Abstract
OBJECTIVE: Changes in fat mass depend on adipogenesis and angiogenesis, mechanisms regulated by the inhibitor of differentiation-3 (ID3). Id3 knockout mice showed attenuated increases in BMI and visceral fat mass. We hypothesized that the ID3 missense variant (rs11574-A) would lead to an attenuated increase over time in fat mass, BMI, waist circumference (WC), and waist-hip ratio (WHR) in humans.
METHODS: The genotyped study populations included the Obesity Research Group - Genetics (ORGGEN) cohort, a cohort of men with obesity (N = 716) and of randomly selected men (N = 826) from the Danish draft register who were examined at mean ages of 20 and 46 years, and the Inter99 (N = 6,116) and Health2006 (N = 2,761) cohorts, two population-based samples of middle-aged people, followed up after 5 years.
RESULTS: In meta-analyses of all data, no association was found between rs11574-A and changes in BMI, WC, WHR, or fat mass. We found an association between rs11574-A and cross-sectional BMI (N = 10,359, β: -0.16 kg/m2per allele, 95% CI: -0.30 to -0.01, P = 0.033) and fat mass (N = 4,188, β: -0.52 kg/m2per allele, 95% CI: -1.03 to -0.01, P = 0.046).
CONCLUSIONS: No consistent impact of the genetic variant on changes in fat mass, BMI, or fat distribution was found in three Danish cohorts.
Originalsprog | Engelsk |
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Tidsskrift | Obesity |
Vol/bind | 26 |
Udgave nummer | 4 |
Sider (fra-til) | 747-754 |
Antal sider | 8 |
ISSN | 1930-7381 |
DOI | |
Status | Udgivet - 2018 |