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PPARγ Pro12Ala 与脂肪摄入量相互作用,影响基于地中海饮食的行为治疗中的肥胖和体重减轻。

PPARγ Pro12Ala interacts with fat intake for obesity and weight loss in a behavioural treatment based on the Mediterranean diet.

机构信息

Department of Physiology, Faculty of Biology, University of Murcia, Murcia, Spain.

出版信息

Mol Nutr Food Res. 2011 Dec;55(12):1771-9. doi: 10.1002/mnfr.201100437. Epub 2011 Nov 21.

Abstract

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.

摘要

范围

本研究的目的是检验过氧化物酶体增殖物激活受体 γ(PPARγ)的 Pro12Ala 多态性是否与胰岛素抵抗、肥胖和体重减轻有关,并分析西班牙超重/肥胖人群中脂肪摄入和 PPARγ 多态性之间的潜在相互作用。

材料和方法

我们招募了 1465 名参加基于地中海饮食的肥胖行为治疗计划的受试者,该计划包括以下内容:饮食治疗、体育活动、营养教育和行为技术。PPARγ2 Pro12Ala 基因型与血浆胰岛素浓度和稳态模型评估胰岛素抵抗之间存在显著相关性。Ala12 基因型受试者的胰岛素水平低于 Pro12Pro 基因型受试者。我们检测到 PPARγ Pro12Ala 多态性与 MUFA 之间的基因-饮食相互作用与 BMI 和体脂肪有关。此外,我们检测到 PPARγ Pro12Ala 多态性与脂肪摄入之间的相互作用与总体重减轻有关(p<0.001)。当总脂肪摄入量较高时,Ala12 携带者的总体重减轻百分比明显低于主要等位基因携带者(p=0.037)。

结论

数据与先前显示 Ala12 等位基因对胰岛素抵抗具有保护作用的结果一致,并复制了先前研究中检测到饮食 MUFA 与 PPARγ2 之间对 BMI 的相互作用。我们检测到 PPARγ Pro12Ala 与脂肪摄入之间的基因-饮食相互作用与体重减轻有关,这可能解释了先前不同研究之间的差异。

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