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Choline, betaine, and L-carnitine are transformed into trimethylamine (TMA) by gut microbiota, absorbed into the liver, and oxidized into trimethylamine-N-oxide (TMAO) by flavin-containing monooxygenases. Elevated TMAO levels may negatively affect human health. As phosphatidylcholine (PC) is the main source of dietary choline, its intake or PC-rich foods may be harmful to human health; however, quantitative comparative information among dietary choline compounds (PC, glycerophosphocholine [GPC], and choline chloride [CC]) regarding in vivo generation of TMAO is lacking. Here, we compared the effects of PC, GPC, and CC on plasma TMAO levels in rats. Furthermore, we investigated their effects on gut microbiota at the genus level. Dietary PC did not affect plasma TMAO levels, whereas dietary GPC and CC significantly increased them. At the genus level, plasma TMAO levels were significantly negatively correlated with relative abundances of Anaerotruncus, Actinomyces, Enterococcus, Dialister, Clostridium XIVa, and Granulicatella; they were significantly positively correlated with that of Coprobacter. Moreover, the relative abundances of Anaerotruncus and Coprobacter were found to predict plasma TMAO levels. Therefore, dietary PC, unlike GPC or CC, does not increase plasma TMAO levels in rats. Furthermore, several gut microbes are associated with changes in plasma TMAO levels in rats fed with choline compounds.

metabolites

Unlike Glycerophosphocholine or Choline Chloride, Dietary Phosphatidylcholine Does Not Increase Plasma Trimethylamine-N-Oxide Levels in Sprague-Dawley Rats