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. 2019 Nov 19;10:1360. doi: 10.3389/fphar.2019.01360

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Copyright © 2019 Yang, Li, Yang, Zhao, Pan, Liang, Tian, Li, Liu, Xing and Wu

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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TMAO potential as a therapeutic target in AS. Dietary choline, L-carnitine, betaine, and other choline-containing compounds are the major nutrient precursors of TMAO, and they are metabolized to TMA by the gut microbiota and various enzymes. Then, TMA can be absorbed in the intestines and delivered to the liver through the portal circulation, where it is converted to TMAO by FMO3. TMAO can be targeted as follows: via the diet, dietary supplements and lifestyle interventions can significantly affect TMAO levels; antibiotics, probiotics, probiotic functional products, and some natural molecules can markedly decrease TMA and TMAO levels by remodeling the gut microbiota; PSE, meldonium, DMB, and CutC/D inhibitors can suppress the generation of TMA; and trigonelline and guggulsterone can inhibit the conversion of TMA to TMAO by inhibiting FMO3. MD, Mediterranean diet; DMB, 3,3-dimethyl-1-butanol; PSE, plant sterol ester.