Bifidobacterium breve and Bifidobacterium longum Attenuate Choline-Induced Plasma Trimethylamine N-Oxide Production by Modulating Gut Microbiota in Mice

Qianqian Wang; Min Guo; Yang Liu; Mengshu Xu; Liuting Shi; Xiu Li; Jianxin Zhao; Hao Zhang; Gang Wang; Wei Chen

doi:10.3390/nu14061222

Bifidobacterium breve and Bifidobacterium longum Attenuate Choline-Induced Plasma Trimethylamine N-Oxide Production by Modulating Gut Microbiota in Mice

Nutrients. 2022 Mar 14;14(6):1222. doi: 10.3390/nu14061222.

Authors

Qianqian Wang^{1

2}, Min Guo^{1

2}, Yang Liu³, Mengshu Xu^{1

2}, Liuting Shi^{1

2}, Xiu Li^{1

2}, Jianxin Zhao^{1

2

4}, Hao Zhang^{1

2

4

5

6}, Gang Wang^{1

2

4}, Wei Chen^{1

2

5}

Affiliations

¹ State Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi 214122, China.
² School of Food Science and Technology, Jiangnan University, Wuxi 214122, China.
³ KLATASDS-MOE, School of Statistics, East China Normal University, Shanghai 200062, China.
⁴ (Yangzhou) Institute of Food Biotechnology, Jiangnan University, Yangzhou 225004, China.
⁵ National Engineering Research Center for Functional Food, Jiangnan University, Wuxi 214122, China.
⁶ Wuxi Translational Medicine Research Center, Jiangsu Translational Medicine Research Institute Wuxi Branch, Wuxi 214122, China.

Abstract

Atherosclerosis is the main cause of myocardial infarction and stroke, and the morbidity and mortality rates of cardiovascular disease are among the highest of any disease worldwide. Excessive plasma trimethylamine-N-oxide (TMAO), an intestinal metabolite, promotes the development of atherosclerosis. Therefore, effective measures for reducing plasma TMAO production can contribute to preventing atherosclerosis. Probiotics are living microorganisms that are beneficial to the human body, and some of them can attenuate plasma TMAO production. To explore the effects of probiotic supplementation on plasma TMAO in choline-fed mice, we intragastrically administered eight strains of Bifidobacterium breve and eight strains of Bifidobacterium longum to mice for 6 weeks. B. breve Bb4 and B. longum BL1 and BL7 significantly reduced plasma TMAO and plasma and cecal trimethylamine concentrations. However, hepatic flavin monooxygenase (FMO) activity, flavin-containing monooxygenase 3 (FMO3), farnesoid X receptor (FXR) protein expression and TMAO fractional excretion were not significantly affected by Bifidobacterium supplementation. The treatment of Bifidobacterium strains modulated the abundances of several genera such as Ruminococcaceae UCG-009, Ruminococcaceae UCG-010, which belong to the Firmicutes that has been reported with cut gene clusters, which may be related to the reduction in intestinal TMA and plasma TMAO. Additionally, a reduction in Ruminococcaceae indicates a reduction in circulating glucose and lipids, which may be another pathway by which Bifidobacterium strains reduce the risk of atherosclerosis. The effect of Bifidobacterium strains on Bacteroides also suggests a relationship between the abundance of this genus and TMA concentrations in the gut. Therefore, the mechanism underlying these changes might be gut microbiota regulation. These Bifidobacterium strains may have therapeutic potential for alleviating TMAO-related diseases.

Keywords: atherosclerosis; choline; gut microbiota; probiotics; trimethylamine; trimethylamine N-oxide.

MeSH terms

Animals
Bifidobacterium breve* / metabolism
Bifidobacterium longum* / metabolism
Choline / metabolism
Gastrointestinal Microbiome* / physiology
Methylamines
Mice
Mice, Inbred C57BL

Substances

Methylamines
trimethyloxamine
Choline

Abstract

MeSH terms

Substances

Grants and funding