The role of dietary creatine
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The daily requirement of a 70-kg male for creatine is about 2 g; up to half of this may be obtained from a typical omnivorous diet, with the remainder being synthesized in the body Creatine is a carninutrient, which means that it is only available to adults via animal foodstuffs, principally skeletal muscle, or via supplements. Infants receive creatine in mother’s milk or in milk-based formulas. Vegans and infants fed on soy-based formulas receive no dietary creatine. Plasma and muscle creatine levels are usually somewhat lower in vegetarians than in omnivores. Human intake of creatine was probably much higher in Paleolithic times than today; some groups with extreme diets, such as Greenland and Alaskan Inuit, ingest much more than is currently typical. Creatine is synthesized from three amino acids: arginine, glycine and methionine (as S-adenosylmethionine). Humans can synthesize sufficient creatine for normal function unless they have an inborn error in a creatine-synthetic enzyme or a problem with the supply of substrate amino acids. Carnivorous animals, such as lions and wolves, ingest much larger amounts of creatine than humans would. The gastrointestinal tract and the liver are exposed to dietary creatine in higher concentrations before it is assimilated by other tissues. In this regard, our observations that creatine supplementation can prevent hepatic steatosis (Deminice et al. J Nutr 141:1799–1804, 2011) in a rodent model may be a function of the route of dietary assimilation. Creatine supplementation has also been reported to improve the intestinal barrier function of the rodent suffering from inflammatory bowel disease.
KeywordsCreatine synthesis Creatine kinase Steatohepatitis Paleolithic diet Intestinal barrier function
Hypoxia inducible transcription factor
This work was supported by Grants from the Canadian Institutes of Health Research (RNL 119957) and the Research Development Corporation (5404-1433-101. We thank Dr. Jennifer R. Stevens for assistance with the figures.
Compliance with ethical standards
Conflict of interest
The authors declare that they have no conflict of interest.
This article is a review summarizing the results and conclusions of published studies on human or animal subjects. All of the work carried out in our laboratories was approved by our local Ethics Committees.
- Carducci C, Birarelli M, Leuzzi V, Carducci C, Battini R, Cioni G, Antonozzi I (2002) Guanidinoacetate and creatine plus creatinine assessment in physiologic fluids: and effective diagnostic tool for the biochemical diagnosis of arginine:glycine amidinotransferase and guanidinoacetate methyltransferase deficiencies. Clin Chem 48:1772–1778PubMedGoogle Scholar
- Glover LE, Bowers BE, Saeedi B, Ehrentraut SF, Campbell EL, Bayless AJ, Dobrinskikh E, Kendrick AA, Kelly CJ, Burgess A, Miller L, Kominsky DJ, Jedlicka P, Colgan SP (2013) Control of creatine metabolism by HIF is an endogenous mechanism of barrier regulation in colitis. Proc Natl Acad Sci USA 110:19820–19825CrossRefPubMedPubMedCentralGoogle Scholar
- Kazak L, Chouchani ET, Jedrychowski MP, Erickson BK, Shinoda K, Cohen P, Vetrivelan R, Lu GZ, Laznik-Bogoslavski D, Hasenfuss SC, Kajimura S, Gygi SP, Spiegelman BM (2015) A creatine-driven substrate cycle enhances energy expenditure and thermogenesis in beige fat. Cell 163:643–655CrossRefPubMedGoogle Scholar
- Nabuurs CI, Choe CU, Veltien A, Kan HE, van Loon LJC, Rodenburg RJT, Matschke J, Wieringa B, Kemp GJ, Isbrandt D, Heerschap A (2013) Disturbed energy metabolism and muscular dystrophy caused by pure creatine deficiency are reversible by creatine intake. J Physiol 591:571–592CrossRefPubMedGoogle Scholar
- Peters BA, Hall MN, Liu X, Parvez F, Siddique AB, Shahriar H, Uddin MN, Islam T, Ilievski V, Graziano JH, Gamble MV (2015) Low-dose creatine supplementation lowers plasma guanidinoacetate, but not plasma homocysteine, in a double-blind, randomized, placebo-controlled trial. J Nutr 145:2245–2252CrossRefPubMedGoogle Scholar
- Petr M, Ŝteffl M, Kohliková E (2013) Effect of the MTHFR 677C/T polymorphism on homocysteinemia in response to creatine supplementation: a case study. Physiol Rev 62:721–729Google Scholar
- Schulze A, Battini R (2007) Pre-symptomatic treatment of creatine biosynthesis defects. In: Salomons GS, Wyss M (eds) Creatine and creatine kinase in health and disease. Springer, New YorkGoogle Scholar
- Sykut-Cegielska J, Gradowska W, Mercimek-Mahmutoglu S, Stӧckler-Ipsiroglu S (2004) Biochemical and clinical characteristics of creatine deficiency syndromes. Acta Biochim Polonica 51:875–882Google Scholar