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Genetic Variation in FADS Has Little Effect on the Association between Dietary PUFA Intake and Cardiovascular Disease.

机译:FaDs的遗传变异对膳食多不饱和脂肪酸摄入量与心血管疾病的关系影响不大。

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摘要

The unclear link between intake of polyunsaturated fatty acids (PUFAs) and risk of cardiovascular disease (CVD) could depend on genetic differences between individuals. Minor alleles of single-nucleotide polymorphisms (SNPs) in the ∆5 fatty acid desaturase (FADS) 1 gene were associated with lower blood concentrations of long-chain ω-3 (n-3) and ω-6 (n-6) PUFAs, indicating an associated loss of function effect. We examined whether the SNP rs174546 in FADS1 modifies the association between PUFA intakes and CVD risk. We included 24,032 participants (62% women, aged 44-74 y) from the Malmö Diet and Cancer cohort without prevalent CVD and diabetes. During a mean follow-up of 14 y, 2648 CVD cases were identified. Diet was assessed by a modified diet history method. Borderline interaction was observed between the α-linolenic acid (ALA) (18:3n-3)-to-linoleic acid (LA) (18:2n-6) intake ratio and FADS genotype on CVD incidence (P = 0.06). The ALA-to-LA intake ratio was inversely associated with CVD risk only among participants homozygous for the minor T-allele (HR for quintile 5 vs. quintile 1 = 0.72; 95% CI: 0.50, 1.04; P-trend = 0.049). When excluding participants reporting unstable food habits in the past (35%), the interaction between the ALA-to-LA intake ratio and FADS genotype on CVD incidence was strengthened and statistically significant (P = 0.04). Additionally, we observed a significant interaction between ALA and FADS genotype on ischemic stroke incidence (P = 0.03). ALA was inversely associated with ischemic stroke only among TT genotype carriers (HR for quintile 5 vs. quintile 1 = 0.50; 95% CI: 0.27, 0.94; P-trend = 0.02). In this large cohort, we found some weak, but not convincing, evidence of effect modification by genetic variation in FADS on the associations between PUFA intakes and CVD risk. For the 11% of the population homozygous for the minor T-allele of rs174546 that associates with lower ∆5 FADS activity, high ALA intake and ALA-to-LA intake ratio may be preferable in the prevention of CVD and ischemic stroke.
机译:多不饱和脂肪酸(PUFA)的摄入量与心血管疾病(CVD)风险之间的不清楚联系可能取决于个体之间的遗传差异。 Δ5脂肪酸去饱和酶(FADS)1基因中的单核苷酸多态性(SNP)的次要等位基因与长链ω-3(n-3)和ω-6(n-6)PUFA的较低血药浓度相关,表示相关的功能丧失效应。我们检查了FADS1中的SNP rs174546是否修饰了PUFA摄入量与CVD风险之间的关联。我们纳入了来自马尔默饮食与癌症研究队列的24,032名参与者(62%的女性,年龄在44-74岁之间),他们没有普遍的CVD和糖尿病。在平均随访14年中,发现2648例CVD病例。通过改良的饮食史方法评估饮食。观察到α-亚麻酸(ALA)(18:3n-3)与亚油酸(LA)(18:2n-6)的摄入比与FADS基因型对CVD发生率之间存在临界相互作用(P = 0.06)。仅在较小的T等位基因纯合的参与者中,ALA与LA的摄入比例与CVD风险呈负相关(五分位数5与五分位数1的HR = 0.72; 95%CI:0.50,1.04; P趋势= 0.049) 。当排除过去报告不稳定饮食习惯的参与者(35%)时,ALA / LA摄入比例与FADS基因型对CVD发生率之间的相互作用得到加强,并具有统计学意义(P = 0.04)。此外,我们观察到ALA和FADS基因型之间在缺血性卒中发生率之间存在显着相互作用(P = 0.03)。仅在TT基因型携带者中,ALA与缺血性卒中呈负相关(五分位数5与五分位数1的HR分别为0.50; 95%CI:0.27、0.94; P趋势= 0.02)。在这一大队列中,我们发现了一些微弱但不令人信服的证据,表明FADS的遗传变异对PUFA摄入量与CVD风险之间的相关性有影响。对于rs174546的较小T等位基因与Δ5FADS活性较低相关的纯合子群体的11%,在预防CVD和缺血性卒中中,较高的ALA摄入量和ALA / LA摄入比可能是优选的。

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