Acetylcarnitine
Acetyl-L-carnitine or ALCAR, is an acetylated form of L-carnitine. It is a dietary supplement and naturally occurs in plants and animals.
Contents
[hide]
1 Biochemical Production and Action
2 Absorption Compared to L-carnitine
3 Health Claims
4 References
5 Other reviews
[edit] 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.[1] 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.[2][3] 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.[4][5] Glucose metabolism increases with administration of either ALCAR[6] or L-carnitine.[7] A portion of L-carnitine is converted to ALCAR after ingestion in humans.[8]
[edit] Absorption Compared to L-carnitine
It has been claimed ALCAR is superior to L-carnitine in terms of bioavailability.[9] Both use the same mechanism for intestinal absorption that improves with sodium.[10] One study shows ALCAR has a lower blood concentration in humans after ingestion[11] possibly because ALCAR is hydrolyzed more in blood.[12] 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.[13]
[edit] Health Claims
ALCAR has the ability to cross the blood-brain barrier and get to the brain blood circulation, where it acts as a powerful antioxidant,[14] which helps in prevention of the brain cells' deterioration. Its supplementation has been shown to be neuroprotective in instances of cerebral ischemia in rats[15] and may be useful in treating peripheral nerve injury.[16] It 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] which pertains to 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. Research into the compound's safety and efficacy in humans is required. 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.[19] ALCAR has also been shown to improve insulin response[20][21] and is proved to have a positive effect on various muscle diseases as well as heart conditions. [22] [23]
[edit] References
^ 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.
^ 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.
^ 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.
^ Kiens B (January 2006). "Skeletal muscle lipid metabolism in exercise and insulin resistance". Physiological Reviews 86 (1): 205–43. doi:10.1152/physrev.00023.2004. PMID 16371598.
^ 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.
^ 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. doi:10.1053/meta.2000.6250. PMID 10877193.
^ 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.
^ 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.
^ 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". Gastroenterology 91 (1): 10–6. PMID 3710058.
^ 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. doi:10.1024/0300-9831.75.1.3. PMID 15830915.
^ 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. doi:10.1196/annals.1320.003. PMID 15591001.
^ 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. doi:10.1113/jphysiol.2006.125799. PMC 2075186. PMID 17331998.
^ Barhwal K, Hota SK, Jain V, Prasad D, Singh SB, Ilavazhagan G (June 2009). "Acetyl-l-carnitine (ALCAR) prevents hypobaric hypoxia-induced spatial memory impairment through extracellular related kinase-mediated nuclear factor erythroid 2-related factor 2 phosphorylation". Neuroscience 161 (2): 501–14. doi:10.1016/j.neuroscience.2009.02.086. PMID 19318118.
^ 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 & Physiology 33 (8): 725–33. doi:10.1111/j.1440-1681.2006.04425.x. PMID 16895547.
^ 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 Surgery 60 (2): 114–8. doi:10.1016/j.bjps.2006.04.017. PMID 17223507.
^ Beal MF (2003). "Bioenergetic approaches for neuroprotection in Parkinson's disease". Annals of Neurology 53 (Suppl 3): S39–47; discussion S47–8. doi:10.1002/ana.10479. PMID 12666097.
^ Hath**** JN, Shao A (October 2006). "Risk assessment for carnitine". Regulatory Toxicology and Pharmacology 46 (1): 23–8. doi:10.1016/j.yrtph.2006.06.007. PMID 16901595.
^ Claudio Teloken, Tulio Graziottin & Patrick E. Teloken (2007). "Oral Therapy for Peyroni's Disease". In Laurence A. Levine M.D. FACS. Peyronies Disease: A Guide to Clinical Management. Humana Press. ISBN 978-1-58829-614-6. Retrieved 2009-06-26.
^ 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". Hypertension 54 (3): 567–74. doi:10.1161/HYPERTENSIONAHA.109.132522. PMID 19620516.
^ 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 Letters 583 (2): 470–4. doi:10.1016/j.febslet.2008.12.053. PMID 19121314.
^ Schroeder MA, Atherton HJ, Ball DR, Cole MA, Heather LC, Griffin JL, Clarke K, Radda GK, Tyler DJ. (August 2009). "Real-time assessment of Krebs cycle metabolism using hyperpolarized 13C magnetic resonance spectroscopy". FASEB J. 23 (8): 2529–2538. doi:10.1096/fj.09-129171. PMC 2717776. PMID 19329759.
^ Kotil K, Kirali M, Eras M, Bilge T, Uzun H. (April 2007). "Neuroprotective effects of acetyl-L-carnithine in experimental chronic compression neuropathy. A prospective, randomized and placebo-control trials.". Turk Neurosurg. 17 (2): 67–77. PMID 17935020.
