Leticia Goni1,2, Dianjianyi Sun3, Yoriko Heianza3, Tiange Wang3, Tao Huang4, J Alfredo Martínez1,2,5,6, Xiaoyun Shang7, George A Bray8, Steven R Smith8, Frank M Sacks9, Lu Qi10,11,12,13. 1. Department of Nutrition, Food Sciences and Physiology, Faculty of Pharmacy and Nutrition, University of Navarra, Pamplona, Navarra, Spain. 2. Faculty of Pharmacy and Nutrition, Centre for Nutrition Research, University of Navarra, Pamplona, Navarra, Spain. 3. Department of Epidemiology, School of Public Health and Tropical Medicine, Tulane University, New Orleans, LA, 70112, USA. 4. Epidemiology Domain, Saw Swee Hock School of Public Health and Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore. 5. Biomedical Research Centre Network in Physiopathology of Obesity and Nutrition (CIBERobn), Institute of Health Carlos III, Madrid, Spain. 6. Navarra Institute for Health Research, Pamplona, Navarra, Spain. 7. Children's Hospital New Orleans, New Orleans, LA, USA. 8. Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, LA, USA. 9. Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA. 10. Department of Epidemiology, School of Public Health and Tropical Medicine, Tulane University, New Orleans, LA, 70112, USA. lqi1@tulane.edu. 11. Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA. lqi1@tulane.edu. 12. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA. lqi1@tulane.edu. 13. Channing Laboratory, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. lqi1@tulane.edu.
Abstract
PURPOSE: A common variant of the melatonin receptor 1B (MTNR1B) gene has been related to increased signaling of melatonin, a hormone previously associated with body fatness mainly through effects on energy metabolism. We examined whether the MTNR1B variant affects changes of body fatness and composition in response to a dietary weight loss intervention. METHODS: The MTNR1B rs10830963 variant was genotyped for 722 overweight and obese individuals, who were randomly assigned to one of four diets varying in macronutrient composition. Anthropometric and body composition measurements (DXA scan) were collected at baseline and at 6 and 24 months of follow-up. RESULTS: Statistically significant interactions were observed between the MTNR1B genotype and low-/high-fat diet on changes in weight, body mass index (BMI), waist circumference (WC) and total body fat (p interaction = 0.01, 0.02, 0.002 and 0.04, respectively), at 6 months of dietary intervention. In the low-fat diet group, increasing number of the sleep disruption-related G allele was significantly associated with a decrease in weight (p = 0.004), BMI (p = 0.005) and WC (p = 0.001). In the high-fat diet group, carrying the G allele was positively associated with changes in body fat (p = 0.03). At 2 years, the associations remained statistically significant for changes in body weight (p = 0.02), BMI (p = 0.02) and WC (p = 0.048) in the low-fat diet group, although the gene-diet interaction became less significant. CONCLUSIONS: The results suggest that carriers of the G allele of the MTNR1B rs10830963 may have a greater improvement in body adiposity and fat distribution when eating a low-fat diet.
RCT Entities:
PURPOSE: A common variant of the melatonin receptor 1B (MTNR1B) gene has been related to increased signaling of melatonin, a hormone previously associated with body fatness mainly through effects on energy metabolism. We examined whether the MTNR1B variant affects changes of body fatness and composition in response to a dietary weight loss intervention. METHODS: The MTNR1Brs10830963 variant was genotyped for 722 overweight and obese individuals, who were randomly assigned to one of four diets varying in macronutrient composition. Anthropometric and body composition measurements (DXA scan) were collected at baseline and at 6 and 24 months of follow-up. RESULTS: Statistically significant interactions were observed between the MTNR1B genotype and low-/high-fat diet on changes in weight, body mass index (BMI), waist circumference (WC) and total body fat (p interaction = 0.01, 0.02, 0.002 and 0.04, respectively), at 6 months of dietary intervention. In the low-fat diet group, increasing number of the sleep disruption-related G allele was significantly associated with a decrease in weight (p = 0.004), BMI (p = 0.005) and WC (p = 0.001). In the high-fat diet group, carrying the G allele was positively associated with changes in body fat (p = 0.03). At 2 years, the associations remained statistically significant for changes in body weight (p = 0.02), BMI (p = 0.02) and WC (p = 0.048) in the low-fat diet group, although the gene-diet interaction became less significant. CONCLUSIONS: The results suggest that carriers of the G allele of the MTNR1Brs10830963 may have a greater improvement in body adiposity and fat distribution when eating a low-fat diet.
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