Macronutrient-specific effect of the genotype on lipid levels in response to 2 year weight-loss diets.

Leticia Goni, Dianjianyi Sun, Yoriko Heianza, Tiange Wang, Tao Huang, Marta Cuervo, J Alfredo Martínez, Xiaoyun Shang, George A Bray, Frank M Sacks, Lu Qi

Journal: Journal of lipid research 2019;59(1):155-161

PMID: 29089366

Abstract

Compelling evidence indicates that lipid metabolism is in partial control of the circadian system. In this context, it has been reported that the melatonin receptor 1B () genetic variant influences the dynamics of melatonin secretion, which is involved in the circadian system as a chronobiotic. The objective was to analyze whether the rs10830963 genetic variant was related to changes in lipid levels in response to dietary interventions with different macronutrient distribution in 722 overweight/obese subjects from the POUNDS Lost trial. We did not find a significant association between the genotype and changes in lipid metabolism. However, dietary fat intake significantly modified genetic effects on 2 year changes in total and LDL cholesterol ( interaction = 0.006 and 0.001, respectively). In the low-fat diet group, carriers of the sleep disruption G allele (minor allele) showed a greater reduction of total cholesterol (β ± SE = -5.78 ± 2.88 mg/dl, = 0.04) and LDL cholesterol (β ± SE = -7.19 ± 2.37 mg/dl, = 0.003). Conversely, in the high-fat diet group, subjects carrying the G allele evidenced a smaller decrease in total cholesterol (β ± SE = 5.81 ± 2.65 mg/dl, = 0.03) and LDL cholesterol (β ± SE = 5.23 ± 2.21 mg/dl, = 0.002). Subjects carrying the G allele of the circadian rhythm-related variant may present a bigger impact on total and LDL cholesterol when undertaking an energy-restricted low-fat diet.

Copyright © 2018 by the American Society for Biochemistry and Molecular Biology, Inc.

Address: Department of Nutrition, Food Sciences, and Physiology University of Navarra, Pamplona, Navarra, Spain.; Centre for Nutrition Research, Faculty of Pharmacy and Nutrition, University of Navarra, Pamplona, Navarra, Spain.; Department of Epidemiology, School of Public Health and Tropical Medicine, Tulane University, New Orleans, LA.; Epidemiology Domain, Saw Swee Hock School of Public Health and Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.; Department of Nutrition, Food Sciences, and Physiology University of Navarra, Pamplona, Navarra, Spain.; Centre for Nutrition Research, Faculty of Pharmacy and Nutrition, University of Navarra, Pamplona, Navarra, Spain.; Biomedical Research Centre Network in Physiopathology of Obesity and Nutrition (CIBERobn), Institute of Health Carlos III, Madrid, Spain.; Navarra Institute for Health Research, Pamplona, Navarra, Spain.; Children's Hospital New Orleans, New Orleans, LA.; Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, LA.; Departments of Nutrition Harvard T. H. Chan School of Public Health, Boston, MA.; Department of Epidemiology, School of Public Health and Tropical Medicine, Tulane University, New Orleans, LA [email protected].; Departments of Nutrition Harvard T. H. Chan School of Public Health, Boston, MA.; Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA.; Channing Laboratory, Brigham and Women's Hospital and Harvard Medical School, Boston, MA.
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