L-carnitine is a non-essential nonproteinaceous amino acid in human nutrition. L-carnitine is manufactured in humans, but can be ingested in the diet, with good sources being animal flesh. L-carnitine is involved in the transport of long chain fatty acids into the mitochondria for oxidation as acylcarnitine esters. Studies involving L-carnitine have shown that it is able to reduce blood sugar levels, increase glucose storage and increase the oxidation of fatty acids through the β-oxidation pathway. L-carnitine may also have allosteric control over key enzymes in glycolysis and gluconeogenesis. Acetyl-L-carnitine is structurally similar to L-carnitine, but with the addition of an acetyl group. Once acetyl-L-carnitine is ingested the acetyl moiety is cleaved from the L-carnitine, and this may produce a more prolonged supply of dietary L-carnitine for use in the metabolism of glucose and fatty acids. Studies investigating the effects of acetyl-L-carnitine show it may be useful as a glucose disposal agent and insulin sensitiser.
For example, in one study researchers administered oral acetyl-L-carnitine at a dose of 1 gram per day to subjects with symptoms of the metabolic syndrome1. The researchers then assessed the changes to the glucose disposal rate. The results of the study were interesting in that acetyl-L-carnitine was effective at reducing the glucose disposal rate but only in those subjects with initial glucose disposal rates of less than 7.9 mg/kg per minute. Subject who were deemed to have adequate glucose disposal rates of over 7.9 mg/kg per minute did not derive a benefit from the acetyl-L-carnitine supplements. In those subjects with poor glucose disposal rates, the acetyl-L-carnitine improved glucose disposal rate from 4.89 to 6.72 mg/kg per minute. The acetyl-L-carnitine also lowered the systolic blood pressure significantly in subjects with both poor and good glucose disposal rates. However, diastolic pressure was reduced only in those subjects with poor glucose disposal rates following acetyl-L-carnitine supplementation.
These results support the contention that acetyl-L-carnitine is an effective glucose disposal agent. The mechanism by which this may occur is not fully understood. However, it may relate to the ability of carnitine compounds to increase fat oxidation. The body weight of the subjects was not measured in this study, but carnitine is known to accelerate the oxidation of fatty acids and weight loss. As the blood pressure correlates with body adiposity, this may explain the lowering of blood pressure. Interestingly the adiponectin plasma concentrations did increase with acetyl-L-carnitine supplementation, and as adiponectin levels are correlated inversely with adiposity, this suggests that body fat may have been reduced during supplementation. Reductions in the lipid content of tissues may have improved insulin sensitivity, which in turn increased glucose disposal rates. Acetyl-L-carnitine is able to protect from oxidative stress, and so its antioxidative role may have contributed to improved insulin sensitivity.
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