The effect of the creatine analogue beta-guanidinopropionic acid on energy metabolism: a systematic review
Oudman I, Clark JF, Brewster LM
PloS one · 76 citas
Cómo se estudió
- Diseño
- Revisión sistemática (indexado por PubMed)
- Estudiado en
- Animales
- Resultado principal
- Marcadores de salud y funcionamiento
Quién lo pagó
- Financiación
- Financiación independiente
- Gobierno
- Nederlandse Organisatie voor Wetenschappelijk Onderzoek
Según 1 financiador declarado y la declaración de financiación del texto completo.
Publicación
- Publicado
- 2013-01-09 · PLoS One · vol. 8 · número 1 · pág. e52879
- Editorial
- Public Library of Science
- Citado
- 86 citas · más que el 64% de estudios similares · 0.8× el promedio de su campo
- Referencias
- 157 trabajos
- Acceso
- Acceso abierto (revista) · CC-BY
- Áreas de investigación
- Muscle metabolism and nutrition · Biochemical effects in animals · Mitochondrial Function and Pathology
- Palabras clave
- beta-guanidinopropionic acid, creatine kinase, energy metabolism, skeletal muscle fatigue, cardiac contractility, brain energy metabolism, phosphocreatine depletion
- MeSH
- muscle, skeletal, cardiovascular system, brain, animals, humans, guanidines, propionates, creatine kinase, administration, oral, energy metabolism
3 autores
- Inge Oudman🇳🇱 · autor de correspondenciaAmsterdam UMC Location University of Amsterdam
- Joseph F. Clark🇺🇸University of Cincinnati
- Lizzy M. Brewster🇳🇱Amsterdam UMC Location University of Amsterdam
Resumen
El texto original del estudio, en el idioma en que se publicó.
Background
Creatine kinase plays a key role in cellular energy transport. The enzyme transfers high-energy phosphoryl groups from mitochondria to subcellular sites of ATP hydrolysis, where it buffers ADP concentration by catalyzing the reversible transfer of the high-energy phosphate moiety (P) between creatine and ADP. Cellular creatine uptake is competitively inhibited by beta-guanidinopropionic acid. This substance is marked as safe for human use, but the effects are unclear. Therefore, we systematically reviewed the effect of beta-guanidinopropionic acid on energy metabolism and function of tissues with high energy demands.
Methods
We performed a systematic review and searched the electronic databases Pubmed, EMBASE, the Cochrane Library, and LILACS from their inception through March 2011. Furthermore, we searched the internet and explored references from textbooks and reviews.
Results
After applying the inclusion criteria, we retrieved 131 publications, mainly considering the effect of chronic oral administration of beta-guanidinopropionic acid (0.5 to 3.5%) on skeletal muscle, the cardiovascular system, and brain tissue in animals. Beta-guanidinopropionic acid decreased intracellular creatine and phosphocreatine in all tissues studied. In skeletal muscle, this effect induced a shift from glycolytic to oxidative metabolism, increased cellular glucose uptake and increased fatigue tolerance. In heart tissue this shift to mitochondrial metabolism was less pronounced. Myocardial contractility was modestly reduced, including a decreased ventricular developed pressure, albeit with unchanged cardiac output. In brain tissue adaptations in energy metabolism resulted in enhanced ATP stability and survival during hypoxia.
Conclusion
Chronic beta-guanidinopropionic acid increases fatigue tolerance of skeletal muscle and survival during ischaemia in animal studies, with modestly reduced myocardial contractility. Because it is marked as safe for human use, there is a need for human data.
Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial (CC BY).
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