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肠道微生物群在响应个性化营养干预时,调节与FTO基因多态性相关的不同脂质代谢结果。

Gut microbiota modulates differential lipid metabolism outcomes associated with FTO gene polymorphisms in response to personalized nutrition intervention.

作者信息

Zheng Jianheng, Wang Feijie, Guo Hongwei, Cheng Junrui, Du Jun, Kan Juntao

机构信息

Nutrilite Health Institute, Shanghai, China.

School of Public Health, Fudan University, Shanghai, China.

出版信息

Front Nutr. 2022 Sep 15;9:985723. doi: 10.3389/fnut.2022.985723. eCollection 2022.

DOI:10.3389/fnut.2022.985723
PMID:36185685
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9520577/
Abstract

BACKGROUND

Interindividual differences in response to personalized nutrition (PN) intervention were affected by multiple factors, including genetic backgrounds and gut microbiota. The fat mass and obesity associated () gene is an important factor related to hyperlipidemia and occurrence of cardiovascular diseases. However, few studies have explored the differences in response to intervention among subjects with different genotypes of , and the associations between gut microbiota and individual responses.

OBJECTIVE

To explore the differential lipid metabolism outcomes associated with gene polymorphisms in response to PN intervention, the altered taxonomic features of gut microbiota caused by the intervention, and the associations between gut microbiota and lipid metabolism outcomes.

METHODS

A total of 400 overweight or obese adults were recruited in the study and randomly divided into the PN group and control group, of whom 318 completed the 12-week intervention. The single nucleotide polymorphism (SNP) of rs1121980 in was genotyped. Gut microbiota and blood lipids were determined at baseline and week 12. Functional property of microbiota was predicted using Tax4Fun functional prediction analysis.

RESULTS

Subjects with the risk genotype of had significantly higher weight and waist circumference (WC) at baseline. Generalized linear regression models showed that the reduction in weight, body mass index (BMI), WC, body fat percentage, total cholesterol (TCHO), and low-density lipoprotein (LDL) was greater in subjects with the risk genotype of and in the PN group. Significant interaction effects between genotype and intervention on weight, BMI, WC, TCHO, and LDL were found after stratifying for specific genotype of . All subjects showed significant increasement in α diversity of gut microbiota after intervention except for those with the non-risk genotype in the control group. Gut microbiota, including and , might be involved in lipid metabolism in response to interventions. The predicted functions of the microbiota in subjects with different genotypes were related to lipid metabolism-related pathways, including fatty acid biosynthesis and degradation.

CONCLUSION

Subjects with the risk genotype of had better response to nutrition intervention, and PN intervention showed better amelioration in anthropometric parameters and blood lipids than the control. Gut microbiota might be involved in modulating differential lipid metabolism responses to intervention in subjects with different genotypes.

TRIAL REGISTRATION

[Chictr.org.cn], identifier [ChiCTR1900026226].

摘要

背景

个体对个性化营养(PN)干预反应的差异受多种因素影响,包括遗传背景和肠道微生物群。脂肪量和肥胖相关()基因是与高脂血症和心血管疾病发生相关的重要因素。然而,很少有研究探讨不同基因型受试者对干预反应的差异以及肠道微生物群与个体反应之间的关联。

目的

探讨与PN干预反应相关的基因多态性的脂质代谢差异结果、干预引起的肠道微生物群分类特征变化以及肠道微生物群与脂质代谢结果之间的关联。

方法

本研究共招募了400名超重或肥胖成年人,随机分为PN组和对照组,其中318人完成了12周的干预。对基因中rs1121980的单核苷酸多态性(SNP)进行基因分型。在基线和第12周时测定肠道微生物群和血脂。使用Tax4Fun功能预测分析预测微生物群的功能特性。

结果

具有风险基因型的受试者在基线时体重和腰围(WC)显著更高。广义线性回归模型显示,具有风险基因型的受试者和PN组体重、体重指数(BMI)、WC、体脂百分比、总胆固醇(TCHO)和低密度脂蛋白(LDL)的降低幅度更大。在按特定基因型分层后,发现基因型与干预对体重、BMI、WC、TCHO和LDL有显著的交互作用。除对照组中非风险基因型的受试者外,所有受试者在干预后肠道微生物群的α多样性均显著增加。肠道微生物群,包括和,可能参与了对干预的脂质代谢。不同基因型受试者中微生物群的预测功能与脂质代谢相关途径有关,包括脂肪酸生物合成和降解。

结论

具有风险基因型的受试者对营养干预反应更好,PN干预在人体测量参数和血脂方面比对照组显示出更好的改善。肠道微生物群可能参与调节不同基因型受试者对干预的脂质代谢差异反应。

试验注册

[Chictr.org.cn],标识符[ChiCTR1900026226]。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3617/9520577/1762be46b83c/fnut-09-985723-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3617/9520577/80859b6ac2f2/fnut-09-985723-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3617/9520577/7695f00c8325/fnut-09-985723-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3617/9520577/1762be46b83c/fnut-09-985723-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3617/9520577/80859b6ac2f2/fnut-09-985723-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3617/9520577/7695f00c8325/fnut-09-985723-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3617/9520577/1762be46b83c/fnut-09-985723-g0003.jpg

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