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. 2022 May 23;12:8664. doi: 10.1038/s41598-022-12720-5

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Graphical Abstract. A significant and stable increase in circulating TMAO occurs after RYGB, which is known to decrease cardiovascular morbidity and mortality. In healthy rodent models in-vivo and in-vitro, we showed that acute exposure of aortas and endothelial cells to TMAO is functionally neutral at concentrations similar to those reported in patients and rodent models post-RYGB. These findings may add a different perspective on the current understanding of TMAO as deleterious molecule promoting endothelial dysfunction and atherosclerosis.