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. 2016 Jul 28;5:F1000 Faculty Rev-1880. [Version 1] doi: 10.12688/f1000research.8459.1

Figure 1. Pathways linking dietary phosphatidylcholine, intestinal microbiota, and incident adverse cardiovascular events.

Figure 1.

Ingested phosphatidylcholine (lecithin), the major dietary source of total choline, is acted on by intestinal lipases to form a variety of metabolic products, including the choline-containing nutrients glycerophosphocholine, phosphocholine, and choline. Choline-containing nutrients that reach the cecum and large bowel may serve as fuel for intestinal microbiota (gut flora), producing trimethylamine (TMA). TMA is rapidly further oxidized to trimethylamine N-oxide (TMAO) by hepatic flavin-containing monooxygenases (FMOs). TMAO enhances the accumulation of cholesterol in macrophages, the accumulation of foam cells in artery walls, and atherosclerosis, all factors that are associated with an increased risk of heart attack, stroke, and death. Choline can also be oxidized to betaine in both the liver and the kidneys. Dietary betaine can serve as a substrate for bacteria to form TMA and presumably TMAO. Reproduced by permission of the Massachusetts Medical Society from: Tang WHW, Wang Z, Levison BS, Koeth RA, Britt EB, Fu X, Wu Y, Hazen SL: Intestinal Microbial Metabolism of Phosphatidylcholine and Cardiovascular Risk. N Engl J Med 2013, 368(17): 1575–1584.