Introduction: The effect of various types of dietary fat on cardiometabolic health continues to be debated, due in part to the high heterogeneity of results following clinical trials investigating the effects of saturated (SFA) and unsaturated fat intake. This variability may be due to genetic differences. Individuals with obesity are at an increased risk for adverse cardiometabolic health and dyslipidemia, and often present with the combined phenotype of elevated triglyceride (TG) and decreased high-density lipoprotein (HDL) cholesterol concentrations. Studying genetic variants relevant to lipid and lipoprotein metabolism can elucidate the mechanisms by which diet might interact with genotype to influence these phenotypes. The objective of this study was to determine relationships of genetic variation, dietary fat intake, and blood lipid concentrations in adults with overweight and obesity. Methods: Genomic DNA, blood lipid concentrations (HDL and TG), and 7-day diet records were obtained from 101 adults (25–45 years of age) with overweight or obesity. Resting energy expenditure (REE) was measured using indirect calorimetry and used to determine implausible intakes using a modified Goldberg method (kilocalories/REE). Genetic variants included 23 single-nucleotide polymorphisms (SNPs) from 15 genes in lipid metabolism pathways. Variants were analyzed with dietary fat intake (total fat, SFA, monounsaturated fat [MUFA], and polyunsaturated fat [PUFA]) via regression analyses. All models were adjusted for age, sex, ancestry, visceral adipose tissue mass, and total kilocalorie intake. The Bonferroni correction was applied for multiple comparisons. Results: Two interactions were detected for TG concentrations. Five gene-diet interactions were associated with HDL concentrations. There was a significant interaction detected between the rs5882 variant of cholesterol-esterase transfer protein (CETP) and MUFA intake to associate with TG concentrations (interaction p = 0.004, R2 = 0.306). Among carriers of the CETP-rs5882 major allele (G), TG concentrations were significantly lower in individuals consuming more than the median MUFA intake (31 g/day) than in those with an intake below the median. Total dietary fat intake interacted with the rs13702 polymorphism of lipoprotein lipase (LPL) to associate with HDL concentrations (interaction p = 0.041, R2 = 0.419), by which individuals with the risk allele (G) had significantly higher HDL concentrations when consuming a higher-fat diet (>92 g/day) than those with a lower-fat diet (56 ± 3 vs. 46 ± 2 mg/dL, p = 0.033). Conclusions: Interactions between dietary intake and genes in lipid metabolism pathways were found to be associated with blood lipid concentrations in adults with overweight and obesity. Fatty acid intake may not modulate blood lipid concentrations uniformly across all individuals. Additional research is needed to determine the biological causes of individual variability in response to dietary intake. Understanding the influence of nutrigenetic interactions on dyslipidemia can aid in the development and implementation of personalized dietary strategies to improve health.

中文翻译：

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脂质代谢途径的遗传变异与饮食相互作用以影响超重和肥胖成人的血脂浓度

介绍：各种膳食脂肪对心脏代谢健康的影响一直存在争议，部分原因是在研究饱和 (SFA) 和不饱和脂肪摄入量影响的临床试验后结果存在高度异质性。这种变异可能是由于遗传差异造成的。肥胖个体患心脏代谢不良和血脂异常的风险增加，并且经常表现为甘油三酯 (TG) 升高和高密度脂蛋白 (HDL) 胆固醇浓度降低的组合表型。研究与脂质和脂蛋白代谢相关的遗传变异可以阐明饮食可能与基因型相互作用以影响这些表型的机制。本研究的目的是确定遗传变异、膳食脂肪摄入量、超重和肥胖成人的血脂浓度。方法：从 101 名超重或肥胖的成年人（25-45 岁）获得基因组 DNA、血脂浓度（HDL 和 TG）和 7 天饮食记录。使用间接量热法测量静息能量消耗 (REE)，并使用改进的 Goldberg 方法（千卡/REE）确定不合理的摄入量。遗传变异包括来自脂质代谢途径中 15 个基因的 23 个单核苷酸多态性 (SNP)。通过回归分析，对饮食脂肪摄入量（总脂肪、SFA、单不饱和脂肪 [MUFA] 和多不饱和脂肪 [PUFA]）进行了分析。所有模型都针对年龄、性别、血统、内脏脂肪组织质量和总卡路里摄入量进行了调整。Bonferroni 校正应用于多重比较。结果：检测到 TG 浓度的两种相互作用。五种基因-饮食相互作用与 HDL 浓度有关。在胆固醇酯酶转移蛋白 (CETP) 的 rs5882 变体和 MUFA 摄入量之间检测到显着的相互作用，与 TG 浓度相关（相互作用 p = 0.004，R2 = 0.306）。在 CETP-rs5882 主要等位基因 (G) 的携带者中，摄入量超过中位数 MUFA 摄入量（31 克/天）的个体的 TG 浓度显着低于摄入量低于中位数的个体。总膳食脂肪摄入量与脂蛋白脂肪酶 (LPL) 的 rs13702 多态性相互作用，从而与 HDL 浓度相关联（相互作用 p = 0.041，R2 = 0.419），由此具有风险等位基因 (G) 的个体在摄入更高浓度的脂肪时具有显着更高的 HDL 浓度- 脂肪饮食（> 92 克/天）比那些低脂肪饮食的人（56 ± 3 对 46 ± 2 毫克/分升，p = 0.033）。结论：发现膳食摄入量与脂质代谢途径基因之间的相互作用与超重和肥胖成人的血脂浓度相关。脂肪酸摄入量可能不会在所有个体中均匀地调节血脂浓度。需要更多的研究来确定个体对饮食摄入量的差异的生物学原因。了解营养遗传相互作用对血脂异常的影响有助于制定和实施个性化饮食策略以改善健康。研究发现，膳食摄入量与脂质代谢途径基因之间的相互作用与超重和肥胖成人的血脂浓度有关。脂肪酸摄入量可能不会在所有个体中均匀地调节血脂浓度。需要更多的研究来确定个体对饮食摄入量的差异的生物学原因。了解营养遗传相互作用对血脂异常的影响有助于制定和实施个性化饮食策略以改善健康。研究发现，膳食摄入量与脂质代谢途径基因之间的相互作用与超重和肥胖成人的血脂浓度有关。脂肪酸摄入量可能不会在所有个体中均匀地调节血脂浓度。需要更多的研究来确定个体对饮食摄入量的差异的生物学原因。了解营养遗传相互作用对血脂异常的影响有助于制定和实施个性化饮食策略以改善健康。