Abstract
Background and Aims : High levels of plasma trimethylamine-N-oxide (TMAO) have been shown to correlate with increased risk of cardio-metabolic diseases including cardiovascular diseases and adverse events after heart failure. TMAO is formed via oxidation of TMA catalysed by flavin-dependent monooxygenases (FMOs) in the human liver, mainly by FMO3. The vast majority of trimethylamine (TMA) is produced by the action of the gut microbiota that produce TMA from dietary substrates including choline, carnitine, and betaine.
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