Acetyl L-Carnitine - How it Works

Background

Lipids are the main source of sustained energy for both heart and skeletal muscle and fatty acids from lipids are the main source of energy for muscles. The reason for this seems to be the energy per gram of lipid is about twice that of polysaccharides and unlike oligosaccharides, lipids are easily stored without the accompanying, hydrating water, making lipids the efficient fuel of choice by a factor of 4 or more. Lipid oxidation to CO2 and H2O occurs within the inner mitochondrial matrix, which is a well-protected space packed with many different enzymes critical for ATP biosynthesis. Unfortunately, this organelle is also the primary target for destruction by undesirable H2O2 and superoxide ion, though some age-related and self-abuse damage can be reversed by liberal intake of L-carnitine and α-lipoic acid⁷.

During energy production from lipids, phophatidyldiacylglycerides and triaceylglycerides are first cleaved by a series of reactions into the component fatty acids, then transported through the cell cytosol to the mitochondrial outer membrane. Next, the enzyme carnitine palmitoyltranferase I (CPT I) binds L-carnitine to the fatty acid to make a neutral acylcarnitine and this neutral molecule is allowed transport into the mitochondrial matrix. After transport, the acyl (fatty acid) group from acylcarnitine is transferred to a free coenzyme A (Co A) with liberation of free carnitine. The enzyme responsible for this action is called carnitine palmitoyltranferase II (CPT II). Finally, the Co A-fatty acid molecule is usually “burned” in a series of reactions called β-oxidation. The free L-carnitine may be allowed back into the cytosol to repeat the fatty acid transport or it may be taken by a hungry nerve cell and used in the biosynthesis of acetylcholine – a neurotransmitter – in this case it is lost from the carnitine-β-oxidation transport cycle.

Utilization of the carnitine-β-oxidation pathway is highly desirable in our modern society, for the tightly controlled biosynthesis of ATP from lipid oxidation is an absolute requirement for continued health. Not only, but carnitine driven β-oxidation is the primary path for riding the body of excess calories. Because this oxidative pathway is so important the body probably needs several grams of acetyl-L-carnitine, daily. For instance, the important nutrients coenzyme Q10 and α-lipoic acid are also important components of the mitochondria and depletion of either of these or L-carnitine leads to irreversible damage to this organelle.

Diet supplementation with L-carnitine is important - People on strict vegetarian diets may not be able to ingest an adequate amount of L-carnitine, for only a few fruits & veggies contain significant amounts. This compounds the problems of sedentary folks on fruit and vegetable diets, for the muscles of obese individuals have drastically reduced ability to oxidize fatty acids which is partly due to both low levels of L-carnitine and low activities of CTP I and II in these muscles⁸. It is well known, from several independent human studies, that obesity is a strong correlate with type II diabetes. Supplementing the diet with L-carnitine can help avoid type II diabetes, Parkinson’s and a range of cardiovascular diseases.

Probably the most exciting development in L-carnitine supplementation is the effect this ingredient has on muscle strength. This is supported by clinical findings of L-carnitine supplements delaying or even preventing cardiovascular disease⁸ and also reducing hospital time for diabetics. Early intervention with 1.5 to 3 grams of L-carnitine, daily, significantly reduces diabetic neuropathy⁵. Bone re-adsorption is inhibited and bone growth stimulated by L-carnitine⁴. At high concentrations L-carnitine suppresses the release of tumor necrosis factor α (TNF-α) and interleukin-12, both factors signaling for osteo-bone cell senescence and death. It even reduces the binding of dexamethasone to bone cells, thus reducing the seriousness of a side-effect of this important drug.

References

1. Tanzer, F., Uzunsel, S. and Atalay, A. (1994). Plasma free carnitine levels in children with malnutrition. Turkish Journal of Pediatrics 36(2): 133-137.
2. Martin, J.J., Versruyssen, A., de Barsy, T. and Ceuterick, C. (1985). Muscle carnitine deficiency in old age. Case report and therapeutic results. Clinical Neurology and Neurosurgery 87(4): 275-281. Hagen, T.M., et al., (1998). Acetyl-L-carnitine fed to old rats partially restores mitochondrial function and ambulatory activity. Proceedings of the National Academy of Science USA 95: 9562-9566.
3. Volek, J.S., et al., (2002). L-Carnitine L-tartrate supplementation favorably affects markers of recovery from exercise stress. American Journal of Physiology, Endocrinology and Metabolism 282: E474-E482.
4. Benvenga, S., et al., (2001). Usefulness of L-carnitine, a naturally occurring peripheral antagonist of thyroid hormone action, in iatrogenic hyperthyroidism: a randomized, double-blind, placebo-controlled clinical trial. Journal of Clinical Endocrinology and Metabolism 86(8): 3579-3594. Colucci, S., et al., (2005). L-Carnitine and isovaleryl L-carnitine fumarate positively affect human osteoblast proliferation and differentiation in vitro. Calcified Tissue International 76(6): 458-465. Manoli, I., Martino M.U., Kino, T. and Alesci, S. (2004). Modulatory effects of L-carnitine on glucocorticoid receptor activity. Annuals of the New York Academy of Science 1033: 147-157.
5. Sima, A.F.A., Calvani, M., Mehra, M. and Amato, A. (2004). Acetyl-L-carnitine improves pain, nerve regeneration and vibratory perception in patients with chronic diabetic neuropathy. Diabetes Care 28(1): 89-101.
6. Borum, P.R. and Taggart, E.M. (1986). Carnitine nutriture of dialysis patients. Journal of the American Dietetic Association 86(5): 644-647.
7. Savitha, S., Sivarajan, K., Haripriya, D., Kokilavani, V. and Panneerselvam, C. (2005). Efficacy of levo carnitine and alpha lipoic acid in ameliorating the decline in mitochondrial enzymes during aging. Clinical Nutrition 24(5): 794-800. Shankar, S.S., Mirzamohammadi, B., Walsh, J.P. and Steinberg, H.O. (2004). L-carnitine may attenuate free fatty acid-induced endothelial dysfunction. Annals of the New York Academy of Science 1033: 189-197.
8. Kim, J.Y., et al., (2000). Lipid oxidation is reduced in obese human skeletal muscle. American Journal of Physiology, Endocrinology and Metabolism 279: E1039-E1044.

Supplement Facts - Acetyl L-Carnitine

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Reference: ConsumerLab.com, Magnesium Supplement Reviews and Quality Ratings, Posted 5/19/09

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