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韩国成年人中低碳水化合物饮食及宏量营养素摄入量与肠道微生物群的关联,以及它们与血脂异常的相互作用。

Association between a low-carbohydrate diet and macronutrient intake with the gut microbiome, and their interaction with dyslipidemia among Korean adults.

作者信息

Chung Sangwon, Shin Ji-Hee, Kim Jung-Ha, Kim Ki Bae, Nam Young-Do, Lim Mi Young

机构信息

Precision Nutrition Research Group, Korea Food Research Institute, 245, Nongsaengmyeong-ro, Wanju-gun, Jeollabuk-do, 55365, Republic of Korea.

Department of Family Medicine, Chung-Ang University Hospital, Chung-Ang University College of Medicine, Seoul, Republic of Korea.

出版信息

Nutr J. 2025 Jul 31;24(1):121. doi: 10.1186/s12937-025-01188-4.

DOI:10.1186/s12937-025-01188-4
PMID:40745546
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12315341/
Abstract

BACKGROUND

The prevalence of dyslipidemia has increased in recent years; however, it remains a modifiable condition through diet and gut microbiome modulation. Yet, evidence from population-based studies remains limited. This study aimed to investigate the relationships among a low-carbohydrate diet (LCD), macronutrient intake, and the gut microbiome, and to evaluate their interaction effects on dyslipidemia in a Korean population.

METHODS

Data were drawn from two population-based studies: the Korean Microbiome Study (KMS) and the Korea National Health and Nutrition Examination Survey (KNHANES). We included 2,178 participants aged 20–80 years from the KMS (2017–2019) and 12,938 participants from the KNHANES (2017–2019). The LCD score and percentage of energy intake from macronutrients were calculated using either a food frequency questionnaire or a 24-hour dietary recall. Dyslipidemia was assessed based on fasting blood tests. Gut microbiota was profiled by sequencing the V3-V4 region of the 16S rRNA gene in the KMS. Multivariate logistic regression models including interaction terms were used to evaluate the joint effects of diet and the gut microbiome on dyslipidemia.

RESULTS

A higher LCD score was associated with lower odds of atherogenic dyslipidemia and low high–density lipoprotein (HDL) cholesterolemia in both studies. Although both studies showed a positive trend for fat intake and a negative trend for carbohydrate intake in relation to hypercholesterolemia, the level of significance differed slightly. We identified 38 microbial genera associated with LCD score and macronutrient intake. Notably, fat intake showed beneficial associations with triglyceride and HDL cholesterol levels in individuals carrying (p for interaction = 0.0017) and 004 (p for interaction = 0.0482), respectively. In contrast, low carbohydrate intake was associated with increased odds of hypercholesterolemia in individuals harboring (odds ratio: 3.79; 95% confidence interval: 2.01–7.17; p for interaction < 0.0001). No significant associations were observed in individuals lacking these genera. Similar interaction effects were observed at the amplicon sequence variant level for and .

CONCLUSIONS

These findings provide population-based evidence for the interactive role of fat and carbohydrate intake with gut microbiota in influencing dyslipidemia among Koreans.

SUPPLEMENTARY INFORMATION

The online version contains supplementary material available at 10.1186/s12937-025-01188-4.

摘要

背景

近年来血脂异常的患病率有所上升;然而,通过饮食和肠道微生物群调节,它仍是一种可改变的状况。然而,基于人群的研究证据仍然有限。本研究旨在调查低碳水化合物饮食(LCD)、宏量营养素摄入与肠道微生物群之间的关系,并评估它们对韩国人群血脂异常的交互作用。

方法

数据来自两项基于人群的研究:韩国微生物组研究(KMS)和韩国国家健康与营养检查调查(KNHANES)。我们纳入了KMS(2017 - 2019年)中2178名年龄在20 - 80岁的参与者以及KNHANES(2017 - 2019年)中12938名参与者。使用食物频率问卷或24小时饮食回顾法计算LCD得分和宏量营养素的能量摄入百分比。根据空腹血液检测评估血脂异常情况。通过对KMS中16S rRNA基因的V3 - V4区域进行测序来分析肠道微生物群。使用包含交互项的多变量逻辑回归模型来评估饮食和肠道微生物群对血脂异常的联合作用。

结果

在两项研究中,较高的LCD得分与致动脉粥样硬化性血脂异常和低高密度脂蛋白(HDL)胆固醇血症的较低几率相关。尽管两项研究均显示脂肪摄入与高胆固醇血症呈正趋势,碳水化合物摄入与高胆固醇血症呈负趋势,但显著性水平略有不同。我们鉴定出38个与LCD得分和宏量营养素摄入相关的微生物属。值得注意的是,在携带(交互作用p = 0.0017)和004(交互作用p = 0.0482)的个体中,脂肪摄入分别与甘油三酯和HDL胆固醇水平呈有益关联。相比之下,在携带的个体中,低碳水化合物摄入与高胆固醇血症几率增加相关(比值比:3.79;95%置信区间:2.01 - 7.17;交互作用p < 0.0001)。在缺乏这些属的个体中未观察到显著关联。在和的扩增子序列变体水平也观察到类似的交互作用。

结论

这些发现为脂肪和碳水化合物摄入与肠道微生物群在影响韩国人血脂异常方面的交互作用提供了基于人群的证据。

补充信息

在线版本包含可在10.1186/s12937 - 025 - 01188 - 4获取的补充材料。

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