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Guanidinoacetic acid in health, sport and exercise
Published in Jay R Hoffman, Dietary Supplementation in Sport and Exercise, 2019
Introduced to medicine and human nutrition approximately 70 years ago by Dr. Henry Borsook from Caltech, guanidinoacetic acid (GAA, also known as glycocyamine, betacyamine or N-amidinoglycine) still drives scientific attention as an intriguing energy-boosting supplement in both athletic and clinical environments. Despite the fact that GAA has been used as a dietary supplement many years before its well-known complement creatine, it still remains far less described in terms of effectiveness and safety, with only two dozen studies evaluating GAA applicability in humans. Nevertheless, recent research has evoked interest for this long-forgotten supplement, with GAA re-appearing as a potent energy-stimulating agent, consumed either as a sole preparation or co-administered with other nutrients. This chapter provides an update on GAA pharmacology, efficacy and safety in medicine, sport and exercise and an overview of possible advanced formulas that contain GAA.
Benefits and drawbacks of guanidinoacetic acid as a possible treatment to replenish cerebral creatine in AGAT deficiency
Published in Nutritional Neuroscience, 2019
GAA (otherwise known as glycocyamine) is further converted to creatine in the second step of the process.2 Hence, AGAT deficiency is characterized by low brain levels of both GAA and creatine, accompanied by mild to moderate intellectual disability, delayed speech development and motor skills, and myopathy.3 Although this disorder has been identified in only a few families,4 severe features of AGAT deficiency require well-targeted treatment protocols to restore brain creatine levels. Traditional management of AGAT deficiency entails long-term oral creatine monohydrate administration (100–800 mg/kg/day) that results in almost complete restoration of brain creatine levels and improvement of clinical characteristics. However, creatine treatment might be somewhat limited due to possible shortcomings in performance and transport of creatine to the brain, at least in some cases of AGAT deficiency.4 Recent studies reported superiority of supplemental GAA vs. creatine to improve brain creatine levels in Yucatan miniature pigs5 and healthy humans,6 suggesting GAA as a possible alternative to creatine to tackle brain creatine levels even in clinical environment. This paper discusses advantages and disadvantages of GAA as a possible treatment to replenish brain creatine levels in AGAT deficiency.
Fabrication of an improved amperometric creatinine biosensor based on enzymes nanoparticles bound to Au electrode
Published in Biomarkers, 2019
Parveen Kumar, Mohit Kamboj, Ranjana Jaiwal, C.S. Pundir
Creatinine (2-amino-1-methyl-5H-imidazol-4-one) is the final result of creatine metabolism, which is present in human blood and expelled from the blood eminently by the kidneys, primarily by glomerular filtration. Creatine is produced mainly in the liver from methylation of glycocyamine. Creatine, at that point is transferred to various organs such as muscles, brain and get phosphorylated to form high energy compound such as phosphocreatine. Creatinine is synthesised in this reaction as a byproduct (Taylor 1989). The concentration of creatinine in blood sera and urine of a healthy person is 45–140 μM and 0.8–2.0 g/day respectively (Kumar et al.2017). Creatinine level is higher in men comparable to women due to its high muscles mass.