PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Creatine pyruvate”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed2001

Neurotoxicity of glutamate uptake inhibition in vivo: correlation with succinate dehydrogenase activity and prevention by energy substrates.

Impairment of glutamate uptake or the reverse action of its transporters has been suggested as the mechanism responsible for the increased glutamate extracellular levels associated with ischemic neuronal damage. In previous studies we have shown that glutamate uptake inhibition by L-trans-pyrrolidine-2,4-dicarboxylate (PDC) in the rat striatum and hippocampus in vivo does not induce neuronal death despite the notable increase in the extracellular levels of glutamate and aspartate. However, PDC intracerebral administration leads to neuronal death in rats chronically injected with the mitochondrial toxin 3-nitropropionic acid (3-NP), an inhibitor of succinate dehydrogenase (SDH). In the present study we have determined the time course of inhibition of SDH activity in the striatum of rats acutely injected with a single dose of 3-NP (20 mg/kg), and studied its relation to PDC neurotoxicity. PDC induced larger lesions when administered during maximum inhibition of SDH activity while smaller lesions were found when it was injected during recovery of enzyme activity. We also studied the neuroprotective effect of different energy substrates such as creatine, pyruvate, and the ketone bodies beta-hydroxybutyrate and acetoacetate in this experimental model. Our results show partial protection with all compounds except for beta-hydroxybutyrate that showed no protection, while MK-801 completely prevented PDC-induced neuronal damage. We believe that the present results might be of relevance for the understanding of the mechanisms responsible for ischemic neuronal death and its prevention.

3-Hydroxybutyric Acid↗
PubMed1994

Fatigue development during electrical stimulation in the masseter muscle of rhesus monkeys (Macaca mulatta).

Fatigue development was investigated in five adult female rhesus monkeys, 9-11 yr old (mean weight, 4.6 kg). After sedation and anaesthesia, silver electrodes were implanted in the anterior and posterior parts of the right masseter; the contralateral muscle was used as a control. The bite force was monitored. Muscle biopsies were obtained from the central part of the masseter and were immediately frozen in liquid nitrogen. After freeze-drying a fluorometric analysis using enzymatic methods for measuring levels of glycogen, glucose, lactate, pyruvate, creatine phosphate, creatine, NADH and NAD was made. The masseters were stimulated for 3 min (100 V, 4 Hz and 2 ms). After a 5-min rest period the stimulation was repeated with the same voltage, frequency and duration. The rhesus monkey masseters were easy to fatigue. After the stimulations 25% of the initial bite force remained. A marked substrate depletion was evident. The precontraction values of glycogen, glucose and phosphocreatine were reduced. The NADH concentration increased and the NAD content decreased. An accumulation of waste products was observed; the pyruvate increased by 92% and the lactate increased by a factor of 3. The substantial substrate depletion in combination with a prominent metabolic waste-product accumulation may induce a decrease in bite-force production.

Animals↗
PubMedDate not supplied

Serum creatine kinase and pyruvate kinase in Duchenne muscular dystrophy carrier detection.

The incidence of elevated serum creatine kinase (CK) and pyruvate kinase (PK) activities was compared in 20 definite carriers of Duchenne muscular dystrophy (DMD), 47 possible carriers, and 42 female controls. When adult age was not regarded as a variable, 70% of the definite carriers had elevated PK, 55% had elevated CK, and 75% had elevated PK or elevated CK or both, 38% of the possible carriers had elevated PK, 19% had elevated CK, and 40% had elevated PK or elevated CK or both. The detection efficiency of the CK test was influenced by the age of the subjects: the upper normal limit of serum CK in the adult controls was at the minimum between 21 and 35 years of age, and CK activity in some carriers declined from elevated to normal levels with increasing age. With these considerations, 70% of definite carriers had elevated CK and 80% had elevated PK and/or CK; 34% of the possible carriers had elevated CK and 43% had elevated PK and/or CK. On the basis of the PK and CK measurements, only 16 of 24 possible carrier mothers were likely to be DMD carriers, implying that the other 8 were non-carrier mothers of new mutant sons.

Adolescent↗
PubMed2003

The effects of ergogenic compounds on myogenic satellite cells.

PURPOSE: A series of studies were conducted in which compounds commonly shown to be ergogenic aids for strength athletes if taken orally were evaluated for their ability to directly induce postnatal muscle stem cell proliferation or differentiation/fusion in vitro. METHODS: Compounds tested were creatine monohydrate, creatine pyruvate, L-glutamine, dehydroepiandrosterone (DHEA), androstenedione, Ma Huang (Ephedra sinensis) extract, and Zhi Shi (Citrus aurantium) extract. Dulbecco's modified eagle medium, supplemented with minimal levels of serum and antibiotics, was used as the initial vehicle for the test compounds. Subsequently, a defined treatment medium termed ITTC was used. Satellite cells were exposed to the test compounds for the indicated times and then evaluated by counting mononucleated and multinucleated (fused) cells. RESULTS: In serum-containing media, none of the treatment groups displayed increased proliferation over that of the control. However, in the differentiation cultures, 0.10% creatine monohydrate increased differentiation over that of the control cultures. When 0.10% creatine monohydrate was added to defined media formulations, all treatments but one demonstrated increased differentiation over the 0.5% serum control. Time course experiments, which followed the effect of 0.10% creatine monohydrate contained in ITTC defined media over 120 h, suggested that cells exposed to this treatment differentiated earlier and to a greater level than cells exposed to ITTC alone. CONCLUSIONS: Creatine in the monohydrate form induced differentiation of myogenic satellite cells. Other agents examined did not increase satellite cell proliferation or differentiation. These results provide initial evidence for a mechanistic understanding of observed effects in vivo of increased muscular size and strength from creatine supplementation.

Analysis of Variance↗
PubMed1993

Recirculating, retrograde heart perfusion according to the Langendorff method for evaluation of MTG--methyl-2-tetradecylglycidate, McNeil 3716--cardiomyopathy.

Recirculating, retrograde heart perfusion according to the Langendorff method was used in an attempt to further elucidate the cardiotoxicity of methyl-2-tetradecylglycidate (McNeil 3716, MTG) and the eccentric hypertrophy elicited by the compound. In subchronic experiments female rats were exposed to MTG 2 x 10 mg/kg and 2 x 25 mg/kg per day for 4 weeks. At various times hearts were perfused ex vivo for up to 2 hr with either 5 mmolar glucose or 0.5 mmolar palmitate as substrate. Substrate uptake (glucose or palmitate) and enzyme release (LDH-lactic dehydrogenase or CPK-creatine-phosphate kinase) were assessed during perfusion. Biochemical analysis (ATP, ADP, AMP, c-AMP, CP, creatine, pyruvate, lactate, glucose-6-phosphate, glycogen, phospholipids, triglycerides and non-esterified fatty acids) were done in hearts before (drug effect) and after perfusion (stress of perfusion). Besides changes in energy metabolism and high-energy phosphate production, as observed in previous experiments (Bachmann et al. 1984) massive changes were seen in energy reserves in heart tissue (ATP, CP, glycogen, phospholipids and triglycerides). As expected, MTG led to significant increases also in non-esterified fatty acids content in hearts.

Adenine Nucleotides↗
PubMed1977

Phosphagen and lactate contents of m. quadriceps femoris of man after exercise.

Muscle biopsies were taken from the m. quadriceps femoris of man immediately after termination of dynamic and isometric exercise. These were analyzed for adenosine triphosphate (ATP), adenosine 5'-diphosphate (ADP), adenosine 5'-phosphate (AMP), phosphorylcreatine (PC), creatine, pyruvate and lactate. Regardless of type, intensity, and duration of the preceding exercise, a general pattern of the relation between high-energy phosphates and lactate content could be observed. PG showed a nonlinear relationship to the muscle lactate content. The ratio of ATP to ADP appeared to decrease linearly when lactate content increased. The relationships are believed to be the consequence of a steady-state condition where muscle pH is one of the major determining factors.

Adenine Nucleotides↗
PubMed2001

Adrenaline increases skeletal muscle glycogenolysis, pyruvate dehydrogenase activation and carbohydrate oxidation during moderate exercise in humans.

1. To evaluate the role of adrenaline in regulating carbohydrate metabolism during moderate exercise, 10 moderately trained men completed two 20 min exercise bouts at 58 +/- 2 % peak pulmonary oxygen uptake (V(O2,peak)). On one occasion saline was infused (CON), and on the other adrenaline was infused intravenously for 5 min prior to and throughout exercise (ADR). Glucose kinetics were measured by a primed, continuous infusion of 6,6-[(2)H]glucose and muscle samples were obtained prior to and at 1 and 20 min of exercise. 2. The infusion of adrenaline elevated (P < 0.01) plasma adrenaline concentrations at rest (pre-infusion, 0.28 +/- 0.09; post-infusion, 1.70 +/- 0.45 nmol l(-1); means +/- S.E.M.) and this effect was maintained throughout exercise. Total carbohydrate oxidation increased by 18 % and this effect was due to greater skeletal muscle glycogenolysis (P < 0.05) and pyruvate dehydrogenase (PDH) activation (P < 0.05, treatment effect). Glucose rate of appearance was not different between trials, but the infusion of adrenaline decreased (P < 0.05, treatment effect) skeletal muscle glucose uptake in ADR. 3. During exercise muscle glucose 6-phosphate (G-6-P) (P = 0.055, treatment effect) and lactate (P < 0.05) were elevated in ADR compared with CON and no changes were observed for pyruvate, creatine, phosphocreatine, ATP and the calculated free concentrations of ADP and AMP. 4. The data demonstrate that elevated plasma adrenaline levels during moderate exercise in untrained men increase skeletal muscle glycogen breakdown and PDH activation, which results in greater carbohydrate oxidation. The greater muscle glycogenolysis appears to be due to increased glycogen phosphorylase transformation whilst the increased PDH activity cannot be readily explained. Finally, the decreased glucose uptake observed during exercise in ADR is likely to be due to the increased intracellular G-6-P and a subsequent decrease in glucose phosphorylation.

Adult↗
PubMed1990

[Study of metabolic myopathies using 1H NMR spectroscopy--analysis of muscle metabolites and muscle autolytic change].

Muscle metabolites of perchloric acid extracts were analyzed using 1H NMR spectroscopy. Several metabolites including lactate, pyruvate, creatine, phosphocreatine, carnitine, acetate and alanine were easily recognized. Muscles frozen with isopentane cooled by liquid nitrogen did not show any significant differences from those directly frozen by liquid nitrogen regarding the contents of metabolites, however moderate delay until freezing the muscle specimens produced considerable biochemical changes. In human application using the biopsied muscle of the patient with myophosphorylase deficiency, in vitro anaerobic glycolysis experiments clearly detects the defect in glycolytic pathway by 1H NMR spectroscopy, revealing the abnormal lactate production blocked between glycogen and glucose-1-phosphate. These data suggests that 1H NMR spectroscopy is useful for analysis of metabolic myopathies.

Anaerobiosis↗
PubMed2004

Phosphorylated derivatives that activate or inhibit mammalian adenosine kinase provide insights into the role of pentavalent ions in AK catalysis.

The enzyme adenosine kinase (AK) exhibits a nearly complete dependency on the presence of pentavalent ions (PVI) such as phosphate, arsenate, and vanadate. To understand its basis, the effect of a large number of phosphorylated compounds on AK activity was examined. Several compounds, such as phosphoribosyl pyrophosphate, phosphoenol pyruvate, creatine phosphate, phosphorous acid, phosphonoformic acid, and inorganic pyrophosphate, were found to substitute for PVI in stimulating AK activity. Similar to PVI, these compounds lowered the Km of AK for adenosine. In contrast, many other structurally related compounds (i.e., phosphonoacetic acid, 2-carboxyethyl phosphonic acid, N-phosphonomethyl glycine, N-phosphonomethyl iminodiacetic acid) inhibited AK activity. These compounds seemed to compete with the activators for binding to AK. Structural comparisons of different compounds indicate that all activating compounds contain a net positive charge on the pentavalent atom (e.g., phosphorous), which should enable it to act as an acceptor for a nucleophilic group. We suggest that a phosphate (or other activator) bound near the active site participates in AK catalysis by forming a transient pentavalent intermediate with a nonbridging oxygen of the beta-phosphate in ATP. This interaction likely facilitates the transfer of gamma-phosphate from ATP to adenosine, thus accounting for the stimulating role of PVI in AK catalysis. The insight provided by these studies concerning the structural features of activators and inhibitors should also prove helpful in the design of more potent inhibitors of AK.

Adenosine Kinase↗
PubMed2001

Dietary supplements: how they are used and regulated.

Overall use of nutrient and botanical dietary supplements (DS) has increased for years across all major categories. Many DS are simply taken as part of a healthy lifestyle, but some are used to reduce risk of or modulate risk factors for specific chronic diseases, such as heart disease (vitamin E, folic acid, garlic), cancer (selenium, vitamin E, garlic) and certain birth defects (folic acid). Other DS are used for short-term benefits such as sleep management (valerian, melatonin) and enhanced physical performance (pyruvate, creatine). DS are regulated under food law, but with certain provisions that apply only to DS. Thus, DS are eligible for Food and Drug Administration (FDA)-authorized health claims under the Nutrition and Labeling Education Act (NLEA). Health claims have already been authorized for folic acid and calcium, but not for several others. In 1994, when the Dietary Supplement Health and Education Act (DSHEA) was passed, it expanded and clarified the definition of DS, specified additional requirements for safety and provided for four types of claims of nutritional support. These include prevention of classic nutritional deficiencies, structure or function (S/F) effects, mechanisms for S/F effects and general well-being. Although S/F effects result from both foods and drugs, representation that a product will treat, cure, mitigate or diagnose a disease is reserved for drugs. Therefore, the wording of S/F claims for DS has become a difficult issue in the proposed DS labeling regulations.

Consumer Product Safety↗
PubMed1983

Energy levels at systole vs. diastole in normal hamster hearts vs. myopathic hamster hearts.

The following studies were carried out to examine energy metabolites and cardiac performance of the failing heart (hereditary cardiomyopathy) of the Syrian hamster (strain UM-X7.1) perfused either by normal or stress conditions, and to determine whether cyclical changes in energy-related metabolites occurred in the glucose-perfused hearts of both normal and heart failure animals. Hamster hearts from 250-day-old animals with moderate heart failure were removed and perfused either as nonworking hearts (Langendorff method, an afterload pressure of 90 mm Hg and 2.5 mM calcium in the perfusate) or as working hearts with stress conditions [an afterload of 110 mm Hg, high calcium concentrations in the perfusate (3.5 mM), and 10(-8) M isoproterenol]. Mechanical parameters (developed pressure and max dP/dt) and measurements of oxygen consumption indicated that both contractility and oxygen consumption had fallen 50% in myopathic hearts, compared with those of normal hamsters perfused with either of the two conditions. By means of a specially designed stimulator-triggered freeze clamp, hearts were terminated at systole and diastole, and tissue content of ATP, ADP, AMP, adenosine, phosphocreatine, creatine, pyruvate, lactate, and inorganic phosphate were analyzed. A 50% reduction in cardiac performance of the cardiomyopathic hamster hearts was associated with a corresponding reduction in systolic ATP, adenosine, and phosphocreatine values, while inorganic phosphate and lactate increased. With glucose as the sole substrate, the high energy phosphates, ATP and phosphocreatine, reached maximum values during diastole and minimum values during systole.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1991

[Study of human muscle biopsies with muscle glycogen storage diseases using 1H nuclear magnetic resonance spectroscopy (NMRS)--analysis of perchloric acid extracts of muscles].

Muscle metabolites of perchloric acid extracts in human muscle biopsies including the cases with muscle glycogen storage diseases (GSD) were analyzed using 1H NMR spectroscopy. Several metabolites such as lactate, pyruvate, creatine, phosphocreatine, acetate, alanine, carnitine and glycogen were recognized. The cases with GSD III and GSD V showed two broad signals at 3.60 and 3.85 ppm which were considered to be the proton signals from the accumulated glycogen. However, in GSD III, the signal at 3.60 ppm was high compared with that at 3.85 ppm suggesting that glycogen was increased in its degree of branching joined by alpha-1,6 linkage. These data suggest that 1H NMR spectroscopy is a useful and simple technique for analysis of muscle glycogen storage diseases as well as lipid myopathies.

Adult↗
PubMed1989

Blood-flow and metabolic response in a contracting canine masticatory muscle.

The mechanical and metabolic characteristics of the canine masseter muscle of seven adult dogs, aged 3 years, weighing 45-55 kg, were evaluated by electrically provoked contractions. The masseter muscle was exposed by careful surgery and stimulated by two silver electrodes placed in the anterior and posterior aspects of the muscle. The bite force was measured with a force transducer. Glycogen, glucose-contents together with lactate, pyruvate, creatine phosphate, NADH and NAD were analysed fluorimetrically. Intra-muscular oxygen tension was continuously recorded by a flexible silver electrode. Blood-flow was measured by the 133Xenon clearance technique. Biopsies were taken at rest and after stimulation. The registered bite force revealed an initial peak, representing maximal force production and thereafter a rapid decline in power output. During the following stimulation events the bite force curve showed decrease in amplitude concerning maximal force as well as duration of bite force production. The blood-flow and oxygen tension were significantly reduced at the end of stimulation. However, after recovery these parameters were normalised to initial values. The glycogen and glucose were depleted after stimulation. The lactate concentration increased about three to four times. The observed changes in NAD and NADH indicate a hypoxic situation in the muscle cells. The oxygen deficit in conjunction with the intramuscular blood-flow impairment and the metabolite variations reflect the energy and redox state in the muscle and may contribute to the decline in bite force production.

Animals↗
PubMed1990

The theory of diazymes and functional coupling of pyruvate kinase and creatine kinase.

The physical-chemical principles governing the interactions of enzymes having common metabolic products are presented. Methods for comparing the dissociation rates of the metabolic product and the rates of enzyme-enzyme interaction are given. Using muscle pyruvate kinase (PK) and creatine kinase (CK) as an example, it is shown that the probability of forming an enzyme-product-enzyme complex is much greater than the rate of ATP dissociation from either enzyme. Experimental evidence using 31P-NMR demonstrates that in the presence of both pyruvate kinase and creatine kinase, there is exchange of phosphate between phosphocreatine and phosphoenolpyruvate without a change in the intermediate, ATP. This confirms the formation of a PK.ATP.CK complex in an aqueous solution without enzyme attachment to a substructure. Enzymes capable of forming these mobile clusters are defined as diazymes, and the criteria for their formation are given. The metabolic implications of diazymes are discussed.

Adenosine Diphosphate↗
PubMed1982

Duchenne muscular dystrophy carrier detection using logistic discrimination: serum creatine kinase, hemopexin, pyruvate kinase, and lactate dehydrogenase in combination.

In the absence of an unambiguous test for identifying Duchenne muscular dystrophy (DMD) heterozygotes, methods are needed for combination of the results of individually equivocal tests as effectively and rationally as possible. Tw used logistic discrimination to assess the effectiveness of measurements of serum creatine kinase, hemopexin, pyruvate kinase, and lactate dehydrogenase alone and in various combinations in identifying DMD carriers. We analyzed 127 serum samples from 63 normal female controls (20-40 years old) and 67 from 38 obligate DMD carriers. The best two tests to use in combination were creatine kinase and hemopexin, and these two, with lactate dehydrogenase, were the best three. t the 95% level (with 5% of controls misclassified), 54% of the carriers were identified by CK alone, whereas 88% were identified by means of the four tests. Although a small proportion of known carriers still cannot be identified, application of the four tests to a group of 45 possible carrier mothers of isolated cases of DMD resolves the population into fairly discrete "normal" and "abnormal" subgroups. Thus, if bias of selection can be eliminated, application of logistic discrimination may permit a direct estimate of the proportion of mothers of affected boys who are homozygous normal.

Adult↗
PubMed1991

Estimate of the intrafamilial correlation for serum creatine kinase and pyruvate kinase in females at risk for Duchenne and Becker muscular dystrophies.

In order to verify the possibility of nonrandom X-inactivation in females heterozygous for Duchenne (DMD) and Becker (BMD) muscular dystrophies, intrafamilial correlations and the heritabilities for serum creatine kinase (CK) and pyruvate kinase (PK) were estimated in a large sample of females belonging to families with affected patients. The results of the present investigation suggest that the apparent intrafamilial correlations for serum CK reported in previous studies in DMD families are not related with the presence of the DMD/BMD gene. Our data do not seem to support the hypothesis of a gene leading to a preferential inactivation of the X-chromosome in females at risk for the dystrophin gene.

Adolescent↗