HIF3A association with adiposity: the story begins before birth

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Abstract

Aim:

Determine if the association of HIF3A DNA methylation with weight and adiposity is detectable early in life.

Material & methods:

We determined HIF3A genotype and DNA methylation patterns (on hybridization arrays) in DNA extracted from umbilical cords of 991 infants. Methylation levels at three CpGs in the HIF3A first intron were related to neonatal and infant anthropometry and to genotype at nearby polymorphic sites.

Results & conclusion:

Higher methylation levels at three previously described HIF3A CpGs were associated with greater infant weight and adiposity. The effect sizes were slightly smaller than those reported for adult BMI. There was also an interaction within cis-genotype. The association between higher DNA methylation at HIF3A and increased adiposity is present in neonates. In this study, no particular prenatal factor strongly influenced HIF3A hypermethylation. Our data nonetheless suggest shared prenatal influences on HIF3A methylation and adiposity.

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Most cited references 21

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High density DNA methylation array with single CpG site resolution.

Marina Bibikova, Bret Barnes, Chan Tsan … (2011)

We have developed a new generation of genome-wide DNA methylation BeadChip which allows high-throughput methylation profiling of the human genome. The new high density BeadChip can assay over 480K CpG sites and analyze twelve samples in parallel. The innovative content includes coverage of 99% of RefSeq genes with multiple probes per gene, 96% of CpG islands from the UCSC database, CpG island shores and additional content selected from whole-genome bisulfite sequencing data and input from DNA methylation experts. The well-characterized Infinium® Assay is used for analysis of CpG methylation using bisulfite-converted genomic DNA. We applied this technology to analyze DNA methylation in normal and tumor DNA samples and compared results with whole-genome bisulfite sequencing (WGBS) data obtained for the same samples. Highly comparable DNA methylation profiles were generated by the array and sequencing methods (average R2 of 0.95). The ability to determine genome-wide methylation patterns will rapidly advance methylation research. Copyright © 2011 Elsevier Inc. All rights reserved.

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Epigenetic mechanisms that underpin metabolic and cardiovascular diseases.

Peter D. Gluckman, Mark Hanson, Tatjana Buklijas … (2009)

Cellular commitment to a specific lineage is controlled by differential silencing of genes, which in turn depends on epigenetic processes such as DNA methylation and histone modification. During early embryogenesis, the mammalian genome is 'wiped clean' of most epigenetic modifications, which are progressively re-established during embryonic development. Thus, the epigenome of each mature cellular lineage carries the record of its developmental history. The subsequent trajectory and pattern of development are also responsive to environmental influences, and such plasticity is likely to have an epigenetic basis. Epigenetic marks may be transmitted across generations, either directly by persisting through meiosis or indirectly through replication in the next generation of the conditions in which the epigenetic change occurred. Developmental plasticity evolved to match an organism to its environment, and a mismatch between the phenotypic outcome of adaptive plasticity and the current environment increases the risk of metabolic and cardiovascular disease. These considerations point to epigenetic processes as a key mechanism that underpins the developmental origins of chronic noncommunicable disease. Here, we review the evidence that environmental influences during mammalian development lead to stable changes in the epigenome that alter the individual's susceptibility to chronic metabolic and cardiovascular disease, and discuss the clinical implications.

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Cohort profile: Growing Up in Singapore Towards healthy Outcomes (GUSTO) birth cohort study.

K Godfrey, , Anne Rifkin-Graboi … (2014)

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Author and article information

Journal

Journal ID (nlm-ta): Epigenomics

Journal ID (iso-abbrev): Epigenomics

Journal ID (publisher-id): EPI

Title: Epigenomics

Publisher: Future Medicine Ltd (London, UK )

ISSN (Print): 1750-1911

ISSN (Electronic): 1750-192X

Publication date (Print): September 2015

Volume: 7

Issue: 6

Pages: 937-950

Affiliations

[1 ]Singapore Institute for Clinical Sciences (SICS), A*STAR, Brenner Centre for Molecular Medicine, 117609, Singapore

[2 ]School of Computer Engineering, Nanyang Technological University (NTU), 639798, Singapore

[3 ]Saw Swee Hock School of Public Health, National University of Singapore (NUS), 117597, Singapore

[4 ]Yong Loo Lin School of Medicine, National University of Singapore (NUS), 119228, Singapore

[5 ]Division of Paediatric Endocrinology & Diabetes, Khoo Teck Puat-National University Children's Medical Institute, National University Health System, 119228, Singapore

[6 ]Department of Medical Genetics, Centre for Molecular Medicine & Therapeutics, Child & Family Research Institute, University of British Columbia, Vancouver, BC, V5Z 4H4 Canada

[7 ]KK Women's and Children's Hospital, 229899, Singapore

[8 ]Ludmer Centre for Neuroinformatics & Mental Health, Douglas University Mental Health Institute, McGill University, Montreal, (Quebec) H4H 1R3, Canada

[9 ]MRC Lifecourse Epidemiology Unit & NIHR Southampton Biomedical Research Centre, University of Southampton & University Hospital Southampton NHS Foundation Trust, Southampton, SO16 6YD, UK

[10 ]Centre for Human Evolution, Adaptation & Disease, Liggins Institute, University of Auckland, Auckland, 1142, New Zealand

Author notes

*Author for correspondence: neerja_karnani@ 123456sics.a-star.edu.sg

**Author for correspondence: joanna_holbrook@ 123456sics.a-star.edu.sg

^‡Authors contributed equally.

Article

DOI: 10.2217/epi.15.45

PMC ID: 4863876

PubMed ID: 26011824

SO-VID: 26660e03-172b-4d60-ab3b-0dd1e4ffd3cb

License:

This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 Unported License

HIF3A association with adiposity: the story begins before birth

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Abstract

Aim:

Material & methods:

Results & conclusion:

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Association of European University Presses (AEUP)

Most cited references 21

High density DNA methylation array with single CpG site resolution.

Epigenetic mechanisms that underpin metabolic and cardiovascular diseases.

Cohort profile: Growing Up in Singapore Towards healthy Outcomes (GUSTO) birth cohort study.

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