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TACSTD2 Gene May Affect Postnatal Growth, Fat Mass

Last Updated: January 06, 2012.

Altered expression of the TACSTD2 gene may be associated with postnatal growth and childhood fat mass, although lack of association between postnatal growth or fat mass and a methylation proxy SNP in this gene may indicate confounding, according to a study published online Dec. 21 in Diabetes.

FRIDAY, Jan. 6 (HealthDay News) -- Altered expression of the TACSTD2 gene may be associated with postnatal growth and childhood fat mass, although lack of association between postnatal growth or fat mass and a methylation proxy SNP in this gene may indicate confounding, according to a study published online Dec. 21 in Diabetes.

Alexandra Groom, M.D., of Newcastle University in the United Kingdom, and colleagues evaluated whether postnatal growth is associated with variability in gene expression and whether genetic variability is associated with later body composition in children. Differentially expressed genes were identified between a group of 121 preterm-born children, followed up at a mean age of 11 years, and 6,990 term-born children followed up at mean ages of 9 and 15 years. Methylation and expression of the TACSTD2 gene were evaluated. A single nucleotide polymorphism (SNP) located in the promoter region of the TACSTD2 gene that correlated highly with local DNA methylation levels was used as a proxy to infer causality between methylation and childhood fat mass.

The researchers found that postnatal growth was associated with differential gene expression in infants born preterm. Specifically, TACSTD2 gene expression was associated with 11-year fat mass, and promoter methylation was associated with postnatal growth and 11-year fat mass. These effects were not observed for the larger term-born cohort. The methylation proxy SNP was not associated with fat mass or postnatal growth in either group.

"In summary, postnatal growth and childhood fat mass were associated with altered TACSTD2 gene expression and promoter methylation. However, the lack of association between fat mass and a methylation proxy SNP in this gene suggests that confounding might explain the observed associations," the authors write.

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