Abstract
L-carnitine supplementation elevates plasma trimethylamine-N-oxide (TMAO), which may participate in atherosclerosis development by affecting cholesterol metabolism. The aim of the current study was to determine the effect of increased plasma TMAO on biochemical markers in the blood following cessation of L-carnitine supplementation. The follow-up measurements were performed on subjects who completed 24 weeks of L-carnitine or placebo supplementation protocol. Blood samples were taken after finishing the supplementation and then 4 and 12 months following the supplementation withdrawal. Four months after cessation of L-carnitine supplementation, plasma TMAO concentration reached a normal level which was stable for the following eight months. During this period, no modifications in serum lipid profile and circulating leukocyte count were noted. TMAO implications in health and disease is widely discussed. The results of this study demonstrate no adverse effects of elevated plasma TMAO, induced by L-carnitine, on the measured parameters at 4 and 12 months after withdrawal of supplementation.
Highlights
Atherosclerosis is a leading cause of vascular disease worldwide, even if several major modifiable risk factors have been identified [1]
Recent studies suggest that trimethylamine N-oxide (TMAO) may participate in the development of atherosclerosis [4]
The aim of the current study was to determine the effect of increased plasma TMAO on biochemical markers in the blood following cessation of L-carnitine supplementation
Summary
Atherosclerosis is a leading cause of vascular disease worldwide, even if several major modifiable risk factors have been identified [1]. The early atherosclerotic lesion is characterized by the accumulation of arterial foam cells derived mainly from cholesterol-loaded macrophages [2]. Recent studies suggest that trimethylamine N-oxide (TMAO) may participate in the development of atherosclerosis [4]. By reducing reverse cholesterol transport, TMAO elevates cholesterol uptake in the vascular wall, leading to macrophage foam cell formation and atherosclerotic lesion development [4,5]. L-carnitine has been suggested as a potential link between red meat consumption and atherosclerosis development [5]. L-carnitine is consumed from red meat but as a supplement due to its potential “fat burning” properties [6]. Dietary L-carnitine supplementation induces TMAO elevation in human blood [7,8,9,10]
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