The oxidation of fatty acids occurs in the mitochondria, but fatty acids are unable to cross the inner mitochondrial membrane unaided. L-carnitine is involved in the shuttle system that allows fatty acids to cross this inner membrane which allows β-oxidation and ATP production to occur. Thus L-carnitine is involved in maintaining high energy phosphate pools in cells to maintain cellular energy levels. Carnitine is synthesised in humans from the amino acids lysine and methionine and is found in high concentrations in muscle. Evidence suggests that carnitine levels fall in hyperlipidaemic conditions (such as diabetes) and in rat models supplemental carnitine is able to normalise levels, modulate lipoproteins and decrease oxidation. Animal experiments show that carnitine may possess antioxidant and lipid lowering effects but the effects are not fully understood in humans.
To investigate the effects of carnitine on lipoprotein levels and oxidation, researchers fed 81 patients with type 2 diabetes 2 g of carnitine or a placebo for 3 months1, while monitoring various biochemical parameters. The results showed that carnitine supplementation decreased LDL cholesterol, triglycerides, apolipoprotein A1 and apolipoprotein B100 plasma levels. Further, there was an increase in HDL cholesterol. This suggests that carnitine supplementation favourably affected the blood lipids that are thought to be potential markers for cardiovascular disease. In addition, carnitine supplementation resulted in a decrease in LDL oxidation as well as TBARS, glycosylated haemoglobin (Hb A1c) and conjugated diene concentrations, suggesting that oxidative stress had been reduced. These results support previous findings from animal studies that showed modulatory effects on oxidation and lipoproteins with carnitine supplementation. Carnitine supplementation did not result in any changes in fasting glucose levels.
Evidence from previous research suggests that supplementation of carnitine may decrease hepatic esterification of fatty acids to glycerol thus decreasing the formation of triglycerides, which would have subsequently be exported in very low density lipoproteins (VLDL) to plasma. Instead the supplemental carnitine may increase the formation of acetylcarnitine, allowing more fatty acids to be passed across the mitochondrial inner membrane with a subsequent increase in the rate of β-oxidation of fatty acids in the mitochondria. Evidence from other research suggests that L-carnitine supplementation increases insulin sensitivity. Because VLDL may contribute to insulin resistance, the decrease in circulating levels of VLDL may be the mechanism that improves the sensitivity of skeletal muscle to glucose after carnitine supplementation. The reduction in oxidation may result from the involvement of carnitine in the regulation of antioxidant enzymes catalase and superoxide dismutase.
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