Nutrition and Genomics Laboratory, Jean Mayer-USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA, USA.
J Nutr. 2011 Dec;141(12):2219-25. doi: 10.3945/jn.111.143826. Epub 2011 Nov 2.
Evidence that physical activity (PA) modulates the association between the fat mass and obesity-associated gene (FTO) and BMI is emerging; however, information about dietary factors modulating this association is scarce. We investigated whether fat and carbohydrate intake modified the association of FTO gene variation with BMI in two populations, including participants in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) study (n = 1069) and in the Boston Puerto Rican Health (BPRHS) study (n = 1094). We assessed energy, nutrient intake, and PA using validated questionnaires. Genetic variability at the FTO locus was characterized by polymorphisms rs9939609 (in the GOLDN) and rs1121980 (in the GOLDN and BPRHS). We found significant interactions between PA and FTO on BMI in the GOLDN but not in the BPRHS. We found a significant interaction between SFA intake and FTO on BMI, which was stronger than that of total fat and was present in both populations (P-interaction = 0.007 in the GOLDN and P-interaction = 0.014 in BPRHS for categorical; and P-interaction = 0.028 in the GOLDN and P-interaction = 0.041 in BPRHS for continuous SFA). Thus, homozygous participants for the FTO-risk allele had a higher mean BMI than the other genotypes only when they had a high-SFA intake (above the population mean: 29.7 ± 0.7 vs. 28.1 ± 0.5 kg/m²; P = 0.037 in the GOLDN and 33.6. ± 0.8 vs. 31.2 ± 0.4 kg/m²; P = 0.006 in BPRHS). No associations with BMI were found at lower SFA intakes. We found no significant interactions with carbohydrate intake. In conclusion, SFA intake modulates the association between FTO and BMI in American populations.
有证据表明，体力活动（PA）调节肥胖相关基因（FTO）和体重指数（BMI）之间的关联；然而，关于调节这种关联的饮食因素的信息却很少。我们研究了脂肪和碳水化合物的摄入量是否会改变 FTO 基因变异与两个人群的 BMI 之间的关联，包括遗传降低血脂药物和饮食网络（GOLDN）研究（n=1069）和波士顿波多黎各健康（BPRHS）研究（n=1094）的参与者。我们使用经过验证的问卷评估了能量、营养素摄入和 PA。FTO 基因座的遗传变异性由多态性 rs9939609（在 GOLDN 中）和 rs1121980（在 GOLDN 和 BPRHS 中）来描述。我们发现 PA 和 FTO 对 BMI 的相互作用在 GOLDN 中显著，但在 BPRHS 中不显著。我们发现 SFA 摄入量与 FTO 对 BMI 的相互作用，其强度强于总脂肪，并且在两个群体中都存在（GOLDN 中分类的 P 交互作用=0.007，BPRHS 中 P 交互作用=0.014；GOLDN 中连续 SFA 的 P 交互作用=0.028，BPRHS 中 P 交互作用=0.041）。因此，FTO 风险等位基因的纯合子参与者只有在 SFA 摄入量较高（高于人群平均值：29.7±0.7 与 28.1±0.5 kg/m²；P=0.037 在 GOLDN 中，33.6.±0.8 与 31.2±0.4 kg/m²；P=0.006 在 BPRHS 中）时，其 BMI 平均值高于其他基因型。在 SFA 摄入量较低时，与 BMI 没有关联。我们没有发现与碳水化合物摄入有关的显著相互作用。总之，SFA 摄入量调节了美国人群中 FTO 与 BMI 之间的关联。
