Acetyl-L-carnitine or ALCAR, is an acetylated form of L-carnitine. It is a dietary supplement. Acetylcarnitine is broken down in the blood by plasma esterases 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. This means it has less bioavailability unless it is entering cells (e.g., brain or muscle) more efficiently from the blood than L-carnitine. L-carnitine is known to not absorb into cells unless there is an insulin spike such as from a carbohydrate load.
ALCAR has the ability to cross the blood–brain barrier and enter the brain, where it acts as a powerful antioxidant. Its supplementation has been shown to be neuroprotective in instances of cerebral ischemia in rats and may be useful in treating peripheral nerve injury as well as spinal cord injury. It has been shown to be of benefit to Alzheimer's patients. It may have some neuroprotective benefit in the treatment of Parkinson's disease, but further research is required. ALCAR is also known to increase sperm motility, which describes the ability of sperm to move vigorously. Since motility is among the most important factors that help in the determination of sperm’s fertilization capability, acetyl-L-carnitine can help sperm cells move more actively, which consequently leads to the improved male fertility.
ALCAR has been shown to be more effective than tamoxifen in improving the curvature and reducing the pain and plaque sizes for men who sought treatment for their Peyronie's disease early and having low curvature deformities. ALCAR has also been shown to improve insulin response. It may induce epigenetic changes that may, in turn, give it utility as a therapeutic agent in neuropathic pain and depression.
^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. 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.
^ abStephens FB, Constantin-Teodosiu D, Greenhaff PL (June 2007). "New insights concerning the role of carnitine in the regulation of fuel metabolism in skeletal muscle". The Journal of Physiology581 (Pt 2): 431–44. doi:10.1113/jphysiol.2006.125799. PMC2075186. PMID17331998.
^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:10.1024/0300-98184.108.40.206. 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.
^Al-Majed AA, Sayed-Ahmed MM, Al-Omar FA, Al-Yahya AA, Aleisa AM, Al-Shabanah OA (August 2006). "Carnitine esters prevent oxidative stress damage and energy depletion following transient forebrain ischaemia in the rat hippocampus". Clinical and Experimental Pharmacology & Physiology33 (8): 725–33. doi:10.1111/j.1440-1681.2006.04425.x. PMID16895547.
^Wilson AD, Hart A, Brännström T, Wiberg M, Terenghi G (2007). "Delayed acetyl-L-carnitine administration and its effect on sensory neuronal rescue after peripheral nerve injury". Journal of Plastic, Reconstructive & Aesthetic Surgery60 (2): 114–8. doi:10.1016/j.bjps.2006.04.017. PMID17223507.
^Samir P. Patel, Patrick G. Sullivan, Travis S. Lyttle, Alexander G. Rabchevsky (2010). "Acetyl-l-carnitine ameliorates mitochondrial dysfunction following contusion spinal cord injury". Journal of Neurochemistry114 (1): 291–301. doi:10.1111/j.1471-4159.2010.06764.x. PMC2897952. PMID20438613.
^Ruggenenti P, Cattaneo D, Loriga G, et al. (September 2009). "Ameliorating hypertension and insulin resistance in subjects at increased cardiovascular risk: effects of acetyl-L-carnitine therapy". Hypertension54 (3): 567–74. doi:10.1161/HYPERTENSIONAHA.109.132522. PMID19620516.
^Zhang Z, Zhao M, Li Q, Zhao H, Wang J, Li Y (January 2009). "Acetyl-l-carnitine inhibits TNF-alpha-induced insulin resistance via AMPK pathway in rat skeletal muscle cells". FEBS Letters583 (2): 470–4. doi:10.1016/j.febslet.2008.12.053. PMID19121314.