The effect of the creatine analogue beta-guanidinopropionic acid on energy metabolism: a systematic review

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#administration-oral #animals #brain #cardiovascular-system #creatine-kinase

The effect of the creatine analogue beta-guanidinopropionic acid on energy metabolism: a systematic review

Oudman et al., 2013 | PLoS One | Systematic Review

Citation

Oudman Inge, Clark Joseph F, Brewster Lizzy M. The effect of the creatine analogue beta-guanidinopropionic acid on energy metabolism: a systematic review. PLoS One. 2013;8(1):e52879. doi:10.1371/journal.pone.0052879

Abstract

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.

Key Findings

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 fati

Outcomes Measured

  • Requires manual extraction

Population

Field Value
Population See abstract
Sample Size See abstract
Age Range See abstract
Condition See abstract

MeSH Terms

  • Administration, Oral
  • Animals
  • Brain
  • Cardiovascular System
  • Creatine Kinase
  • Energy Metabolism
  • Guanidines
  • Humans
  • Muscle, Skeletal
  • Propionates

Evidence Classification

  • Level: Systematic Review
  • Publication Types: Journal Article, Research Support, Non-U.S. Gov't, Systematic Review
  • Vertical: creatine

Provenance

Source extracted via PubMed E-utilities API on 2026-04-09