Abstract

Aim: Following the ingestion of red meat, chicken, eggs and dairy products, L-carnitine and phosphatidylcholine undergo microbic and hepatic metabolism, leading to the formation of trimethylamine-N-oxide (TMAO). Recent metabolomic studies positively associated plasma levels of TMAO with incident and prevalent cardiovascular disease, but the mechanisms accounting for this relation are still lacking. The aim of this work is to evaluate TMAO capacity to impair lipid metabolism in cultured macrophages.

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