Changes of glycogen metabolism in phosphorylcreatine-depleted muscles taken from rats fed with beta-guanidine propionate

Tata, Vincenzo De; Bergamini, Z. Gori; Bergamini, Ettore

doi:10.3109/13813458909075056

Cited by 3 publications

(3 citation statements)

References 24 publications

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“…In line with this, GLUT-4 protein content, a sarcolemmal insulin responsive glucose transporter, increased in 4 studies of which one provided a percentage increase; 45% in type I and 33% in type II fiber predominant muscle [21], [31], [68], [79]. Consequently, studies showed an 94.3% (SD 43.5) increased skeletal muscle glycogen content after βGPA (Figure S1) [25], [26], [33], [37], [68], [80]. Results for plasma glucose were more pronounced in diabetic than non-diabetic animals; fasting glucose levels were decreased by resp.…”

Section: Resultsmentioning

confidence: 66%

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: 66%

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

2013

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“…5, 262, 263, 528, 556, 656, 718, 719, 725, 802, 889, 983, , 1073; an increase in GLUT-4 glucose transporter activity (802); an increase (or decrease?) in hexokinase activity (183,184,262,718,802); a decrease in glycolytic enzymes and lactate content as well as an increase in glycogen content (184,724,802,887,983,1044); a decrease in AMP deaminase protein content and activity which, however, was unrelated to actual IMP production (800, 827); a shift in myosin isoenzyme expression from fast-type myosins to slow-type myosins, coupled with a decreased energy cost of maintaining tension (ϭ higher contractile economy) (3-5, 556, 656, 657, 801); a decrease in CK activity (183,656,718,719,887); an increase in ␤-adrenoceptor density in soleus and extensor digitorum longus muscle (726); a decrease in parvalbumin content (657); as well as an up to 50% decrease in ATP content in fast-twitch muscles (e.g., Refs. 656,724,801,889,983).…”

Section: B Cr Analog Administration As a Means Of Studying Ck Functimentioning

confidence: 99%

Creatine and Creatinine Metabolism

Wyss

Kaddurah‐Daouk

2000

Physiological Reviews

2,423

2,103

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The goal of this review is to present a comprehensive survey of the many intriguing facets of creatine (Cr) and creatinine metabolism, encompassing the pathways and regulation of Cr biosynthesis and degradation, species and tissue distribution of the enzymes and metabolites involved, and of the inherent implications for physiology and human pathology. Very recently, a series of new discoveries have been made that are bound to have distinguished implications for bioenergetics, physiology, human pathology, and clinical diagnosis and that suggest that deregulation of the creatine kinase (CK) system is associated with a variety of diseases. Disturbances of the CK system have been observed in muscle, brain, cardiac, and renal diseases as well as in cancer. On the other hand, Cr and Cr analogs such as cyclocreatine were found to have antitumor, antiviral, and antidiabetic effects and to protect tissues from hypoxic, ischemic, neurodegenerative, or muscle damage. Oral Cr ingestion is used in sports as an ergogenic aid, and some data suggest that Cr and creatinine may be precursors of food mutagens and uremic toxins. These findings are discussed in depth, the interrelationships are outlined, and all is put into a broader context to provide a more detailed understanding of the biological functions of Cr and of the CK system.

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“…In the presence of glucose and ATP, it can make glucose-6-phosphate (via glycolytic metabolism) and increase anaerobic ATP production. However, no significant change in hexokinase II abundance was found in advanced age rat compared to young [39]. More tissue-based model-data are needed to understand the change in ATP production and export in advanced age.…”

Section: Atp Supply In Advanced Agementioning

confidence: 99%

Age-related changes of myocardial ATP supply and demand mechanisms

Yaniv

Juhaszova

Sollott

2013

Trends in Endocrinology & Metabolism

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In advanced age, the resting myocardial oxygen consumption (M V̇O2) and cardiac work (CW) in the rat remain intact. However, M V̇O2, CW and cardiac efficiency achieved at high demand are decreased with age, compared to maximal values in the young. Whether this deterioration is due to decrease in myocardial ATP demand, ATP supply, or the control mechanisms that match them, remains controversial. Here we discuss evolving perspectives of age-related changes of myocardial ATP supply and demand mechanisms, and critique experimental models used to investigate aging. Specifically, we evaluate experimental data collected at the level of isolated mitochondria, tissue, or organism, and discuss how mitochondrial energetic mechanisms change in advanced age, both at basal and high energy demand levels.

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Changes of glycogen metabolism in phosphorylcreatine-depleted muscles taken from rats fed with beta-guanidine propionate

Cited by 3 publications

References 24 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

Creatine and Creatinine Metabolism

Age-related changes of myocardial ATP supply and demand mechanisms

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