TY - JOUR
T1 - Objectively measured physical activity, sedentary behavior, and genetic predisposition to obesity in U.S. Hispanics/Latinos
T2 - Results from the hispanic community health study/study of Latinos (HCHS/SOL)
AU - Moon, Jee Young
AU - Wang, Tao
AU - Sofer, Tamar
AU - North, Kari E.
AU - Isasi, Carmen R.
AU - Cai, Jianwen
AU - Gellman, Marc D.
AU - Moncrieft, Ashley E.
AU - Sotres-Alvarez, Daniela
AU - Argos, Maria
AU - Kaplan, Robert C.
AU - Qi, Qibin
N1 - Funding Information:
Acknowledgments. The authors thank the staff and participants of HCHS/SOL for their important contributions. A complete list of HCHS/SOL staff and investigators can be found in Ann Epidemiol 2010;20:642–649 or at http:// sites.cscc.unc.edu/hchs/. Funding. The baseline examination of the HCHS/SOL was carried out as a collaborative study supported by the National Heart, Lung, and Blood Institute (NHLBI) to the University of North Carolina (contract N01-HC65233), the University of Miami (contract N01-HC65234), the Albert Einstein College of Medicine (contract N01-HC65235), Northwestern University (contract N01-HC65236), and San Diego State University (contract N01-HC65237). The following institutes/centers/offices contributed to the first funding period of the HCHS/SOL through a transfer of funds to the NHLBI: National Institute on Minority Health and Health Disparities, the National Institute of Deafness and Other Communications Disorders, the National Institute of Dental and Craniofacial Research, the National Institute of Diabetes and Digestive and Kidney Diseases, the National Institute of Neurological Disorders and Stroke, and the National Institutes of Health Office of Dietary Supplements. The Genetic Analysis Center at the University of Washington was supported by the NHLBI (contract HHSN268201300005C AM03) and the National Institute of Dental and Craniofacial Research (contract MOD03). Genotyping efforts were supported by the NHLBI (HSN 26220/20054C), the National Center for Advancing Translational Sciences (Clinical and Translational Science Award grant UL1TR000123), and the National Institute of Diabetes and Digestive and Kidney Diseases Diabetes Research Center (grant DK063491). Q.Q. is supported by a Scientist Development Award (K01HL129892) from the NHLBI. Duality of Interest. No conflicts of interest relevant to this article were reported. Author Contributions. J.-Y.M. and Q.Q. designed the study and wrote the manuscript. J.Y.-M. performed statistical analysis. T.W., K.E.N., C.R.I., J.C., M.D.G., A.E.M., M.A., and R.C.K. contributed to the discussion and edited and reviewed the manuscript. T.S. and D.S.-A. researched and reviewed data and edited and reviewed the manuscript. Q.Q. is the guarantor of this work and, as such, had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. Prior Presentation. Parts of this study were presented in abstract and poster form at the American Heart Association’s (AHA’s) EPI/LIFESTYLE Scientific Sessions, Portland, OR, 7–10 March 2017; CHARGE Investigator meeting, New York, NY, 23– 24 March 2017; and Best of AHA Specialty Conferences Invitation for Abstracts Scientific Session, Anaheim, CA, 11–15 November 2017.
Publisher Copyright:
© 2017 by the American Diabetes Association.
PY - 2017/12/1
Y1 - 2017/12/1
N2 - 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 BMIassociated single nucleotide polymorphisms (SNPs). Genetic association with BMI was stronger in individuals with lower MVPA (first tertile) versus higher MVPA (third tertile) (b = 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) (b = 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.
AB - 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 BMIassociated single nucleotide polymorphisms (SNPs). Genetic association with BMI was stronger in individuals with lower MVPA (first tertile) versus higher MVPA (third tertile) (b = 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) (b = 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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U2 - 10.2337/db17-0573
DO - 10.2337/db17-0573
M3 - Article
C2 - 28986399
AN - SCOPUS:85035311985
VL - 66
SP - 3001
EP - 3012
JO - Diabetes
JF - Diabetes
SN - 0012-1797
IS - 12
ER -
