Elsevier

Metabolism

Volume 41, Issue 2, February 1992, Pages 135-136
Metabolism

The exogenous origin of trimethylamine in the mouse

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Abstract

Although it is now generally regarded that the origin of urinary trimethylamine (TMA) is via the action of intestinal microflora on precursors such as choline, little direct evidence exists. The normal production of urinary TMA was shown to be absent in germ-free mice and greatly reduced in antibiotic-pretreated animals. Cohabitation of germ-free mice with conventional animals restored their ability to excrete TMA. This study invokes a fundamental role for the intestinal microflora in the provision of TMA from precursors within the food.

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    The relevance of TMAO in CVDs was proposed a decade ago, particularly in the formation of atherosclerotic plaques (Wang et al., 2011). It was found that choline can be catabolized by the intestinal microbiota after ingestion to produce TMAO gas (Al-Waiz et al., 1992), which is then absorbed and metabolized by the hepatic flavin monooxygenase (FMO) family of enzymes, FMO3, to form TMAO (Lang et al., 1998). Another study found that specific intestinal microbiota and TMAO levels were associated with thrombogenic potential (Zhu et al., 2016).

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Supported by the Arabian Gulf University (M.A.-W.).

1

M.M. was the recipient of a fellowship from SIZ for Science of Vojvodina, Novi Sad, Yugoslavia.

2

Dr Mikov's present address is Department of Pharmacology and Toxicology, University of Novi Sad, Faculty of Medicine, 21001 Novi Sad, POB 98, Yugoslavia.

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