APOA2, dietary fat, and body mass index: replication of a gene-diet interaction in 3 independent populations.
APOA2, dietary fat, and body mass index: replication of a gene-diet interaction in 3 independent populations.
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DOI：
10.1001/archinternmed.2009.343
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发表时间：
2009-11-09
影响因子：
--
通讯作者：
Ordovas, Jose M.
中科院分区：
文献类型：
--
作者：
Corella, Dolores;Peloso, Gina;Arnett, Donna K.;Demissie, Serkalem;Cupples, L. Adrienne;Tucker, Katherine;Lai, Chao-Qiang;Parnell, Laurence D.;Coltell, Oscar;Lee, Yu-Chi;Ordovas, Jose M.
营养遗传学研究遗传变异对饮食和健康之间相互作用的作用，旨在提供更个性化的饮食建议。然而，复制率很低。我们的目的是在独立人群中研究功能性APOA 2多态性、食物摄入量和体重指数（BMI）之间的相互作用，以复制研究结果并提高其证据水平。在三个独立的人群中进行了横断面、随访（20年）和病例对照分析。我们分析了来自三个美国人群的3，462名受试者中APOA 2 - 265 T>C多态性和饱和脂肪（SATFAT）摄入量对BMI和肥胖的基因-饮食相互作用：Fragrance（1，454名白人），GOLDN（1，078名白人）和波士顿-波多黎各研究（930名加勒比裔西班牙人）。CC受试者的患病率范围为11- 15%。我们确定了所有三个人群中APOA 2 - 265 T>C和SATFAT对BMI的统计学显著相互作用。因此，CC和TT+TC受试者之间的BMI差异幅度因SATFAT而异。在所有研究中，高摄入量（>= 22 g/d）的基因型BMI平均增加6.2%（范围为4.3%-7.9%; P<0.05），但低摄入量的基因型BMI没有增加。同样，CC基因型与所有人群中肥胖患病率的升高显著相关，仅在高SATFAT分层中。荟萃分析估计CC与TT+TC受试者相比肥胖：OR=1.84，95%CI：1.38-2.47; P<0.0001，在高SATFAT分层中，但在低SATFAT分层中未检测到相关性（OR=0.81，95%CI：0.59-1.11;P=0.181）。这是第一次，基因-饮食相互作用影响BMI和肥胖已经强烈和一致地复制在三个独立的人群。
Nutrigenetics studies the role of genetic variation on interactions between diet and health aimed at providing more personalized dietary advice. However, replication has been very low. Our aim was to study the interaction between a functional APOA2 polymorphism, food intake and body mass index (BMI) in independent populations to replicate findings and to increase their evidence level. Cross-sectional, follow-up (20 years) and case-control analyses were undertaken in three independent populations. We analyzed gene-diet interactions between the APOA2 -265T>C polymorphism and saturated fat (SATFAT) intake on BMI and obesity in 3,462 subjects from three American populations: Framingham (1,454 Whites), GOLDN (1,078 Whites) and Boston-Puerto Rican studies (930 Hispanics of Caribbean origin). Prevalence of CC subjects ranged from 11-15%. We identified statistically significant interactions between the APOA2 -265T>C and SATFAT on BMI in all three populations. Thus, the magnitude of the difference in BMI between the CC and TT+TC subjects differed by SATFAT. A mean increase of 6.2% BMI (ranging from 4.3%-7.9%; P<0.05), was observed between genotypes with high (>=22g/d), but not with low SATFAT intake in all studies. Likewise, the CC genotype was significantly associated with higher obesity prevalence in all populations only in the high-SATFAT stratum. Meta-analysis estimations of obesity for CC compared with TT+TC subjects were: OR=1.84, 95%CI:1.38-2.47; P<0.0001 in the high-SATFAT stratum, but no association was detected in the low-SATFAT stratum (OR=0.81, 95%CI:0.59-1.11;P=0.181). For the first time, a gene-diet interaction influencing BMI and obesity has been strongly and consistently replicated in three independent populations.
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