Choline, phosphatidylcholine and L-carnitine are cleaved by the gut microbiota to trimethylamine (TMA), which is oxidized to trimethylamine-N-oxide (TMAO) in the liver. TMAO seems to be proatherogenic in animal models and plasma levels are associated with risk of cardiovascular and other diseases in humans (2, 3). Circulating TMAO increases during renal failure, and has been regarded as an uremic toxin (4).
Assessment of choline status in relation to cardiovascular risk.
Matrix: EDTA plasma is preferred if sarcosine is not measured simultaneously.
Volume: Minimum volume is 60 µL, but 200 µL is optimal and allows reanalysis.
Preparation and stability: The blood sample must be centrifuged and the plasma/serum fraction put on ice, and frozen.
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2. Cho, C.E., and Caudill, M.A. (2017). Trimethylamine-N-oxide: Friend, foe, or simply caught in the cross-fire? Trends Endocrinol Metab 28, 121-130.
3. Subramaniam, S., and Fletcher, C. (2018) Trimethylamine N-oxide: breathe new life. Br J Pharmacol 175, 1344-1353.
4. Rysz, J., Franczyk, B., Ławiński, J., Olszewski, R., Ciałkowska-Rysz, A., & Gluba-Brzózka, A. (2021). The impact of CKD on uremic toxins and gut microbiota. Toxins (Basel), 13, 252.