Creatine
From Wikipedia, the free encyclopedia
| Creatine | |
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| Chemical name | 2-(carbamimidoyl-methyl- amino)acetic acid |
| Synonyms | (α-methylguanido)acetic acid Creatin Kreatin methylguanidinoacetic acid N-amidinosarcosine |
| Chemical formula | C4H9N3O2 |
| Molecular mass | 131.13 g/mol |
| CAS number | [57-00-1] |
| EINECS number | 200-306-6 |
| Melting point | dec. at 303 °C |
| SMILES | CN(CC(=O)O)C(=N)N |
| Disclaimer and references | |
Creatine is a nitrogenous organic acid that naturally occurs in vertebrates and helps to supply energy to muscle cells. Creatine was identified in 1832 when Michel Eugène Chevreul discovered it as a component of skeletal muscle which he later named creatine after the Greek word for flesh, Kreas.
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[edit] Function
Creatine (by way of conversion to and from creatine phosphate) functions as part of a system based on arginine/phosphoarginine that operates in many invertebrates. The presence of this energy shuttle keeps the ATP/ADP ratio high which ensures that the free energy of ATP remains high and minimizes the loss of adenosine nucleotides, which would cause cellular dysfunction. Such high energy phosphate buffers are known as phosphagens.
[edit] Synthesis
In the human body, creatine is synthesized mainly in the liver by the use of parts from three different amino acids - arginine, glycine, and methionine. 95% of it is later stored in the skeletal muscles, with the rest in the brain, heart, and testes.
Arg - Arginine; GAMT - Guanidinoacetate N-methyltransferase; GAMT - Glycine amidinotransferase; Gly - Glycine; Met - Methionine; SAH - S-adenosyl homocysteine; SAM - S-adenosyl methionine.
The enzyme GAMT [guanidinoacetate N-methyltransferase, also known as L-arginine:glycine amidinotransferase (AGAT), EC 2.1.4.1], is a mitochondrial enzyme responsible for catalyzing the first rate-limiting step of creatine biosynthesis, and is primarily expressed in the kidneys.
The second enzyme in the pathway (GAMT, guanidinoacetate N-methyltransferase, EC:2.1.1.2) is primarily expressed in the liver.
Genetic deficiencies in the creatine biosynthetic pathway lead to various severe neurological defects.
[edit] Sources
In humans, typically half of stored creatine originates from food (mainly from meat and fish). However, endogenous synthesis of creatine in the liver is sufficient for normal activities. This is evidenced by the fact that, even though vegetables do not contain creatine, vegetarians do not suffer from creatine deficiency.[citation needed] Vegetarian creatine can be obtained via chemical synthesis using plant-derived amino acids.
[edit] Creatine and the treatment of muscular diseases
Creatine supplementation has been, and continues to be, investigated as a possible therapeutic approach for the treatment of muscular, neurological and neuromuscular diseases (arthritis, congestive heart failure, disuse atrophy, gyrate atrophy, McArdle's disease, Huntington's disease, miscellaneous neuromuscular diseases, mitochondrial diseases, muscular dystrophy, neuroprotection, etc.).
Two scientific studies have indicated that creatine may be beneficial for neuromuscular disorders. First, a study (Klivenyi et al. 1999) by MDA-funded researcher M. Flint Beal of Cornell University Medical Center demonstrated that creatine was twice as effective as the prescription drug riluzole in extending the lives of mice with the degenerative neural disease amyotrophic lateral sclerosis (ALS, or Lou Gehrig's disease). Beal suspects that the neuroprotective effects of creatine in the mouse model of ALS are due either to an increased availability of energy to injured nerve cells or to a blocking of the chemical pathway that leads to cell death.
Second, a study by Canadian researchers Mark Tarnopolsky and Joan Martin of McMaster University Medical Centre in Hamilton, Ontario found that creatine can cause modest increases in strength in people with a variety of neuromuscular disorders. The latter paper was published in the March 1999 issue of Neurology.
[edit] Creatine as a diagnostic of kidney function
Hospitals and doctors routinely measure blood creatinine levels to determine kidney function. Creatine is broken down to creatinine, which is eliminated through the kidneys; if kidney function is impaired, creatinine levels will rise.
[edit] See also
- Acetyl-L-carnitine
- Adenosine triphosphate (ATP)
- Citric acid cycle (Krebs cycle)
- Creatine Ethyl Ester
- Coenzyme Q10
- Idebenone
- Lipoic acid
- Pyritinol
- Vitamin B5
- Nitric oxide
- Links to external chemical sources
[edit] References
- Burke DG, Chilibeck PD, Parise G, Tarnopolsky MA, Candow DG. (2003). "Effect of alpha-lipoic acid combined with creatine monohydrate on human skeletal muscle creatine and phosphagen concentration.". Int J Sport Nutr Exerc Metab. Sep (13). PMID 14669930. .
- Dangott B, Schultz E, Mozdziak PE. (2000). "Dietary creatine monohydrate supplementation increases satellite cell mitotic activity during compensatory hypertrophy". International Journal of Sports Medicine 2000 Jan (21(1):): 13-6. PMID 10683092. .
- Hespel P, Op't Eijnde B, Van Leemputte M, Urso B, Greenhaff PL, Labarque V, Dymarkowski S, Van Hecke P, Richter EA. (2001). "Oral creatine supplementation facilitates the rehabilitation of disuse atrophy and alters the expression of muscle myogenic factors in humans". J Physiol. 2001 Oct 15 (536(Pt 2)): 625-33. PMID 11600695. .
- Hultman E, Soderlund K, Timmons JA, et al. (1996). "Muscle creatine loading in men.". J Appl Physiol (81): 232-237. PMID 8828669. .
- Juhn MS. (2003). "Popular sports supplements and ergogenic aids". Sports Med. 33 (2): 921-39. PMID 12974658.
- Klivenyi P, Ferrante RJ, Matthews RT, Bogdanov MB, Klein AM, Andreassen OA, Mueller G, Wermer M, Kaddurah-Daouk R, Beal MF. (mar 1999). "Neuroprotective effects of creatine in a transgenic animal model of amyotrophic lateral sclerosis.". Nature Medicine. 5 (3): 347-350. PMID 10086395. .
- Powers ME et al. (2003). "Creatine Supplementation Increases Total Body Water Without Altering Fluid Distribution". Journal of Athletic Training 38 (1): 44-50. PMID 12937471. .
- Rae C, Digney AL, McEwan SR, Bates TC. (2003). "Oral creatine monohydrate supplementation improves cognitive performance; a placebo-controlled, double-blind cross-over trial.". Proceedings of the Royal Society of London - Biological Sciences 270 (1529): 2147-2150. PMID 14561278. .
- Robinson TM et al. (2000). "Dietary creatine supplementation does not affect some haematological indices, or indices of muscle damage and hepatic and renal function". British Journal of Sports Medicine 34: 284-288. PMID 10953902. .
- Schroeder C et al. (2001). "The effects of creatine dietary supplementation on anterior compartment pressure in the lower leg during rest and following exercise". Clin J Sport Med. 11 (2): 87-95. PMID 11403120.
[edit] External links
- NCBI Online Mendelian Inheritance In MAN (OMIM) GATM human mutation record
- Quackwatch on creatine
- BBC News - Creatine 'boosts brain power'
- Review article on creatine's function in the neurological context (from the Science Creative Quarterly)
