Abstract:
AIM:We tested the hypothesis that the obesity-associated FTO SNP rs9939609 would be associated with clinically significant weight gain (≥ 5% of initial body weight) in the first year of university; a time identified as high risk for weight gain. METHODS:We collected anthropometric data from university students (n = 1,411, mean age: 22.4 ± 2.5 years, 49.1% male) at the beginning and end of the academic year. DNA was analysed for FTO rs9939609. Associations of FTO genotype with BMI at baseline were analysed using ANCOVA, and with risk of 5% weight gain over follow-up with logistic regression; both analyses adjusting for age and sex. The alpha level was reduced to 0.0125 to account for multiple testing. RESULTS:Using an additive model, FTO status was not associated with higher BMI at baseline (22.2 vs. 21.9 kg/m2, p = 0.059). Dropout was high but unrelated to genotype. Among the 310 (21.9%) completing follow-up, those with AT genotypes had twice the odds of ≥ 5% weight gain compared with TTs (OR = 2.05, 95% CI = 1.05-4.01, p = 0.036), but this was no longer significant after Bonferroni correction. There was a trend for AA carriers for ≥ 5% weight gain compared with TT carriers (p = 0.089), but sample size was small. CONCLUSION:This study provides nominal evidence for the genetic susceptibility hypothesis, but findings need to be replicated.
journal_name
Obes Factsjournal_title
Obesity factsauthors
Meisel SF,Beeken RJ,van Jaarsveld CH,Wardle Jdoi
10.1159/000434733subject
Has Abstractpub_date
2015-01-01 00:00:00pages
243-51issue
4eissn
1662-4025issn
1662-4033pii
000434733journal_volume
8pub_type
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