Blood trimethylamine-N-oxide originates from microbiota mediated breakdown of phosphatidylcholine and absorption from small Intestine
Elevated serum trimethylamine-N-oxide (TMAO) was previously reported to be associated with an elevated risk for cardiovascular events. TMAO originates from the microbiota-dependent breakdown of food-derived phosphatidylcholine (PC) to trimethylamine (TMA), which is oxidized by hepatic flavin-contain...
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| Main Authors: | , , , , , , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
January 27, 2017
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| In: |
PLOS ONE
Year: 2017, Volume: 12, Issue: 1, Pages: e0170742 |
| ISSN: | 1932-6203 |
| DOI: | 10.1371/journal.pone.0170742 |
| Online Access: | Verlag, LF, Volltext: http://dx.doi.org/10.1371/journal.pone.0170742 Verlag, LF, Volltext: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0170742 
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| Author Notes: | Wolfgang Stremmel, Kathrin V. Schmidt, Vera Schuhmann, Frank Kratzer, Sven F. Garbade, Claus-Dieter Langhans, Gert Fricker, Jürgen G. Okun |
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| 245 | 1 | 0 | |a Blood trimethylamine-N-oxide originates from microbiota mediated breakdown of phosphatidylcholine and absorption from small Intestine |c Wolfgang Stremmel, Kathrin V. Schmidt, Vera Schuhmann, Frank Kratzer, Sven F. Garbade, Claus-Dieter Langhans, Gert Fricker, Jürgen G. Okun |
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| 520 | |a Elevated serum trimethylamine-N-oxide (TMAO) was previously reported to be associated with an elevated risk for cardiovascular events. TMAO originates from the microbiota-dependent breakdown of food-derived phosphatidylcholine (PC) to trimethylamine (TMA), which is oxidized by hepatic flavin-containing monooxygenases to TMAO. Our aim was to investigate the predominant site of absorption of the bacterial PC-breakdown product TMA. A healthy human proband was exposed to 6.9 g native phosphatidylcholine, either without concomitant treatment or during application with the topical antibiotic rifaximin, or exposed only to 6.9 g of a delayed-release PC formulation. Plasma and urine concentrations of TMA and TMAO were determined by electrospray ionization tandem mass spectrometry (plasma) and gas chromatography-mass spectrometry (urine). Native PC administration without concomitant treatment resulted in peak plasma TMAO levels of 43 ± 8 μM at 12 h post-ingestion, which was reduced by concomitant rifaximin treatment to 22 ± 8 μM (p < 0.05). TMAO levels observed after delayed-release PC administration were 20 ± 3 μM (p < 0.001). Accordingly, the peak urinary concentration at 24 h post-exposure dropped from 252 ± 33 to 185 ± 31 mmol/mmol creatinine after rifaximin treatment. In contrast, delayed-release PC resulted in even more suppressed urinary TMAO levels after the initial 12-h observation period (143 ± 18 mmol/mmol creatinine) and thereafter remained within the control range (24 h: 97 ± 9 mmol/mmol creatinine, p < 0.001 24 h vs. 12 h), indicating a lack of substrate absorption in distal intestine and large bowel. Our results showed that the microbiota in the small intestine generated the PC breakdown product TMA. The resulting TMAO, as a cardiovascular risk factor, was suppressed by topical-acting antibiotics or when PC was presented in an intestinally delayed release preparation. | ||
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