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. 2017 Dec;66(12):3001-3012.
doi: 10.2337/db17-0573. Epub 2017 Oct 6.

Objectively Measured Physical Activity, Sedentary Behavior, and Genetic Predisposition to Obesity in U.S. Hispanics/Latinos: Results From the Hispanic Community Health Study/Study of Latinos (HCHS/SOL)

Affiliations

Objectively Measured Physical Activity, Sedentary Behavior, and Genetic Predisposition to Obesity in U.S. Hispanics/Latinos: Results From the Hispanic Community Health Study/Study of Latinos (HCHS/SOL)

Jee-Young Moon et al. Diabetes. 2017 Dec.

Abstract

Studies using self-reported data suggest a gene-physical activity interaction on obesity, yet the influence of sedentary behavior, distinct from a lack of physical activity, on genetic associations with obesity remains unclear. We analyzed interactions of accelerometer-measured moderate to vigorous physical activity (MVPA) and time spent sedentary with genetic variants on obesity among 9,645 U.S. Hispanics/Latinos. An overall genetic risk score (GRS), a central nervous system (CNS)-related GRS, and a non-CNS-related GRS were calculated based on 97 BMI-associated single nucleotide polymorphisms (SNPs). Genetic association with BMI was stronger in individuals with lower MVPA (first tertile) versus higher MVPA (third tertile) (β = 0.78 kg/m2 [SE, 0.10 kg/m2] vs. 0.39 kg/m2 [0.09 kg/m2] per SD increment of GRS; Pinteraction = 0.005), and in those with more time spent sedentary (third tertile) versus less time spent sedentary (first tertile) (β = 0.73 kg/m2 [SE, 0.10 kg/m2] vs. 0.44 kg/m2 [0.09 kg/m2]; Pinteraction = 0.006). Similar significant interaction patterns were observed for obesity risk, body fat mass, fat percentage, fat mass index, and waist circumference, but not for fat-free mass. The CNS-related GRS, but not the non-CNS-related GRS, showed significant interactions with MVPA and sedentary behavior, with effects on BMI and other adiposity traits. Our data suggest that both increasing physical activity and reducing sedentary behavior may attenuate genetic associations with obesity, although the independence of these interaction effects needs to be investigated further.

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Figures

Figure 1
Figure 1
Associations of total physical activity, MVPA, and sedentary behavior with BMI and other adiposity traits according to tertiles (T) of overall GRS. Data are effect sizes per 100 counts/min increments of total physical activity, per 10-min increment of MVPA, and per 1-h increment of sedentary time for BMI, fat mass, fat percentage, fat mass index, fat-free mass, and waist circumference, adjusting for sampling weight, field center, age, sex, the five principal components for population structure, education, income, employment, smoking, alcohol use, energy intake, and AHEI as fixed effects, and genetic relatedness, household, and block groups as random effects. Diff, difference; Pint, Pinteraction.
Figure 2
Figure 2
Interactions of total physical activity, MVPA, and sedentary behavior with the overall GRS for obesity risk. Data are odds ratios (95% CIs) for obesity risk (BMI ≥30 vs. <30 kg/m2) per 1-SD increment of the overall GRS according to tertiles (T) of total physical activity, MVPA, and sedentary behavior, adjusting for sampling weight, field center, age, sex, five principal components for population structure, education, income, employment, smoking, alcohol use, energy intake, and AHEI as fixed effects, and genetic relatedness, household, and block groups as random effects.
Figure 3
Figure 3
BMI among individuals grouped by tertiles (T) of the overall GRS and tertiles of total physical activity (A), MVPA (B), and sedentary time (C). Solid lines indicate the estimated BMI levels across tertiles of total physical activity, MVPA, or sedentary behavior by individuals with low (GRS T1), medium (GRS T2) and high (GRS T3) genetic risk for obesity. Dashed lines indicate the projected BMI levels among individuals with medium (GRS T2) and high (GRS T3) genetic risk for obesity, assuming no gene–environment interactions. The dashed lines are parallel to the black solid line of the estimated BMI levels among individuals with low genetic risk (GRS T1) for obesity. Values are means (95% CIs), adjusted for sampling weight, field center, age, sex, five principal components for population structure, education, income, employment, smoking, alcohol use, energy intake, and AHEI as fixed effects, and genetic relatedness, household, and block groups as random effects.
Figure 4
Figure 4
Interactions of MVPA and sedentary behavior with the CNS-related GRS and the non-CNS-related GRS on BMI, body composition measures, and waist circumference. Data are effect sizes (95% CIs) per 1-SD increment of the CNS-related GRS and the non-CNS-related GRS on BMI, fat mass, fat percentage, fat mass index, fat-free mass, and waist circumference, adjusting for sampling weight, field center, age, sex, five principal components for population structure, education, income, employment, smoking, alcohol use, energy intake, and AHEI as fixed effects, and genetic relatedness, household, and block groups as random effects. Diff, difference; Pint, Pinteraction; T, tertile.

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