食品与发酵工业 >

2022 , Vol. 48 >Issue 16: 11 - 17

DOI: https://doi.org/10.13995/j.cnki.11-1802/ts.031344

研究报告

罗伊氏乳杆菌CCFM8631对由胆碱导致的血浆氧化三甲胺和盲肠三甲胺水平升高的影响

  • 王茜茜 ,
  • 张婷 ,
  • 梁明 ,
  • 赵建新 ,
  • 张灏 ,
  • 王刚 ,
  • 陈卫
展开
  • 1(江南大学 食品学院,江苏 无锡,214122)
    2(无限极(中国)有限公司,广东 广州,510645)
博士研究生(王刚教授和梁明为共同通信作者,E-mail:wanggang@jiangnan.edu.cn;Fiona.Liang@infinitus-int.com)

收稿日期: 2022-03-01

  修回日期: 2022-03-17

  网络出版日期: 2022-09-16

基金资助

国家自然科学基金面上项目(31972052)

收起

Effect of Lactobacillus reuteri CCFM8631 on choline-induced elevation of plasma trimethylamine-N-oxide and cecal trimethylamine levels

  • WANG Qianqian ,
  • ZHANG Ting ,
  • LIANG Ming ,
  • ZHAO Jianxin ,
  • ZHANG Hao ,
  • WANG Gang ,
  • CHEN Wei
Expand
  • 1(School of Food Science and Technology, Jiangnan University, Wuxi 214122, China)
    2(Infinitus (China) Company Ltd., Guangzhou 510645, China)

Received date: 2022-03-01

  Revised date: 2022-03-17

  Online published: 2022-09-16

Fold

摘要

血浆氧化三甲胺是一种与肠道微生物相关的胆碱代谢物,已发现血浆中高浓度的氧化三甲胺是促进动脉粥样硬化的独立风险因素。降低血浆氧化三甲胺的含量,对预防心血管疾病起着重要作用。该研究以期得到具有降低血浆氧化三甲胺(trimethylamine-N-oxide,TMAO)和盲肠三甲胺(trimethylamine , TMA)效果的乳杆菌,为动脉粥样硬化性心血管疾病的防治开发新的功能性乳杆菌。为了分析乳杆菌降低氧化三甲胺的能力,该研究分别用3株不同种的乳杆菌灌胃胆碱饲料喂养的小鼠,采用液相质谱联用的方法检测小鼠血浆TMAO和盲肠TMA水平,同时采用Illumina MiSeq高通量测序技术分析小鼠粪便菌群的多样性及物种组成。结果显示罗伊氏乳杆菌CCFM8631可以显著降低小鼠血浆TMAO和盲肠TMA含量。以上这种降低作用并非是通过影响肝脏黄素单氧化酶3(flavin-containing monooxygenase 3,FMO3)和法尼酯X受体(recombinant farnesoid X receptor,FXR)蛋白的表达以及肝脏FMO的活性实现的,而与乳酸菌对肠道菌群的调节有关。

关键词： 肠道菌群; 氧化三甲胺; 三甲胺; 动脉粥样硬化; 罗伊氏乳杆菌

本文引用格式

王茜茜 , 张婷 , 梁明 , 赵建新 , 张灏 , 王刚 , 陈卫 . 罗伊氏乳杆菌CCFM8631对由胆碱导致的血浆氧化三甲胺和盲肠三甲胺水平升高的影响[J]. 食品与发酵工业, 2022 , 48(16) : 11 -17 . DOI: 10.13995/j.cnki.11-1802/ts.031344

Abstract

Cardiovascular diseases have the highest mortality and morbidity rates in the world, for which atherosclerosis (AS) is the main pathologic basis. AS occurrence and development are related to vascular inflammation, hypercholesterolemia and oxidative stress. In recent years, researchers have found that gut microbiota play a key role in the occurrence and development of AS. High plasma trimethylamine-N-oxide (TMAO) concentrations, mainly from choline metabolite by gut microbiota or from fish intake, have been found to be an independent risk factor for promoting AS. TMAO promotes AS occurrence and development in several ways. Ingesting dietary components that reduce TMAO production may be a promising strategy by which to prevent AS. Given the role of gut microbiota in the pathogenesis of TMAO-induced AS, gut microbiota offers a potential therapeutic target for preventing and treating cardiovascular disease. Dietary composition affects the community structure of intestinal microorganisms and gut microbiota quickly adapt to dietary changes. In the light of growing evidence of the relationship between gut microbiota and chronic diseases, probiotics have received increasing attention as intervention targets. Probiotics show specificity and functionality for alleviating chronic diseases and reducing inflammation, and preclinical studies have been demonstrated to relieve liver damage, reduce weight and remit colitis. In order to analyze the ability of Lactobacillus to reduce TMAO, in this study, three different strains of Lactobacillus were given choline-fed mice by gavage. The levels of plasma TMAO and cecal trimethylamine (TMA) in mice were detected by liquid chromatography-mass spectrometry (HPLC-MS/MS), and the diversity and species composition of mouse fecal microbiota were analyzed by Illumina MiSeq high-throughput sequencing technology. It was found that Lactobacillus reuteri CCFM8631 could significantly reduce the contents of plasma TMAO and cecal TMA. This reduction was not achieved by affecting the expression of hepatic FMO3 and FXR proteins and the enzymatic activity of hepatic FMOs, but is related to the regulation of gut microbiota by lactic acid bacteria.

Key words： gut microbiota; trimethylamine-N-oxide; trimethylamine; atherosclerosis; Lactobacillus reuteri

参考文献

[1] ABBAFATI C, ABBAS K M, ABBASI M, et al.Global burden of 369 diseases and injuries in 204 countries and territories, 1990—2019:A systematic analysis for the Global Burden of Disease Study 2019 [J].Lancet, 2020, 396(10 258):1 204-1 222.
[2] MENSAH G A, ROTH G A, FUSTER V.The Global Burden of Cardiovascular Diseases and Risk Factors 2020 and Beyond [J].Journal of the American College of Cardiology, 2019, 74(20):2 529-2 532.
[3] ZHOU M G, WANG H D, ZENG X Y, et al.Mortality, morbidity, and risk factors in China and its provinces, 1990—2017:A systematic analysis for the Global Burden of Disease Study 2017 [J].The Lancet, 2019, 394(10 204):1 145-1 158.
[4] LIU S W, LI Y C, ZENG X Y, et al.Burden of Cardiovascular Diseases in China, 1990—2016 Findings From the 2016 Global Burden of Disease Study[J].JAMA Cardiology, 2019, 4(4):342-345.
[5] TURNBAUGH P J, LEY R E, MAHOWALD M A, et al.An obesity-associated gut microbiome with increased capacity for energy harvest [J].Nature, 2006, 444(7 122):1 027-1 031.
[6] WANG Z N, KLIPFELL E, BENNETT B J, et al.Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease [J].Nature, 2011, 472(7 341):57-63.
[7] KOETH R A, WANG Z N, LEVISON B S, et al.Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis [J].Nature Medicine, 2013, 19(5):576-585.
[8] TANG W H W, WANG Z N, LEVISON B S, et al.Intestinal microbial metabolism of phosphatidylcholine and cardiovascular risk[J].The New England Journal of Medicine, 2013, 368(17):1 575-1 584.
[9] TANG W H W, HAZEN S L.The contributory role of gut microbiota in cardiovascular disease[J].The Journal of Clinical Investigation, 2014, 124(10):4 204-4 211.
[10] HEIANZA Y, MA W J, MANSON J E, et al.Gut microbiota metabolites and risk of major adverse cardiovascular disease events and death:A systematic review and meta-analysis of prospective studies[J].Journal of the American Heart Association, 2017, 6(7):e004947.
[11] QIU L, TAO X Y, XIONG H, et al.Lactobacillus plantarum ZDY04 exhibits a strain-specific property of lowering TMAO via the modulation of gut microbiota in mice [J].Food Function, 2018, 9(8):4 299-4 309.
[12] QIU L, YANG D, TAO X Y, et al.Enterobacter aerogenes ZDY01 attenuates choline-induced trimethylamine N-oxide levels by remodeling gut microbiota in mice[J].Journal of Microbiology and Biotechnology Letters, 2017, 27(8):1 491-1 499.
[13] OCQUE A J, STUBBS J R, NOLIN T D.Development and validation of a simple UHPLC-MS/MS method for the simultaneous determination of trimethylamine N-oxide, choline, and betaine in human plasma and urine [J].Journal of Pharmaceutical and Biomedical Analysis, 2015, 109:128-135.
[14] ZHAO X Q, ZEISEL S H, ZHANG S C.Rapid LC-MRM-MS assay for simultaneous quantification of choline, betaine, trimethylamine, trimethylamine N-oxide, and creatinine in human plasma and urine [J].Electrophoresis, 2015, 36(18):2 207-2 214.
[15] BENNETT B J, DE AGUIAR VALLIM T Q, WANG Z N, et al.Trimethylamine-N-oxide, a metabolite associated with atherosclerosis, exhibits complex genetic and dietary regulation[J].Cell Metabolism, 2013, 17(1):49-60.
[16] MAO B Y, LI D Y, ZHAO J X, et al.Metagenomic insights into the effects of fructo-oligosaccharides(FOS) on the composition of fecal microbiota in mice[J].Journal of Agricultural and Food Chemistry, 2015, 63(3):856-863.
[17] CAPORASO J G, KUCZYNSKI J, STOMBAUGH J, et al.QIIME allows analysis of high-throughput community sequencing data [J].Nature Methods, 2010, 7(5):335-336.
[18] CHONG J, LIU P, ZHOU G Y, et al.Using MicrobiomeAnalyst for comprehensive statistical, functional, and meta-analysis of microbiome data [J].Nature Protocols, 2020, 15(3):799-821.
[19] SEGATA N, IZARD J, WALDRON L, et al.Metagenomic biomarker discovery and explanation [J].Genome Biology, 2011, 12(6): R60.
[20] BARBERN A, BATES S T, CASAMAYOR E O, et al.Using network analysis to explore co-occurrence patterns in soil microbial communities [J].The ISME Journal, 2012, 6(2):343-351.
[21] Probiotics Society of The Chinese Institute of Food Science A, Technology.Scientific consensus on probiotics(2020) [J].Journal of Chinese Institute Of Food Science and Technology, 2020, 20(5):303-307.
[22] YATES A A, SCHLICKER S A, SUITOR C W.Dietary reference intakes:The new basis for recommendations for calcium and related nutrients, B vitamins, and choline [J].Journal of the American Dietetic Association, 1998, 98(6):699-706.
[23] PENRY J T, MANORE M M.Choline:An important micronutrient for maximal endurance-exercise performance? [J].International Journal of Sport Nutrition and Exercise Metabolism, 2008, 18(2):191-203.
[24] CORBIN K D, ZEISEL S H.Choline metabolism provides novel insights into nonalcoholic fatty liver disease and its progression [J].Current Opinion in Gastroenterology, 2012, 28(2):159-165.
[25] SHERRIFF J L, O'SULLIVAN T A, PROPERZI C, et al.Choline, its potential role in nonalcoholic fatty liver disease, and the case for human and bacterial genes[J].Advances in Nutritions, 2016, 7(1):5-13.
[26] UFNAL M.Trimethylamine, a toxic precursor of trimethylamine oxide, lost in medical databases[J].Journal of Nutrition, 2020, 150(2):419.
[27] WILLING B P, DICKSVED J, HALFVARSON J, et al.A pyrosequencing study in twins shows that gastrointestinal microbial profiles vary with inflammatory bowel disease phenotypes[J].Gastroenterology, 2010, 139(6):1 844-1 854.
[28] BCKHED F, DING H, WANG T, et al.The gut microbiota as an environmental factor that regulates fat storage [J].Proceedings of the National Academy of Sciences of the United States of America, 2004, 101(44):15 718-15 723.
[29] LIU B N, ZHANG Y L, WANG R, et al.Western diet feeding influences gut microbiota profiles in apoE knockout mice [J].Lipids in Health and Disease, 2018, 17(1):1-8.
[30] WANG K, JIN X L, LI Q Q, et al.Propolis from different geographic origins decreases intestinal inflammation and bacteroides spp.populations in a model of dss-induced colitis[J].Molecular Nutrition & Food Research, 2018, 62(17):1800080.
Options
文章导航

/

〈 〉

技术支持：北京玛格泰克科技发展有限公司