APOA5 gene variation modulates the effects of dietary fat intake on body mass index and obesity risk in the Framingham Heart Study
APOA5 gene variation modulates the effects of dietary fat intake on body mass index and obesity risk in the Framingham Heart Study
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DOI：
10.1007/s00109-006-0147-0
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发表时间：
2007-02-01
影响因子：
4.7
通讯作者：
Ordovas, Jose M.
中科院分区：
文献类型：
--
作者：
Corella, Dolores;Lai, Chao-Qiang;Ordovas, Jose M.
饮食是一个重要的环境因素，与我们的基因相互作用，以调节发展血脂紊乱的可能性，从而，心血管疾病的风险。我们的目的是在一项大规模人群研究中研究饮食摄入是否调节APOA 5基因变异和体重之间的关联。具体来说，我们研究了APOA 5 - 1131 T> C和56 C> G（S19 W）多态性与常量营养素摄入（总脂肪，碳水化合物和蛋白质）之间的相互作用，以及它们与参与Fragile Offspring研究的1，073名男性和1，207名女性的体重指数（BMI）和肥胖风险的关系。我们发现APOA 5 - 1131 T> C单核苷酸多态性（SNP;但不是56 C> G）和BMI的总脂肪摄入量之间存在一致且统计学显著的相互作用。这种相互作用具有剂量依赖性，未检测到性别的统计学显著异质性。在-1131T主要等位基因纯合子的受试者中，BMI随着总脂肪摄入量的增加而增加。相反，这种增加不存在于-1131C次要等位基因的携带者中。因此，我们发现在确定肥胖和超重风险方面存在显着的相互作用。载脂蛋白A5 - 1131 C微小等位基因携带者肥胖风险较低（OR，0.61，95%; CI，0.39 - 0.98; P= 0.032）和超重风险（OR，0.63，95%; CI，0.41-0.96; P= 0.031）与高脂肪摄入组TT受试者相比（>= 30%的能量），但当脂肪摄入量较低时则不存在（肥胖和超重的OR分别为1.16，95%; CI，0.77-1.74; P= 0.47和OR=1.15，95%; CI，0.77-1.71; P= 0.48）。当分析特定脂肪酸组时，单不饱和脂肪酸对这些相互作用显示出最高的统计学显著性。总之，APOA 5 - 1131 T> C SNP存在于大约13%的该人群中，调节脂肪摄入对男性和女性BMI和肥胖风险的影响。
Diet is an important environmental factor interacting with our genes to modulate the likelihood of developing lipid disorders and, consequently, cardiovascular disease risk. Our objective was to study whether dietary intake modulates the association between APOA5 gene variation and body weight in a large population-based study. Specifically, we have examined the interaction between the APOA5-1131T > C and 56C > G (S19W) polymorphisms and the macronutrient intake ( total fat, carbohydrate, and protein) in their relation to the body mass index (BMI) and obesity risk in 1,073 men and 1,207 women participating in the Framingham Offspring Study. We found a consistent and statistically significant interaction between the APOA5-1131T > C single-nucleotide polymorphism ( SNP; but not the 56C > G) and total fat intake for BMI. This interaction was dose-dependent, and no statistically significant heterogeneity by gender was detected. In subjects homozygous for the - 1131T major allele, BMI increased as total fat intake increased. Conversely, this increase was not present in carriers of the - 1131C minor allele. Accordingly, we found significant interactions in determining obesity and overweight risks. APOA5-1131C minor allele carriers had a lower obesity risk ( OR, 0.61, 95%; CI, 0.39 - 0.98; P= 0.032) and overweight risk ( OR, 0.63, 95%; CI, 0.41-0.96; P= 0.031) compared with TT subjects in the high fat intake group (>= 30% of energy) but not when fat intake was low ( OR, 1.16, 95%; CI, 0.77-1.74; P= 0.47 and OR=1.15, 95%; CI, 0.77-1.71; P= 0.48) for obesity and overweight, respectively). When specific fatty acid groups were analyzed, monounsaturated fatty acids showed the highest statistical significance for these interactions. In conclusion, the APOA5-1131T > C SNP, which is present in approximately 13% of this population, modulates the effect of fat intake on BMI and obesity risk in both men and women.