassARRAY system, varied greatly at particular CpG sites. Of 68 CpGs studied, 31 had a median methylation >5% and a 5-95% range >10%. Independently of sex, there were strong correlations of the degree of methylation in specific CpGs in eNOS with childhood fat mass (Pearson correlation rp 50.42, n566) and trunk/limb fat ratio (rp 50.33, n566), and in RXRA methylation with fat mass and percentage fat mass (rp 50.32 and 0.29, respectively, n564) (all p,0.005, taking account of methylation at other CpG sites). Methylation at these sites was not linked to birth weight. Controlling for sex, perinatal epigenetic marks explained more than 40% of the variance in body composition at age 9 years.

Conclusions: Epigenetic marks at birth predict a significant proportion of the variance in later childhood adiposity, indicating that substantial components of later metabolic disease risk are induced before birth. Perinatal epigenetic analysis may have utility in identifying individual vulnerability to later chronic non-communicable disease. MAH and JSJ are supported by the British Heart Foundation. PDG and AS are funded by the National Research Centre for Growth and Development (New Zealand). BSE is supported by the Agency for Science, Technology and Research (Singapore). This work was supported by the charity WellChild (previously Children Nationwide), by the University of Southampton, by the UK Medical Research Council and the EpiGen consortium.
S44-S44
Godfrey, Keith M.
0931701e-fe2c-44b5-8f0d-ec5c7477a6fd
Gluckman, Peter D.
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Lillycrop, Karen A.
eeaaa78d-0c4d-4033-a178-60ce7345a2cc
Burdge, Graham C.
09d60a07-8ca1-4351-9bf1-de6ffcfb2159
Rodford, J.L.
c5962404-a31b-44ac-be66-c3762d1f9b14
Slater-Jefferies, J.L.
e46c711a-9d4c-436a-b853-828df69bb4d7
McLean, C
a8f9c5b4-d79d-4f72-850a-ff1cf9885a6d
Sheppard, A
1920e080-034f-49e1-9039-29a3ad89cd19
Crozier, S.R.
a97b1967-f6af-413a-8eb0-69fa25534d68
Emerald, B.S.
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Gale, Catharine R.
5bb2abb3-7b53-42d6-8aa7-817e193140c8
Cooper, C.
e05f5612-b493-4273-9b71-9e0ce32bdad6
Hanson, Mark A.
1952fad1-abc7-4284-a0bc-a7eb31f70a3f
Godfrey, Keith M.
0931701e-fe2c-44b5-8f0d-ec5c7477a6fd
Gluckman, Peter D.
ef2e8b92-0b76-4a12-bd7c-01b0674f94d3
Lillycrop, Karen A.
eeaaa78d-0c4d-4033-a178-60ce7345a2cc
Burdge, Graham C.
09d60a07-8ca1-4351-9bf1-de6ffcfb2159
Rodford, J.L.
c5962404-a31b-44ac-be66-c3762d1f9b14
Slater-Jefferies, J.L.
e46c711a-9d4c-436a-b853-828df69bb4d7
McLean, C
a8f9c5b4-d79d-4f72-850a-ff1cf9885a6d
Sheppard, A
1920e080-034f-49e1-9039-29a3ad89cd19
Crozier, S.R.
a97b1967-f6af-413a-8eb0-69fa25534d68
Emerald, B.S.
36ae23a7-8650-4f3e-8af0-38413d49fdb3
Gale, Catharine R.
5bb2abb3-7b53-42d6-8aa7-817e193140c8
Cooper, C.
e05f5612-b493-4273-9b71-9e0ce32bdad6
Hanson, Mark A.
1952fad1-abc7-4284-a0bc-a7eb31f70a3f

Godfrey, Keith M., Gluckman, Peter D., Lillycrop, Karen A., Burdge, Graham C., Rodford, J.L., Slater-Jefferies, J.L., McLean, C, Sheppard, A, Crozier, S.R., Emerald, B.S., Gale, Catharine R., Cooper, C. and Hanson, Mark A. (2009) Abstract. Epigenetic marks at birth predict childhood body composition at age 9 years. Journal of Developmental Origins of Health and Disease, 1, supplement Programme and Abstracts of the 6th World Congress on Developmental Origins of Heath and Disease, 19-22 November 2009, Santiago, Chile, S44-S44. (doi:10.1017/S2040174409990018).

Record type: Article

Abstract

Objective: While genomic variation explains only a modest proportion of the risk of cardiovascular and metabolic disease, animal models demonstrate that maternal environmental influences alter epigenetic processes in the offspring, with important effects on their later body composition and cardiometabolic function. Whether such processes operate in humans has not been examined.

Methods: Using DNA extracted from stored umbilical cord tissue from healthy neonates who were subsequently extensively phenotyped, we related the DNA methylation status of specific CpGs 5’ from candidate genes to body composition measured by DXA scanning at age 9 years. Appropriate institutional ethics committee clearance and participants’ informed consent were obtained.

Results: Methylation, measured by the Sequenom MassARRAY system, varied greatly at particular CpG sites. Of 68 CpGs studied, 31 had a median methylation >5% and a 5-95% range >10%. Independently of sex, there were strong correlations of the degree of methylation in specific CpGs in eNOS with childhood fat mass (Pearson correlation rp 50.42, n566) and trunk/limb fat ratio (rp 50.33, n566), and in RXRA methylation with fat mass and percentage fat mass (rp 50.32 and 0.29, respectively, n564) (all p,0.005, taking account of methylation at other CpG sites). Methylation at these sites was not linked to birth weight. Controlling for sex, perinatal epigenetic marks explained more than 40% of the variance in body composition at age 9 years.

Conclusions: Epigenetic marks at birth predict a significant proportion of the variance in later childhood adiposity, indicating that substantial components of later metabolic disease risk are induced before birth. Perinatal epigenetic analysis may have utility in identifying individual vulnerability to later chronic non-communicable disease. MAH and JSJ are supported by the British Heart Foundation. PDG and AS are funded by the National Research Centre for Growth and Development (New Zealand). BSE is supported by the Agency for Science, Technology and Research (Singapore). This work was supported by the charity WellChild (previously Children Nationwide), by the University of Southampton, by the UK Medical Research Council and the EpiGen consortium.

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Published date: October 2009
Organisations: Human Development & Health

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Local EPrints ID: 355546
URI: http://eprints.soton.ac.uk/id/eprint/355546
PURE UUID: dd350423-cdc1-4944-b711-646feaf84acb
ORCID for Keith M. Godfrey: ORCID iD orcid.org/0000-0002-4643-0618
ORCID for Karen A. Lillycrop: ORCID iD orcid.org/0000-0001-7350-5489
ORCID for Graham C. Burdge: ORCID iD orcid.org/0000-0002-7665-2967
ORCID for J.L. Slater-Jefferies: ORCID iD orcid.org/0000-0001-8325-1320
ORCID for Catharine R. Gale: ORCID iD orcid.org/0000-0002-3361-8638
ORCID for C. Cooper: ORCID iD orcid.org/0000-0003-3510-0709
ORCID for Mark A. Hanson: ORCID iD orcid.org/0000-0002-6907-613X

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Date deposited: 02 Sep 2013 12:50
Last modified: 18 Mar 2024 03:03

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Contributors

Author: Peter D. Gluckman
Author: J.L. Rodford
Author: C McLean
Author: A Sheppard
Author: S.R. Crozier
Author: B.S. Emerald
Author: C. Cooper ORCID iD
Author: Mark A. Hanson ORCID iD

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