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Not to be confused with carnosine or creatine.
Clinical data
AHFS/ Micromedex Detailed Consumer Information
  • US: B (No risk in non-human studies)
Routes of
Oral, intravenous
ATC code A16AA01 (WHO) (L form)
Legal status
Legal status
Pharmacokinetic data
Bioavailability <10%
Protein binding None
Metabolism slightly
Excretion Urine (>95%)
CAS Number 541-15-1 YesY
PubChem (CID) 288
DrugBank DB00583 N
ChemSpider 282 YesY
KEGG C00318 YesY
ChEBI CHEBI:17126 YesY
Chemical and physical data
Formula C7H15NO3
Molar mass 161.199 g/mol
3D model (Jmol) Interactive image
 NYesY (what is this?)  (verify)

Carnitine is an amino acid derivative and nutrient involved in lipid (fat) metabolism in mammals and other eukaryotes. It is in the chemical compound classes of β-hydroxyacids and quaternary ammonium compounds, and because of the hydroxyl-substituent, it exists in two stereoisomers, the biologically active enantiomer L-carnitine (R form), and the essentially biologically inactive D-carnitine.[1][better source needed] Both are available through chemical synthesis,[not verified in body] and the L-form is continuously biosynthesized in eukaryotic organisms from the proteinogenic amino acids lysine and methionine.[2] In such eukaryotic cells, it is specifically required for the transport of fatty acids from the intermembraneous space in the mitochondria into the mitochondrial matrix during the catabolism of lipids, in the generation of metabolic energy.[1][better source needed] Carnitine was originally found as a growth factor for mealworms[3] and labeled vitamin BT, although carnitine is not by biochemical definition a true vitamin.[4][5] It is used efficaciously, clinically, in the treatment of some conditions, e.g. systemic primary carnitine deficiency,[6] and it is available over the counter as a nutritional supplement, though its efficacy for most conditions for which it is advertised is controversial or not yet established.[7][8]

Biosynthesis and metabolism[edit]

In animals, the biosynthesis of R-carnitine (L) occurs primarily in the liver and kidneys from the amino acids lysine (via trimethyllysine) and methionine.[9]

Carnitine transports long-chain acyl groups from fatty acids into the mitochondrial matrix, so they can be broken down through β-oxidation to acetyl CoA to obtain usable energy via the citric acid cycle.[1] In some organisms, such as fungi, the acetate is used in the glyoxylate cycle for gluconeogenesis and formation of carbohydrates. Fatty acids must be activated before being covalently linked to the carnitine molecule to form acylcarnitine for transport. The free fatty acid in the cytosol is first adenylated by reaction with ATP, then attached with a thioester bond to coenzyme A (CoA), with expulsion of AMP. This reaction is catalyzed by the enzyme fatty acyl-CoA synthetase and driven to completion by inorganic pyrophosphatase.

The acyl group on CoA can now be transferred to carnitine and the resulting acylcarnitine transported into the mitochondrial matrix.[1] This occurs via a series of similar steps:[citation needed]

  1. Acyl CoA is transferred to the hydroxyl group of carnitine by carnitine acyltransferase I (palmitoyltransferase) located on the outer mitochondrial membrane
  2. Acylcarnitine is shuttled inside by a carnitine-acylcarnitine translocase
  3. Acylcarnitine is converted to acyl CoA by carnitine acyltransferase II (palmitoyltransferase) located on the inner mitochondrial membrane. The liberated carnitine returns to the cytosol.

Carnitine acyltransferase I and peroxisomal carnitine octanoyl transferase (CROT) undergo allosteric inhibition by malonyl-CoA, an intermediate in fatty acid biosynthesis,[citation needed] to prevent futile cycling between β-oxidation and fatty acid synthesis.[citation needed]

Human genetic disorders, such as primary carnitine deficiency, carnitine palmitoyltransferase I deficiency, carnitine palmitoyltransferase II deficiency and carnitine-acylcarnitine translocase deficiency, affect different steps of this process.[10]

Physiological effects[edit]


A link between dietary consumption of carnitine and atherosclerosis has been proposed.[11] There is evidence that carnitine lowers the risk of mortality due to arrythmias, after an acute myocardial infarction.[citation needed] When intestinal bacteria are exposed to carnitine from food, they produce the byproduct, trimethylamine, which is oxidised in the liver to trimethylamine N-oxide (TMAO), which may be associated with atherosclerosis;[according to whom?][citation needed] the risk of cardiovascular events is higher in those with high TMAO levels, independent of the observed level of carnitine.[citation needed] The presence of TMAO-producing bacteria is reportedly a consequence of subject's consuming diets rich in meat.[according to whom?][citation needed] Vegetarian and vegans who ate a single meal of meat had much lower levels of TMAO in their bloodstream than did regular meat-eaters, which was ascribed to the lower levels of the intestinal bacteria that convert carnitine into TMAO.[12]

A further study reported evidence of a second path for atherogenic activity of carnitine, passing through a different metabolite, γ-butyrobetaine (γBB).[13]

Effects on bone mass[edit]

[needs update]

Carnitine concentration in cells diminishes as humans age,[citation needed] affecting fatty acid metabolism in various tissues.[citation needed] Bone is affected, in particular, as it requires the continuous reconstructive and metabolic functions of osteoblasts for maintenance of its mass.[citation needed] A 2008 study reported that supplementing rat diets with L-carnitine decreased bone turnover and increased bone mineral density in ovariectomized females.[14][non-primary source needed]

Effect on thyroid hormone action[edit]

[needs update] A 2001 report suggested that L-carnitine may be useful in preventing and reversing hyperthyroid symptoms.[15][non-primary source needed] A 2004 study reported that L-carnitine acts as a peripheral antagonist of thyroid hormone action; in particular, L-carnitine inhibited both triiodothyronine (T3) and thyroxine (T4) entry into the cell nuclei.[16][non-primary source needed]

Possible health effects[edit]

Carnitine has been proposed as a supplement to treat a variety of health conditions including heart attack,[17][18] heart failure,[citation needed] angina,[19][better source needed] narcolepsy,[20][non-primary source needed] and diabetic neuropathy,[21][dubious ][better source needed] but not improving exercise performance,[19] nor wasting syndrome (weight loss).[21][dubious ][better source needed] In all of these cases the results are preliminary or proposed, and not part of an established medical treatment.[21][better source needed]

People with epileptic disorders/vulnerability are advised, on product monographs and pharmacy databases, to avoid carnitine and its derivatives as it is claimed to promote epileptic discharges. It now appears that this advice has been misguided. According to a systematic review of epileptics treated with valproic acid, these claims are unsubstantiated both in the scientific literature and in clinical practice and may have done more harm than good.[22] This is unfortunate as many epileptics actually have decreased levels of carnitine (especially those under valproate treatment) and might need to supplement with this substance in order to avoid troubling side effects (e.g., hepatotoxicity, hyperammonemic encephalopathy). The exact reason for these cautionary notes against carnitine is not known. One possibility is that a well-intended, but ultimately false, disclaimer has propagated uncontrollably throughout pharmacy texts and electronic databases worldwide. Another possibility is that some of the side effects of carnitine (e.g., overstimulation, dizziness, headache, nausea) may mimic, and thus be mistaken for, a mild epileptic fit.



The highest concentrations of carnitine are found in red meat.[23][24] It can be found at significantly lower levels in many other foods including nuts and seeds (e.g. pumpkin, sunflower, sesame), legumes or pulses (beans, peas, lentils, peanuts), vegetables (artichokes, asparagus, beet greens (young leaves of the beetroot), broccoli, brussels sprouts, collard greens, garlic, mustard greens, okra, parsley, kale), fruits (apricots, bananas), cereals (buckwheat, corn, millet, oatmeal, rice bran, rye, whole wheat, wheat bran, wheat germ) and other foods (bee pollen, brewer's yeast, carob).[citation needed]

Product Quantity Carnitine
Lamb 100 g 190 mg
Beef steak 100 g 95 mg
Ground beef 100 g 94 mg
Pork 100 g 27.7 mg
Bacon 100 g 23.3 mg
Tempeh 100 g 19.5 mg
Cod fish 100 g  5.6 mg
Chicken breast 100 g  3.9 mg
American cheese 100 g  3.7 mg
Ice cream 100 mL  3.7 mg
Whole milk 100 mL  3.3 mg
Avocado one medium 2 mg[25]
Cottage cheese 100 g  1.1 mg
Whole-wheat bread 100 g  0.36 mg
Asparagus 100 g  0.195 mg
White bread 100 g  0.147 mg
Macaroni 100 g  0.126 mg
Peanut butter 100 g  0.083 mg
Rice (cooked) 100 g  0.0449 mg
Egg 100 g  0.0121 mg
Orange juice 100 mL  0.0019 mg
Lentil 100 g 2.1 mg[26]
Potato 100 g 2.4 mg[26]
Sweet Potato 100 g 1.1 mg[26]
Banana 100 g 0.2 mg[26]
Carrot 100 g 0.3 mg[26]
Apple (without skin) 100 g 0.2 mg[26]
Raisin 100 g 0.8 mg[26]

In general, 20 to 200 mg are ingested per day by those on an omnivorous diet, whereas those on a strict vegetarian or vegan diet may ingest as little as 1 mg/day.[citation needed] However, even strict vegetarians (vegans) show no signs of carnitine deficiency, despite the fact that most dietary carnitine is derived from animal sources.[23][24] No advantage appears to exist in giving an oral dose greater than 2 g at one time, since absorption studies indicate saturation at this dose.[27]

Health Canada[edit]

Other sources may be found in over-the-counter vitamins, energy drinks and various other products. Products containing L-carnitine can now be marketed as "natural health products" in Canada. As of 2012, Parliament has allowed carnitine products and supplements to be imported into Canada (Health Canada). The Canadian government did issue an amendment in December 2011 allowing the sale of L-carnitine without a prescription.[28]


Levocarnitine was approved by the U.S. Food and Drug Administration as a new molecular entity under the brand name Carnitor on December 27, 1985.[29]

See also[edit]


  1. ^ a b c d Mehta, Sweety (2013). "Activation and Transportation of Fatty Acids to the Mitochondria via the Carnitine Shuttle with Animation [self-published learning resource]" (online). Disclaimer: does not evaluate or guarantee the accuracy of any articles, videos or other posted information on the Author Network (“PAN”)… see Disclaimer. 
  2. ^ Steiber A.; J. Kerner; C. Hoppel (2004). "Carnitine: a Nutritional, Biosynthetic, and Functional perspective". Mol. Aspects Med. 25 (5–6): 455–73. doi:10.1016/j.mam.2004.06.006. PMID 15363636. 
  3. ^ Fraenkel, G.; Blewett, M.; Coles, M. (1948-06-19). "BT, A New Vitamin of the B-Group and its Relation to the Folic Acid Group, and Other Anti-Anæmia Factors". Nature. 161 (4103): 981–983. doi:10.1038/161981a0. ISSN 0028-0836. Retrieved 2016-09-04. 
  4. ^ Bremer, J. (1983). "Carnitine—Metabolism and Functions". Physiol. Rev. 63: 1420–1480. Retrieved 22 January 2016. 
  5. ^ Carter, H. E.; Bhattacharyya, P. K.; Weidman, K. R.; Fraenkel, G. (1952). "Chemical Studies on vitamin BT. Isolation and characterization as carnitine". Arch. Biochem. Biophys. 38: 405–416. 
  6. ^ Stanley, Charles A.; Bennett, Michael J.; Longo, Nicolo (2000). "Plasma Membrane Carnitine Transport Defect". In Scriver, C.W.; Beaudet, A.L.; Sly, W.S.; Valle, D. Metabolic and Molecular Bases of Inherited Disease (8th ed.). New York, NY, USA: McGraw Hill. doi:10.1036/ommbid.297. ISBN 0-07-913035-6. Retrieved 22 January 2016. 
  7. ^ Johri, A.M.; D.K. Heyland; M.F. Hétu; B. Crawford & J.D. Spence (2014). "Carnitine Therapy for the Treatment of Metabolic Syndrome and Cardiovascular Disease: Evidence and Controversies" (print, online review). Nutr. Metab. Cardiovasc. Dis. 24 (8, Aug.): 808–814. doi:10.1016/j.numecd.2014.03.007. Retrieved 22 January 2016. 
  8. ^ Dambrova, M.; E. Liepinsh (2015). "Risks and Benefits of Carnitine Supplementation in Diabetes" (print, online review). Exp. Clin. Endocrinol. Diabetes. 123 (2, Feb.): 95–100. doi:10.1055/s-0034-1390481. Retrieved 22 January 2016. 
  9. ^ "L-Carnitine". Archived from the original on 2007-05-08. Retrieved 2007-06-01. 
  10. ^ Olpin S (2005). "Fatty acid oxidation defects as a cause of neuromyopathic disease in infants and adults". Clin. Lab. 51 (5–6): 289–306. PMID 15991803. 
  11. ^ Brown, J. Mark; Stanley L. Hazen (2015). "The Gut Microbial Endocrine Organ: Bacterially Derived Signals Driving Cardiometabolic Diseases". Annu. Rev Med. 66: 343–359. doi:10.1146/annurev-med-060513-093205. PMC 4456003Freely accessible. PMID 25587655. 
  12. ^ Koeth, Robert A.; Zeneng Wang; Bruce S. Levison; Jennifer A. Buffa; Elin Org; Brendan T. Sheehy; Earl B. Britt; Xiaoming Fu; Yuping Wu; Lin Li; Jonathan D. Smith; Joseph A. DiDonato; Jun Chen; Hongzhe Li; Gary D. Wu; James D. Lewis; Manya Warrier; J. Mark Brown; Ronald M. Krauss; W. H. Wilson Tang; Frederic D. Bushman; Aldons J. Lusis & Stanley L. Hazen (2013). "Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis". Nature Medicine. 19 (5): 576–85. doi:10.1038/nm.3145. PMC 3650111Freely accessible. PMID 23563705. 
  13. ^ Koeth, Robert A.; Bruce S. Levison; Miranda K. Culley; Jennifer A. Buffa; Zeneng Wang; Jill C. Gregory; Elin Org; Yuping Wu; Lin Li; Jonathan D. Smith; W.H. Wilson Tang; Joseph A. DiDonato; Aldons J. Lusis; Stanley L. Hazen (2014). "γ-Butyrobetaine Is a Proatherogenic Intermediate in Gut Microbial Metabolism of L-Carnitine to TMAO". Cell Metabolism. 20 (5): 799–812. doi:10.1016/j.cmet.2014.10.006. PMC 4255476Freely accessible. PMID 25440057. Retrieved 22 January 2016. 
  14. ^ Hooshmand S, Balakrishnan A, Clark RM, Owen KQ, Koo SI, Arjmandi BH (Aug 2008). "Dietary L-Carnitine Supplementation Improves Bone Mineral Density by Suppressing Bone Turnover in Aged Ovariectomized Rats". Phytomedicine. 15 (8): 595–601. doi:10.1016/j.phymed.2008.02.026. PMID 18539446. 
  15. ^ Benvenga S, Ruggeri RM, Russo A, Lapa D, Campenni A, Trimarchi F (Aug 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". The Journal of Clinical Endocrinology and Metabolism. 86 (8): 3579–94. doi:10.1210/jcem.86.8.7747. PMID 11502782. 
  16. ^ Benvenga S, Amato A, Calvani M, Trimarchi F (Nov 2004). "Effects of carnitine on thyroid hormone action". Ann N Y Acad Sci. 1033: 158–167. doi:10.1196/annals.1320.015. PMID 15591013. 
  17. ^ Dinicolantonio, J. J.; Lavie, C. J.; Fares, H.; Menezes, A. R.; o'Keefe, J. H. (2013). "L-Carnitine in the Secondary Prevention of Cardiovascular Disease: Systematic Review and Meta-analysis" (pdf). Mayo Clinic Proceedings. 88 (6): 544–51. doi:10.1016/j.mayocp.2013.02.007. PMID 23597877. 
  18. ^ Marcovina, S. M.; Sirtori, C.; Peracino, A.; Gheorghiade, M.; Borum, P.; Remuzzi, G.; Ardehali, H. (2013). "Translating the Basic Knowledge of Mitochondrial Functions to Metabolic Therapy: Role of L-Carnitine". Translational Research. 161 (2): 73–84. doi:10.1016/j.trsl.2012.10.006. PMC 3590819Freely accessible. PMID 23138103. 
  19. ^ a b Pekala, J.; Patkowska-Sokoła, B.; Bodkowski, R.; Jamroz, D.; Nowakowski, P.; Lochyński, S.; Librowski, T. (2011). "L-Carnitine—Metabolic Functions and Meaning in Humans [sic.] Life". Current Drug Metabolism. 12 (7): 667–78. doi:10.2174/138920011796504536. PMID 21561431. 
  20. ^ Miyagawa, T; Kawamura, H; Obuchi, M; Ikesaki, A; Ozaki, A; Tokunaga, K; Inoue, Y; Honda, M (2013). "Effects of oral L-carnitine administration in narcolepsy patients: A randomized, double-blind, cross-over and placebo-controlled trial". PLoS ONE. 8 (1): e53707. doi:10.1371/journal.pone.0053707. PMC 3547955Freely accessible. PMID 23349733. [non-primary source needed]
  21. ^ a b c Ehrlich, Steven D. (2014). "Supplement: Carnitine (L-carnitine)" (online). Complementary and Alternative Medicine Guide (December 28). Retrieved 21 January 2016. [Author] Steven D. Ehrlich, NMD [Naturopathic Medical Doctor], Solutions Acupuncture, a private practice specializing in complementary and alternative medicine, Phoenix, AZ. Review provided by VeriMed Healthcare Network.  See Naturopathy.
  22. ^ Zeiler FA, Sader N, Gillman LM, West M (2016). "Levocarnitine induced seizures in patients on valproic acid: A negative systematic review". Seizure. 36: 36–39. doi:10.1016/j.seizure.2016.01.020. PMID 26889779. 
  23. ^ a b "L-Carnitine – Linus Pauling Institute – Oregon State University". 
  24. ^ a b Lombard, K. A.; Olson, A. L.; Nelson, S. E.; Rebouche, C. J. (1989-08-01). "Carnitine status of lactoovovegetarians and strict vegetarian adults and children". The American Journal of Clinical Nutrition. 50 (2): 301–306. ISSN 0002-9165. PMID 2756917. 
  25. ^ Rebouche CJ. Carnitine. In: Shils ME, Olson JA, Shike M, Ross AC, eds. Modern Nutrition in Health and Disease. 9th ed. Philadelphia: Lippincott, Williams & Wilkins; 1999:505-512. Cited by Jane Higdon (2002), see Oregon State U, accessed 12 January 2016
  26. ^ a b c d e f g Demarquoy, Jean; Georges, Béatrice; Rigault, Caroline; Royer, Marie-Charlotte; Clairet, Amélie; Soty, Maud; Lekounoungou, Serge; Le Borgne, Françoise (2004-06-01). "Radioisotopic determination of l-carnitine content in foods commonly eaten in Western countries". Food Chemistry. 86 (1): 137–142. doi:10.1016/j.foodchem.2003.09.023. 
  27. ^ Bain, Marcus A.; Milne, Robert W.; Evans, Allan M. (2006-10-01). "Disposition and metabolite kinetics of oral L-carnitine in humans". Journal of Clinical Pharmacology. 46 (10): 1163–1170. doi:10.1177/0091270006292851. ISSN 0091-2700. PMID 16988205. 
  28. ^ "Regulations Amending the Food and Drug Regulations". 
  29. ^ FDA approval letter

Further reading[edit]

The following are good secondary sources on the subject of this article.

External links[edit]