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 l-carnitine 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.
Keywords: Atherosclerosis; Cardiovascular disease; Carnitine; Choline; Gut microbiota; Trimethylamine-N-oxide.
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