Foods rich in cholesterol and fats are also often rich in the indicated dietary nutrients PC (lecithin), choline, and carnitine. Following ingestion, gut microbiota can use these nutrients as a carbon fuel source. While mammals do not have the enzyme, gut microbes have TMA lyases, which can cleave the C-N bond of these nutrients, releasing the TMA moiety as a waste product. Transport via the portal circulation brings the TMA to a cluster of hepatic enzymes, the FMOs (particularly FMO3), that efficiently oxidize TMA, thus forming TMAO. TMAO enters the circulation, where it is predominantly excreted by the kidneys. TMAO has been shown to affect cholesterol and sterol metabolism in animal models, enhancing macrophage cholesterol accumulation and atherosclerosis development. In multiple human studies, elevated TMAO has been independently associated with prevalent CVD and incident risks for MI, stroke, death, and revascularization. [O], oxidation.