Consumption of dietary fiber and APOA5 genetic variants in metabolic syndrome: baseline data from the Korean Medicine Daejeon Citizen Cohort Study

IF 3.9 2区医学 Q2 NUTRITION & DIETETICS

Nutrition & Metabolism Pub Date : 2024-04-05 DOI:10.1186/s12986-024-00793-0

Jimi Kim, Younghwa Baek, Siwoo Lee

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Abstract

Consumption of dietary fiber has been suggested as an important aspect of a healthy diet to reduce the risk of metabolic syndrome (MetS), including cardiovascular disease. The role of fiber intake in MetS might differ by individual genetic susceptibility. APOA5 encodes a regulator of plasma triglyceride levels, which impacts the related mechanisms of MetS. This study investigated the association between dietary fiber and the risk of MetS, assessing their associations according to APOA5 genetic variants. A total of 1985 participants aged 30–55 years were included from a cross-sectional study based on the Korean Medicine Daejeon Citizen Cohort study at baseline (2017–2019). Dietary fiber intake was measured using a semiquantitative food frequency questionnaire. The APOA5 polymorphisms (rs2266788 A > G, rs662799 A > G, and rs651821 T > C) were genotyped using the Asia Precision Medicine Research Array. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (95% CIs). A higher consumption of dietary fiber was associated with a lower prevalence of MetS (P = 0.025). Among the components of MetS, an inverse association with dietary fiber was observed in increased waist circumference (OR, 95% CI = 0.60, 0.41–0.88, P for trend = 0.009) and elevated triglycerides (OR, 95% CI = 0.69, 0.50–0.96, P for trend = 0.012). Regarding the interaction with APOA5 genetic variants, a stronger association with dietary fiber intake was shown in G allele carriers of rs662799 than in A/A carriers (OR, 95% CI = 2.34, 1.59–3.44, P for interaction = 0.024) and in C allele carriers of rs651821 than in T/T carriers (OR, 95% CI = 2.35, 1.59–3.46, P for interaction = 0.027). The findings of this study suggest that the benefits of dietary fiber on the risk of MetS could be modified by genetic variants of the APOA5 gene, providing a more effective strategy for preventing MetS.

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代谢综合征中的膳食纤维摄入量和 APOA5 基因变异：韩国医学大田市民队列研究的基线数据

摄入膳食纤维被认为是健康饮食的一个重要方面，可降低代谢综合征（MetS）（包括心血管疾病）的风险。纤维摄入在代谢综合征中的作用可能因个体遗传易感性而异。APOA5 编码血浆甘油三酯水平的调节因子，它影响 MetS 的相关机制。本研究调查了膳食纤维与 MetS 风险之间的关联，并根据 APOA5 基因变异评估了两者之间的关联。在一项基于韩国医学大田市民队列研究的横断面研究（2017-2019 年）中，共纳入了 1985 名年龄在 30-55 岁之间的参与者。膳食纤维摄入量通过半定量食物频率问卷进行测量。使用亚洲精准医学研究阵列对 APOA5 多态性（rs2266788 A > G、rs662799 A > G 和 rs651821 T > C）进行了基因分型。采用逻辑回归法估算了几率比（OR）和 95% 置信区间（95% CI）。膳食纤维摄入量越高，MetS患病率越低（P = 0.025）。在 MetS 的组成成分中，观察到腰围增加（OR，95% CI = 0.60，0.41-0.88，趋势 P = 0.009）和甘油三酯升高（OR，95% CI = 0.69，0.50-0.96，趋势 P = 0.012）与膳食纤维呈负相关。关于与 APOA5 基因变异的交互作用，rs662799 的 G 等位基因携带者比 A/A 携带者（OR，95% CI = 2.34，1.59-3.44，交互作用的 P = 0.024）和 rs651821 的 C 等位基因携带者比 T/T 携带者（OR，95% CI = 2.35，1.59-3.46，交互作用的 P = 0.027）与膳食纤维摄入量有更强的关联。这项研究的结果表明，膳食纤维对 MetS 风险的益处可能会因 APOA5 基因的遗传变异而改变，从而为预防 MetS 提供更有效的策略。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Nutrition & Metabolism 医学-营养学

CiteScore

8.40

自引率

0.00%

发文量

审稿时长

4-8 weeks

期刊介绍： Nutrition & Metabolism publishes studies with a clear focus on nutrition and metabolism with applications ranging from nutrition needs, exercise physiology, clinical and population studies, as well as the underlying mechanisms in these aspects. The areas of interest for Nutrition & Metabolism encompass studies in molecular nutrition in the context of obesity, diabetes, lipedemias, metabolic syndrome and exercise physiology. Manuscripts related to molecular, cellular and human metabolism, nutrient sensing and nutrient–gene interactions are also in interest, as are submissions that have employed new and innovative strategies like metabolomics/lipidomics or other omic-based biomarkers to predict nutritional status and metabolic diseases. Key areas we wish to encourage submissions from include: -how diet and specific nutrients interact with genes, proteins or metabolites to influence metabolic phenotypes and disease outcomes; -the role of epigenetic factors and the microbiome in the pathogenesis of metabolic diseases and their influence on metabolic responses to diet and food components; -how diet and other environmental factors affect epigenetics and microbiota; the extent to which genetic and nongenetic factors modify personal metabolic responses to diet and food compositions and the mechanisms involved; -how specific biologic networks and nutrient sensing mechanisms attribute to metabolic variability.