In recent years, a number of studies have alluded to the importance of the intestinal microflora in
controlling whole-body metabolic homeostasis and organ physiology. In particular, it has been suggested
that the hepatic production of trimethylamine-N-oxide (TMAO) from gut microbiota-derived trimethylamine
(TMA) may enhance cardiovascular risk via promoting atherosclerotic lesion development.
The source of TMA production via the gut microbiota appears to originate from 2 principle sources, either
phosphatidylcholine/choline and/or L-carnitine. Therefore, it has been postulated that consumption of
these dietary sources, which are often found in large quantities in red meats, may be critical factors
promoting cardiovascular risk. In contrast, a number of studies demonstrate beneficial properties for Lcarnitine
consumption against metabolic diseases including skeletal muscle insulin resistance and
ischemic heart disease. Furthermore, fish are a significant source of TMAO, but dietary fish consumption
and fish oil supplementation may exhibit positive effects on cardiovascular health. In this mini-review
we will discuss the discrepancies regarding L-carnitine supplementation and its possible negative effects
on cardiovascular risk through potential increases in TMAO production, as well as its positive effects
on metabolic health via increasing glucose metabolism in the muscle and heart.