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Trimethylamine-N-Oxide, a Metabolite Associated with Atherosclerosis, Exhibits Complex Genetic and Dietary Regulation
Trimethylamine-N-oxide levels linked to artery disease are influenced by genes and diet
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Abstract
Circulating trimethylamine-N-oxide (TMAO) levels are strongly associated with atherosclerosis.
- Two flavin mono-oxygenase enzymes, FMO1 and FMO3, convert trimethylamine (TMA) into TMAO.
- FMO3 has 10-fold higher specific activity than FMO1 in this conversion process.
- Overexpression of FMO3 in mice significantly increases plasma TMAO levels, while silencing FMO3 reduces TMAO levels.
- Hepatic FMO3 expression is lower in males than females in both humans and mice, primarily influenced by androgens.
- Dietary bile acids induce FMO3 expression through the farnesoid X receptor (FXR).
- Inbred strains of mice indicate a significant correlation between FMO3 and TMAO, with TMAO levels explaining 11% of the variation in atherosclerosis.
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