Acetyl-L-carnitine or ALCAR, is an acetylated form of L-carnitine. It is naturally produced by the body, although it is often taken as a dietary supplement. Acetylcarnitine is broken down in the blood by plasmaesterases to carnitine which is used by the body to transport fatty acids into the mitochondria for breakdown.
ALCAR is an acetylated derivative of L-carnitine. During strenuous exercise, a large portion of L-carnitine and unused acetyl-CoA are converted to ALCAR and CoA inside mitochondria by carnitine O-acetyltransferase. The ALCAR is transported outside the mitochondria where it converts back to the two constituents. The L-carnitine is cycled back into the mitochondria with acyl groups to facilitate fatty acid utilization, but excess acetyl-CoA may block it. Excess acetyl-CoA causes more carbohydrates to be used for energy at the expense of fatty acids. This occurs by different mechanisms inside and outside the mitochondria. ALCAR transport decreases acetyl-CoA inside the mitochondria, but increases it outside. Glucose metabolism in diabetics improves with administration of either ALCAR or L-carnitine. ALCAR decreases glucose consumption in favor of fat oxidation in non-diabetics. A portion of L-carnitine is converted to ALCAR after ingestion in humans.
It has been claimed ALCAR is superior to L-carnitine in terms of bioavailability. Both use the same mechanism for intestinal absorption that improves with sodium. One study shows ALCAR has a lower blood concentration in humans after ingestion possibly because ALCAR is hydrolyzed more in blood.
Early research which seemed to suggest Acetylcarnitine had potential as a treatment for dementia were not strongly substantiated by later research, and the substance is not routinely used for this purpose.
^Zeyner A, Harmeyer J (1999). "Metabolic functions of L-carnitine and its effects as feed additive in horses. A review". Archiv Für Tierernährung52 (2): 115–38. doi:10.1080/17450399909386157. PMID10548966.
^Lopaschuk GD, Gamble J (October 1994). "The 1993 Merck Frosst Award. Acetyl-CoA carboxylase: an important regulator of fatty acid oxidation in the heart". Canadian Journal of Physiology and Pharmacology72 (10): 1101–9. doi:10.1139/y94-156. PMID7882173.
^Giancaterini A, De Gaetano A, Mingrone G, et al. (June 2000). "Acetyl-L-carnitine infusion increases glucose disposal in type 2 diabetic patients". Metabolism: Clinical and Experimental49 (6): 704–8. doi:10.1053/meta.2000.6250. PMID10877193.
^Cao Y, Wang YX, Liu CJ, Wang LX, Han ZW, Wang CB (2009). "Comparison of pharmacokinetics of L-carnitine, acetyl-L-carnitine and propionyl-L-carnitine after single oral administration of L-carnitine in healthy volunteers". Clinical and Investigative Medicine32 (1): E13–9. PMID19178874.
^Jane Higdon, Ph.D. (October 2002). L-Carnitine. Linus Pauling Institute at Oregon State University.
^Hamilton JW, Li BU, Shug AL, Olsen WA (July 1986). "Carnitine transport in human intestinal biopsy specimens. Demonstration of an active transport system". Gastroenterology91 (1): 10–6. PMID3710058.
^Eder K, Felgner J, Becker K, Kluge H (January 2005). "Free and total carnitine concentrations in pig plasma after oral ingestion of various L-carnitine compounds". International Journal for Vitamin and Nutrition Research75 (1): 3–9. doi:10.1024/0300-9818.104.22.168. PMID15830915.
^Rebouche CJ (November 2004). "Kinetics, pharmacokinetics, and regulation of L-carnitine and acetyl-L-carnitine metabolism". Annals of the New York Academy of Sciences1033: 30–41. doi:10.1196/annals.1320.003. PMID15591001.