Possible role of creatine concentrations in the brain in regulating appetite and weight

Galbraith, Richard A.; Furukawa, Masaru; Li, Muyao

doi:10.1016/j.brainres.2006.05.032

Cited by 31 publications

(19 citation statements)

References 31 publications

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“…In five studies with numerical information on ad libitum food intake, there was no evidence of reduced food intake (data not shown) [12], [20], [35], [56], [60]. One study proposed weight loss due a central hypophagic effect, showing that ßGPA (single intrathecal injection) resulted in a 9-fold increased Fos expression, a measure of hypothalamus activity, in rats [61].…”

Section: Resultsmentioning

confidence: 98%

The Effect of the Creatine Analogue Beta-guanidinopropionic Acid on Energy Metabolism: A Systematic Review

2013

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BackgroundCreatine 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.MethodsWe 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.ResultsAfter 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.ConclusionChronic 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.

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Section: Resultsmentioning

confidence: 98%

The Effect of the Creatine Analogue Beta-guanidinopropionic Acid on Energy Metabolism: A Systematic Review

2013

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“…Weight gain is the only consistent side effect of creatine supplementation and most likely reflects an increase in muscular mass either due to increased muscle protein synthesis or water retention in the initial days 37. Cerebral creatine might also have an effect on appetite47 and growth hormone secretion 48…”

Section: Discussionmentioning

confidence: 99%

Phenotype and genotype in 101 males with X-linked creatine transporter deficiency

et al. 2013

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“…The diverse phenotypic spectrum of neurological symptoms observed in AGAT-, GAMT-and SLC6A8-deficient patients shows the importance of Cr for psychomotor development and cognitive functions and is probably explained by the wide pattern of AGAT, GAMT and SLC6A8 expression in the mammalian brain (see below). The recently proposed roles of Cr as cotransmitter on GABA postsynaptic receptors ) and of regulator of appetite and weight on specific hypothalamic nuclei (Galbraith et al 2006) might also contribute to this phenotypic diversity. The more complex phenotype of GAMT deficiency, including intractable epilepsy, extrapyramidal movement syndromes and abnormalities in basal ganglia is probably due to the toxicity, and particularly the epileptogenic action, of brain GAA accumulation characteristic of GAMT deficiency (Schulze et al 2001), which may occur through activation of GABA A receptors by GAA (Neu et al 2002).…”

Section: Introductionmentioning

confidence: 99%

Creatine deficiency syndromes and the importance of creatine synthesis in the brain

et al. 2011

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Creatine deficiency syndromes, due to deficiencies in AGAT, GAMT (creatine synthesis pathway) or SLC6A8 (creatine transporter), lead to complete absence or very strong decrease of creatine in CNS as measured by magnetic resonance spectroscopy. Brain is the main organ affected in creatine-deficient patients, who show severe neurodevelopmental delay and present neurological symptoms in early infancy. AGAT-and GAMT-deficient patients can be treated by oral creatine supplementation which improves their neurological status, while this treatment is inefficient on SLC6A8-deficient patients. While it has long been thought that most, if not all, of brain creatine was of peripheral origin, the past years have brought evidence that creatine can cross blood-brain barrier, however, only with poor efficiency, and that CNS must ensure parts of its creatine needs by its own endogenous synthesis. Moreover, we showed very recently that in many brain structures, including cortex and basal ganglia, AGAT and GAMT, while found in every brain cell types, are not coexpressed but are rather expressed in a dissociated way. This suggests that to allow creatine synthesis in these structures, guanidinoacetate must be transported from AGAT-to GAMT-expressing cells, most probably through SLC6A8. This new understanding of creatine metabolism and transport in CNS will not only allow a better comprehension of brain consequences of creatine deficiency syndromes, but will also contribute to better decipher creatine roles in CNS, not only in energy as ATP regeneration and buffering, but also in its recently suggested functions as neurotransmitter or osmolyte.

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Possible role of creatine concentrations in the brain in regulating appetite and weight

Cited by 31 publications

References 31 publications

The Effect of the Creatine Analogue Beta-guanidinopropionic Acid on Energy Metabolism: A Systematic Review

The Effect of the Creatine Analogue Beta-guanidinopropionic Acid on Energy Metabolism: A Systematic Review

Phenotype and genotype in 101 males with X-linked creatine transporter deficiency

Creatine deficiency syndromes and the importance of creatine synthesis in the brain

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