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

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 and eight strains of to mice for 6 weeks. Bb4 and 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 supplementation. The treatment of strains modulated the abundances of several genera such as UCG-009, UCG-010, which belong to the Firmicutes that has been reported with gene clusters, which may be related to the reduction in intestinal TMA and plasma TMAO. Additionally, a reduction in indicates a reduction in circulating glucose and lipids, which may be another pathway by which strains reduce the risk of atherosclerosis. The effect of strains on 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 strains may have therapeutic potential for alleviating TMAO-related diseases.