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PPAR γ Pro12Ala interacts with fat intake for obesity and weight loss in a behavioural treatment based on the Mediterranean diet
Author(s) -
Garaulet Marta,
Smith Caren E,
HernándezGonzález Teresa,
Lee YuChi,
Ordovás Jose M.
Publication year - 2011
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201100437
Subject(s) - insulin resistance , endocrinology , medicine , genotype , obesity , overweight , weight loss , peroxisome proliferator activated receptor , allele , polymorphism (computer science) , mediterranean diet , biology , insulin , population , receptor , genetics , gene , environmental health
Scope: The goal of this study was to examine whether the Pro12Ala polymorphism of peroxisome proliferator‐activated receptor γ ( PPAR γ) is associated with insulin resistance, obesity and weight loss and to analyze potential interactions between fat intake and PPAR γ 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 PPAR γ2 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 PPAR γ Pro12Ala polymorphism and MUFA for BMI and body fat. Furthermore, we detected an interaction between the PPAR γ 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 PPAR γ2 for BMI. Our detection of a gene–diet interaction between PPAR γ Pro12Ala and fat intake for weight loss may explain previous discrepancies among different studies.

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