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首页> 外文期刊>The Journal of Nutrition: Official Organ of the American Institute of Nutrition >APOA5 Gene Variation Interacts with Dietary Fat Intake to Modulate Obesity and Circulating Triglycerides in a Mediterranean Population
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APOA5 Gene Variation Interacts with Dietary Fat Intake to Modulate Obesity and Circulating Triglycerides in a Mediterranean Population

机译：APOA5基因变异与膳食脂肪摄入相互作用，以调节肥胖症和地中海人口中循环甘油三酸酯。

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APOA5 is one of the strongest regulators of plasma TG concentrations; nevertheless, its mechanisms of action are poorly characterized. Genetic variability at the APOA5 locus has also been associated with increased cardiovascular disease risk; however, this predisposition could be attenuated in the context of a prudent diet as traditionally consumed in the Mediterranean countries. We have investigated the interaction between a single nucleotide polymorphism (SNP) at the APOA5 gene (-1131T C) and dietary fat that may modulate TG-rich lipoprotein concentrations and anthropometric measures in overweight and obese participants. We recruited 1465 participants from a Spanish population (20–65 y old; BMI 25–40 kg/m2) attending outpatient obesity clinics. Consistent with previous reports, we found an association between the APOA5-1131T C SNP and TG-rich lipoprotein concentrations that were higher in carriers of the minor allele than in noncarriers (P 0.001). Moreover, we found a significant genotype-dietary fat interaction for obesity traits. Participants homozygous for the ?1131T major allele had a positive association between fat intake and obesity, whereas in those carrying the APOA5?1131C minor allele, higher fat intakes were not associated with higher BMI. Likewise, we found genotype-dietary fat interactions for TG-rich lipoproteins (P 0.001). In conclusion, we have replicated previous gene-diet interactions between APOA5 -1131T C SNP and fat intake for obesity traits and detected a novel interaction for TG-rich lipoprotein concentrations. Our data support the hypothesis that the minor C-allele may protect those consuming a high-fat diet from obesity and elevated concentrations of TG-rich lipoproteins.
机译：APOA5是血浆TG浓度最强的调节剂之一。但是，其作用机理还很差。 APOA5基因座的遗传变异性也与心血管疾病风险增加有关。但是，在地中海国家传统上饮食谨慎的情况下，这种倾向可能会减弱。我们研究了APOA5基因（-1131T> C）上的单核苷酸多态性（SNP）与膳食脂肪之间的相互作用，该脂肪可能调节超重和肥胖参与者中富含TG的脂蛋白浓度和人体测量学。我们从西班牙人口（20-65岁; BMI 25-40 kg / m2）的门诊肥胖诊所招募了1465名参与者。与以前的报告一致，我们发现APOA5-1131T> C SNP与富含TG的脂蛋白浓度之间的相关性，次要等位基因的携带者高于非携带者（P <0.001）。此外，我们发现肥胖性状的显着基因型-饮食脂肪相互作用。 ≥1131T主要等位基因纯合的参与者在脂肪摄入和肥胖之间呈正相关，而那些携带APOA5≥1131C较小等位基因的参与者中，较高的脂肪摄入与较高的BMI不相关。同样，我们发现富含TG的脂蛋白的基因型-饮食脂肪相互作用（P <0.001）。总之，我们已经复制了APOA5 -1131T> C SNP与肥胖特征的脂肪摄入之间的先前基因-饮食相互作用，并检测了富含TG的脂蛋白浓度的新型相互作用。我们的数据支持以下假设：次要C等位基因可以保护那些食用高脂饮食的人免受肥胖和富含TG的脂蛋白浓度的影响。

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