Postnatal growth and DNA methylation are associated with differential gene expression of the TACSTD2 gene and childhood fat mass

Groom, Alexandra, Potter, Catherine, Swan, Daniel C., Fatemifar, Ghazaleh, Evans, David M., Ring, Susan M., Turcot, Valerie, Pearce, Mark S., Embleton, Nicholas D., Smith, George Davey, Mathers, John C. and Relton, Caroline L. (2012) Postnatal growth and DNA methylation are associated with differential gene expression of the TACSTD2 gene and childhood fat mass. Diabetes, 61 2: 391-400. doi:10.2337/db11-1039


Author Groom, Alexandra
Potter, Catherine
Swan, Daniel C.
Fatemifar, Ghazaleh
Evans, David M.
Ring, Susan M.
Turcot, Valerie
Pearce, Mark S.
Embleton, Nicholas D.
Smith, George Davey
Mathers, John C.
Relton, Caroline L.
Title Postnatal growth and DNA methylation are associated with differential gene expression of the TACSTD2 gene and childhood fat mass
Journal name Diabetes   Check publisher's open access policy
ISSN 0012-1797
1939-327X
Publication date 2012
Sub-type Article (original research)
DOI 10.2337/db11-1039
Open Access Status
Volume 61
Issue 2
Start page 391
End page 400
Total pages 10
Place of publication Alexandria, VA, United States
Publisher American Diabetes Association
Language eng
Abstract Rapid postnatal growth is associated with increased risk of childhood adiposity. The aim of this study was to establish whether this pathway is mediated by altered DNA methylation and gene expression. Two distinct cohorts, one preterm (n = 121) and one term born (n = 6,990), were studied. Exploratory analyses were performed using microarrays to identify differentially expressed genes in whole blood from children defined as "slow"(n = 10) compared with "rapid" (n = 10) postnatal (term to 12 weeks corrected age) growers. Methylation within the identified TACSTD2 gene was measured in both cohorts, and rs61779296 genotype was determined by Pyrosequencing or imputation and analyzed in relation to body composition at 9-15 years of age. In cohort 1, TACSTD2 expression was inversely correlated with methylation (P = 0.016), and both measures were associated with fat mass (expression, P = 0.049; methylation, P = 0.037). Although associated with gene expression (cohort 1, P = 0.008) and methylation (cohort 1, P = 2.98 × 10 -11; cohort 2, P = 3.43 × 10 -15), rs61779296 was not associated with postnatal growth or fat mass in either cohort following multiple regression analysis. Hence, the lack of association between fat mass and a methylation proxy SNP suggests that reverse causation or confounding may explain the initial association between fat mass and gene regulation. Noncausal methylation patterns may still be useful predictors of later adiposity.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: UQ Diamantina Institute Publications
 
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