The Effect of Different L-Carnitine Administration Routes on the Development of Atherosclerosis in ApoE Knockout Mice

Scope: l-Carnitine (LC) is abundant in red meat and is widely added to health in the body is obtained from dietary supplements and food. This study focuses on the adverse effects of oral intake.[1] LC was first isolated from meat supplementation of 1.3% LC in ApoE−/− mice and whether the parenteral in the early 1900s. Later, in the 1950s, administration of LC (subcutaneously, sub) has any impact on the the metabolic function of this new com- pound was realized.[2] In the following development of atherosclerosis. years, extensive research was conducted Methods and results: Mice are randomly divided into three groups (n = 15). to help understand the biological func- All mice are fed a high-fat diet (HFD). The number of Ly6Chi monocytes; tion and metabolic role of LC in the body. degree of atherosclerosis; plasma LC, γ -butyrobetaine (γ BB), and LC is known to shuttle free fatty trimethylamine-N-oxide (TMAO) levels; and microbial community acids from the cytosol into the mito- chondrial matrix for β-oxidation and composition are analyzed. Compared with the HFD and HFD ± LC (sub) energy production. LC is also an an- groups, the number of Ly6Chi monocytes, atherosclerotic plaque area, and tioxidant, acting as a free radical scav- plasma γBB and TMAO levels are increased in the HFD ± LC (oral) group enger to protect cells from relative oxy- (p < 0.001). Plasma LC levels in the HFD ± LC (sub) group are higher than gen species.[3,4] However, the evidence those in other groups. The levels of γ BB, TMAO, and Ly6Chi monocytes are supporting the cardioprotective efficacy positively correlated with atherosclerotic plaque area (p < 0.01), and TMAO is of LC is controversial. Treatment with LC has been shown to protect against positively correlated with Bacteroidetes and negatively correlated with ischemia-reperfusion injury and improve Firmicutes at the phylum level. exercise tolerance and activity levels Conclusion: In contrast with oral LC administration, subcutaneous LC in patients with cardiovascular disease administration, which bypasses its conversion to TMAO in the liver, does not (CVD).[5–9] However, other studies have have a detrimental effect on the development of atherosclerosis in male shown that oral LC supplementation has ApoE−/− mice. Taking LC parenterally may be preferable among patients who no significant benefit in terms of all- cause mortality, heart failure, unstable require LC supplementation. angina,