PPARγ Pro12Ala interacts with fat intake for obesity and weight loss in a behavioural treatment based on the Mediterranean diet
Article first published online: 21 NOV 2011
Copyright © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
Molecular Nutrition & Food Research
Volume 55, Issue 12, pages 1771–1779, December 2011
How to Cite
Garaulet, M., Smith, C. E., Hernández-González, T., Lee, Y.-C. and Ordovás, J. M. (2011), PPARγ Pro12Ala interacts with fat intake for obesity and weight loss in a behavioural treatment based on the Mediterranean diet. Mol. Nutr. Food Res., 55: 1771–1779. doi: 10.1002/mnfr.201100437
- Issue published online: 2 DEC 2011
- Article first published online: 21 NOV 2011
- Manuscript Accepted: 3 SEP 2011
- Manuscript Revised: 20 AUG 2011
- Manuscript Received: 30 JUN 2011
- Government of Education, Science and Research of Murcia. Grant Number: BIO/FFA 07/01-0004
- The Spanish Government of Science and Innovation. Grant Number: AGL2008-01655/ALI
- National Heart, Lung, and Blood Institute. Grant Number: HL-54776
- National Institute of Diabetes and Digestive and Kidney Diseases. Grant Number: DK075030
- US Department of Agriculture Research. Grant Numbers: 53-K06-5-10, 58-1950-9-001
- Fat intake;
- Gene–environment interaction;
- Peroxisome proliferator-activated receptor γ
Scope: The goal of this study was to examine whether the Pro12Ala polymorphism of peroxisome proliferator-activated receptor γ (PPARγ) is associated with insulin resistance, obesity and weight loss and to analyze potential interactions between fat intake and PPARγ polymorphism in a Spanish overweight/obese population.
Materials and methods: We recruited 1465 subjects enrolled in a behavioural treatment program for obesity based on a Mediterranean diet, which included the following: dietary treatment, physical activity, nutritional education and behavioral techniques. A significant association was found between PPARγ2 Pro12Ala genotype and plasma insulin concentration and homeostasis model assessment insulin resistance. Subjects with the Ala12 genotype had lower insulin levels than those with the Pro12Pro genotype. We detected a gene–diet interaction between the PPARγ Pro12Ala polymorphism and MUFA for BMI and body fat. Furthermore, we detected an interaction between the PPARγ Pro12Ala polymorphism and fat intake for total weight loss (p<0.001). When total fat intake was high, Ala12-carriers exhibited a significantly lower percentage of total weight loss than major-allele-carriers (p=0.037).
Conclusion: Data are consistent with previous results showing a protective role for the Ala12 allele against insulin resistance, and replicate an earlier study that detected an interaction between dietary MUFA and PPARγ2 for BMI. Our detection of a gene–diet interaction between PPARγ Pro12Ala and fat intake for weight loss may explain previous discrepancies among different studies.