Dietary allicin reduces transformation of L-carnitine to TMAO through impact on gut microbiota

• Low dose carnitine induced the functional ability of gut microbiota for TMAO production.
• Dietary allicin helped the host to prevent TMAO formation from carnitine intake.
• Allicin played a role as a functional modulator of gut microbiota through its antimicrobial property.

Trimethylamine N-oxide (TMAO) was recently discovered as a novel and independent risk factor for promoting atherosclerosis while it has been found to be generated from dietary carnitine through metabolism of gut microbiota for decades. Antibiotics were found to successfully inhibit the pathway of gut microbiota-dependent TMAO formation, as well as prevention of atherosclerosis. However, the side effects and resistance potential of antibiotics limit their potential application. Allicin is a well-established antimicrobial phytochemical naturally found in fresh blended garlic and easily acquired from diet. Here we demonstrated that the plasma TMAO levels in C57BL/6 mice fed with dietary carnitine were 4–22 times greater than that in the control chow diet group during carnitine challenge test. Interestingly, the differences of plasma TMAO level were not seen when comparing mice in carnitine plus allicin diet group with the control chow diet group. The results of this study suggest that dietary allicin may be capable of protecting the host from producing TMAO when carnitine is consumed through its impact on gut microbiota. Allicin and dietary fresh garlic containing allicin may be used as functional foods for the prevention of atherosclerosis.