Open Access Articles- Top Results for Acetylcarnitine


Systematic (IUPAC) name
Clinical data
AHFS/ International Drug Names
  • Over-the-counter
Pharmacokinetic data
Bioavailability >10
Half-life 4.2 hours[1]
3040-38-8 7pxY
PubChem CID 7045767
ChemSpider 5406074 7pxY
ChEBI CHEBI:57589 7pxY
ChEMBL CHEMBL1697733 7pxN
Chemical data
Formula C9H17NO4
 14pxN (what is this?)  (verify)

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 plasma esterases to carnitine which is used by the body to transport fatty acids into the mitochondria for breakdown.[2]

Biochemical production and action

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.[2][3] 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.[4][5] 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.[6][7] Glucose metabolism in diabetics improves with administration of either ALCAR[8] or L-carnitine.[9] ALCAR decreases glucose consumption in favor of fat oxidation in non-diabetics.[10] A portion of L-carnitine is converted to ALCAR after ingestion in humans.[11]

Absorption compared to L-carnitine

It has been claimed ALCAR is superior to L-carnitine in terms of bioavailability.[2][12] Both use the same mechanism for intestinal absorption that improves with sodium.[13] One study shows ALCAR has a lower blood concentration in humans after ingestion[14] possibly because ALCAR is hydrolyzed more in blood.[15]

Health effects

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.[16]

ALCAR may have some neuroprotective benefit in the treatment of Parkinson's disease, but further research is required.[17] ALCAR is also known to increase sperm motility.[18]

It has been suggested ALCAR may have potential as a drug for treating peripheral neuropathic pain.[19]

Ethanol neurotoxicity

Acetylcarnitine has been shown to reduce ethanol-induced neurotoxicity in mice.[20]


  1. ^ "Acetyl-L-carnitine. Monograph." (PDF). Alternative Medicine Review 15 (1): 76–83. April 2010. PMID 20359271. 
  2. ^ a b c Activation and transportation of fatty acids to the mitochondria via the carnitine shuttle.
  3. ^ Zeyner A, Harmeyer J (1999). "Metabolic functions of L-carnitine and its effects as feed additive in horses. A review". Archiv Für Tierernährung 52 (2): 115–38. PMID 10548966. doi:10.1080/17450399909386157. 
  4. ^ Longnus SL, Wambolt RB, Barr RL, Lopaschuk GD, Allard MF (October 2001). "Regulation of myocardial fatty acid oxidation by substrate supply". American Journal of Physiology. Heart and Circulatory Physiology 281 (4): H1561–7. PMID 11557544. 
  5. ^ Lysiak W, Lilly K, DiLisa F, Toth PP, Bieber LL (January 1988). "Quantitation of the effect of L-carnitine on the levels of acid-soluble short-chain acyl-CoA and CoASH in rat heart and liver mitochondria". The Journal of Biological Chemistry 263 (3): 1151–6. PMID 3335535. 
  6. ^ Kiens B (January 2006). "Skeletal muscle lipid metabolism in exercise and insulin resistance". Physiological Reviews 86 (1): 205–43. PMID 16371598. doi:10.1152/physrev.00023.2004. 
  7. ^ 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 Pharmacology 72 (10): 1101–9. PMID 7882173. doi:10.1139/y94-156. 
  8. ^ 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 Experimental 49 (6): 704–8. PMID 10877193. doi:10.1053/meta.2000.6250. 
  9. ^ Mingrone G, Greco AV, Capristo E et al. (February 1999). "L-carnitine improves glucose disposal in type 2 diabetic patients". Journal of the American College of Nutrition 18 (1): 77–82. PMID 10067662. doi:10.1080/07315724.1999.10718830. 
  10. ^ Stephens 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 Physiology 581 (Pt 2): 431–44. PMC 2075186. PMID 17331998. doi:10.1113/jphysiol.2006.125799. 
  11. ^ 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 Medicine 32 (1): E13–9. PMID 19178874. 
  12. ^ Jane Higdon, Ph.D. (October 2002). "L-Carnitine". Linus Pauling Institute at Oregon State University. 
  13. ^ Hamilton JW, Li BU, Shug AL, Olsen WA (July 1986). "Carnitine transport in human intestinal biopsy specimens. Demonstration of an active transport system". Gastroenterology 91 (1): 10–6. PMID 3710058. 
  14. ^ 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 Research 75 (1): 3–9. PMID 15830915. doi:10.1024/0300-9831.75.1.3. 
  15. ^ Rebouche CJ (November 2004). "Kinetics, pharmacokinetics, and regulation of L-carnitine and acetyl-L-carnitine metabolism". Annals of the New York Academy of Sciences 1033: 30–41. PMID 15591001. doi:10.1196/annals.1320.003. 
  16. ^ Hudson S, Tabet N (2003). "Acetyl-L-carnitine for dementia". Cochrane Database Syst Rev (Systematic review) (2): CD003158. PMID 12804452. doi:10.1002/14651858.CD003158. 
  17. ^ Beal MF (2003). "Bioenergetic approaches for neuroprotection in Parkinson's disease". Annals of Neurology 53 (Suppl 3): S39–47; discussion S47–8. PMID 12666097. doi:10.1002/ana.10479. 
  18. ^ [unreliable medical source?]Hathcock JN, Shao A (October 2006). "Risk assessment for carnitine". Regulatory Toxicology and Pharmacology 46 (1): 23–8. PMID 16901595. doi:10.1016/j.yrtph.2006.06.007. 
  19. ^ Chiechio S, Copani A, Gereau RW, Nicoletti F (2007). "Acetyl-L-carnitine in neuropathic pain: experimental data". CNS Drugs. 21 Suppl 1: 31–8; discussion 45–6. PMID 17696591. doi:10.2165/00023210-200721001-00005. 
  20. ^ PMID 20708681 (PubMed)
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