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PubMed2004

Blood-to-retina transport of creatine via creatine transporter (CRT) at the rat inner blood-retinal barrier.

The purpose of this study was to elucidate the mechanisms of blood-to-retina creatine transport across the blood-retinal barrier (BRB) in vivo and in vitro, and to identify the responsible transporter(s). The creatine transport across the BRB in vivo and creatine uptake in an in vitro model of the inner BRB (TR-iBRB2 cells) were examined using [(14)C]creatine. Identification and localization of the creatine transporter (CRT) were carried out by RT-PCR, western blot, and immunoperoxidase electron microscopic analyses. An in vivo intravenous administration study suggested that [(14)C]creatine is transported from the blood to the retina against the creatine concentration gradient that exists between the retina and blood. [(14)C]Creatine uptake by TR-iBRB2 cells was saturable, Na(+)- and Cl(-)-dependent and inhibited by CRT inhibitors, suggesting that CRT is involved in creatine transport at the inner BRB. RT-PCR and western blot analyses demonstrated that CRT is expressed in rat retina and TR-iBRB2 cells. Moreover, using an immunoperoxidase electron microscopic analysis, CRT immunoreactivity was found at both the luminal and abluminal membranes of the rat retinal capillary endothelial cells. In conclusion, CRT is expressed at the inner BRB and plays a role in blood-to-retina creatine transport across the inner BRB.

Animals↗
PubMed1994

Comparison of the value of novel rapid measurement of myoglobin, creatine kinase, and creatine kinase-MB with the electrocardiogram for the diagnosis of acute myocardial infarction.

OBJECTIVE: To determine whether serum myoglobin, creatine kinase, and creatine kinase-MB measured at admission by rapid, compact, and easy to use automated quantitative analysers (results within 10 min) helped the early identification of acute myocardial infarction. The results were compared with the data obtained from the electrocardiograms recorded at admission. DESIGN: A prospective study. SETTING: Coronary care unit. PATIENTS: 94 consecutive patients with suspected myocardial infarction. Myocardial infarction was subsequently confirmed in 44 patients and excluded in 50. METHODS: All admission serum myoglobin, creatine kinase, and creatine kinase-MB were measured by clinical staff using analysers in the coronary care unit. An admission electrocardiogram was obtained from all patients. RESULTS: The sensitivity, specificity, and predictive accuracy for diagnosing myocardial infarction were: electrocardiogram 68%, 100%, and 85%; myoglobin 57%, 100%, and 80%; creatine kinase (threshold of 190 U/l) 34%, 98%, and 68%; creatine kinase-MB (threshold of 25 U/l) 43%, 100%, and 73%. When the electrocardiographic and myoglobin data were combined the sensitivity improved to 91%, diagnostic accuracy to 96%, with specificity of 100%. The results for the electrocardiogram and creatine kinase-MB were 80%, 90%, 100% respectively and those for the electrocardiogram with creatine kinase were 80%, 89%, 98% respectively. CONCLUSIONS: Admission myoglobin, creatine kinase, and creatine kinase-MB measurements were not as useful as the electrocardiogram for the diagnosis of acute myocardial infarction. Combining the electrocardiogram and myoglobin data substantially improved the sensitivity and predictive accuracy for the diagnosis of acute myocardial infarction.

Blood Chemical Analysis↗
PubMed1986

The isoelectric focusing of creatine kinase variants: I. The heterogeneity of creatine kinase in human heart cytosol and mitochondria.

Creatine kinase isoenzymes in cytosolic and mitochondrial fractions from human cardiac tissues were studied by analytical and preparative isoelectric focusing (IEF), electrophoresis and immunoinhibition. Analytical IEF on agarose gels revealed many creatine kinase variants in human cardiac cytosol prepared by extraction with a hypotonic medium. The bands located at approximately pH 5.5 were shown to contain creatine kinase-MB and minute creatine kinase-BB bands by electrophoresis. Two bands which focused closely together in IEF (pH 6.85-7.0) showed an electrophoretic migration pattern similar to creatine kinase-MM. One of them (IP 6.85) showed a complete inhibition by anti-creatine kinase-M antibodies, whereas the other showed only 50% inhibition. Increasing the salt concentration of tris-HCl (0.1 mol/l) in the extraction medium resulted in additional creatine kinase variants. They were characterized by high alkaline isoelectric points and were not inhibited by anti-creatine kinase-M antibodies. These variants corresponded to two cathodic bands in electrophoresis. The treatment of washed mitochondria with phosphate buffer resulted in a release of mitochondrial variants with different isoelectric points, as shown by analytical IEF in agarose gels. The same pattern was obtained by using preparative IEF. Variants with high alkaline isoelectric points gave rise to two cathodic bands upon electrophoresis. These two bands resembled those present in cytosol after extraction with high salt concentration. No complete inhibition with anti-creatine kinase-M was observed in any of the eluates. The mitochondrial variants exhibited different affinities towards creatine phosphate and ADP. Variants with higher alkaline isoelectric points showed lower Km-values for these substrates than those with less alkaline isoelectric points.

Creatine Kinase↗
PubMed2005

Effect of a defined lacto-ovo-vegetarian diet and oral creatine monohydrate supplementation on plasma creatine concentration.

This study examined the effects that preceding creatine supplementation with a lacto-ovo-vegetarian diet would have on plasma creatine concentration. Twenty-six healthy moderately fit omnivorous men were assigned to either a 26-day lacto-ovo-vegetarian (LOV; n = 12) or omnivorous (Omni; n = 14) diet. On day 22, subjects were also assigned in a double-blind manner either creatine monohydrate (CM; 0.3 g.kg(-1).day(-1) + 20 g Polycose) or an equivalent dose of placebo (PL) for 5 days. Blood samples were taken on days 1, 22 and 27. Consuming a LOV diet for 21 days was effective in reducing plasma creatine concentration (p < 0.01) in the LOV group. Regardless of diet, the CM group showed an increase in plasma creatine concentrations from day 22 to 27, whereas the PL group's levels remained the same (p < 0.05). Although the LOV diet caused a deprivation effect in plasma creatine concentration relative to the Omni diet, concurrent supplementation with creatine resulted in no difference in plasma creatine concentrations between the LOV and Omni diet groups. Dietary advice should be provided to LOV athletes that supplementation with creatine may help to increase their muscle stores of creatine, and thus their ATP resynthesis capabilities, to levels similar to those of omnivores.

Administration, Oral↗
PubMed1994

Creatine in humans with special reference to creatine supplementation.

Since the discovery of creatine in 1832, it has fascinated scientists with its central role in skeletal muscle metabolism. In humans, over 95% of the total creatine (Crtot) content is located in skeletal muscle, of which approximately a third is in its free (Crf) form. The remainder is present in a phosphorylated (Crphos) form. Crf and Crphos levels in skeletal muscle are subject to individual variations and are influenced by factors such as muscle fibre type, age and disease, but not apparently by training or gender. Daily turnover of creatine to creatinine for a 70kg male has been estimated to be around 2g. Part of this turnover can be replaced through exogenous sources of creatine in foods, especially meat and fish. The remainder is derived via endogenous synthesis from the precursors arginine, glycine and methionine. A century ago, studies with creatine feeding concluded that some of the ingested creatine was retained in the body. Subsequent studies have shown that both Crf and Crphos levels in skeletal muscle can be increased, and performance of high intensity intermittent exercise enhanced, following a period of creatine supplementation. However, neither endurance exercise performance nor maximal oxygen uptake appears to be enhanced. No adverse effects have been identified with short term creatine feeding. Creatine supplementation has been used in the treatment of diseases where creatine synthesis is inhibited.

Adolescent↗
PubMed1995

Creatine supplementation in chronic heart failure increases skeletal muscle creatine phosphate and muscle performance.

BACKGROUND: Cardiac creatine levels are depressed in chronic heart failure. Oral supplementation of creatine to healthy volunteers has been shown to increase physical performance. AIM: To evaluate the effects of creatine supplementation on ejection fraction, symptom-limited physical endurance and skeletal muscle strength in patients with chronic heart failure. METHODS: With a double-blind, placebo-controlled design 17 patients (age 43-70 years, ejection fraction < 40) were supplemented with creatine 20 g daily for 10 days. Before and on the last day of supplementation ejection fraction was determined by radionuclide angiography as was symptom-limited 1-legged knee extensor and 2-legged exercise performance on the cycle ergometer. Muscle strength as unilateral concentric knee extensor performance (peak torque, Nm at 180 degrees/s) was also evaluated. Skeletal muscle biopsies were taken for the determination of energy-rich phosphagens. RESULTS: Ejection fraction at rest and at work did not change. Performance before creatine supplementation did not differ between placebo and creatine groups. While no change was seen in the placebo group compared to baseline, creatine supplementation increased skeletal muscle total creatine and creatine phosphate by 17 +/- 4% (P < 0.05) and 12 +/- 4% (P < 0.05), respectively. Increments were seen only in patients with < 140 mmol total creatine/kg d.w. (P < 0.05). One-legged performance (21%, P < 0.05), 2-legged performance (10%, P < 0.05), and peak torque, Nm (5%, P < 0.05) increased. Both peak torque and 1-legged performance increased linearly with increased skeletal muscle phosphocreatine (P < 0.05). The increments in 1-legged, 2-legged and peak torque were significant compared to the placebo group, (P < 0.05). CONCLUSIONS: One week of creatine supplementation to patients with chronic heart failure did not increase ejection fraction but increased skeletal muscle energy-rich phosphagens and performance as regards both strength and endurance. This new therapeutic approach merits further attention.

Administration, Oral↗
PubMed2005

Supranormal myocardial creatine and phosphocreatine concentrations lead to cardiac hypertrophy and heart failure: insights from creatine transporter-overexpressing transgenic mice.

BACKGROUND: Heart failure is associated with deranged cardiac energy metabolism, including reductions of creatine and phosphocreatine. Interventions that increase myocardial high-energy phosphate stores have been proposed as a strategy for treatment of heart failure. Previously, it has not been possible to increase myocardial creatine and phosphocreatine concentrations to supranormal levels because they are subject to tight regulation by the sarcolemmal creatine transporter (CrT). METHODS AND RESULTS: We therefore created 2 transgenic mouse lines overexpressing the myocardial creatine transporter (CrT-OE). Compared with wild-type (WT) littermate controls, total creatine (by high-performance liquid chromatography) was increased in CrT-OE hearts (66+/-6 nmol/mg protein in WT versus 133+/-52 nmol/mg protein in CrT-OE). Phosphocreatine levels (by 31P magnetic resonance spectroscopy) were also increased but to a lesser extent. Surprisingly, CrT-OE mice developed left ventricular (LV) dilatation (LV end-diastolic volume: 21.5+/-4.3 microL in WT versus 33.1+/-9.6 microL in CrT-OE; P=0.002), substantial LV dysfunction (ejection fraction: 64+/-9% in WT versus 49+/-13% in CrT-OE; range, 22% to 70%; P=0.003), and LV hypertrophy (by 3-dimensional echocardiography and magnetic resonance imaging). Myocardial creatine content correlated closely with LV end-diastolic volume (r=0.51, P=0.02), ejection fraction (r=-0.74, P=0.0002), LV weight (r=0.59, P=0.006), LV end-diastolic pressure (r=0.52, P=0.02), and dP/dt(max) (r=-0.69, P=0.0008). Despite increased creatine and phosphocreatine levels, CrT-OE hearts showed energetic impairment, with increased free ADP concentrations and reduced free-energy change levels. CONCLUSIONS: Overexpression of the CrT leads to supranormal levels of myocardial creatine and phosphocreatine, but the heart is incapable of keeping the augmented creatine pool adequately phosphorylated, resulting in increased free ADP levels, LV hypertrophy, and dysfunction. Our data demonstrate that a disturbance of the CrT-mediated tight regulation of cardiac energy metabolism has deleterious functional consequences. These findings caution against the uncritical use of creatine as a therapeutic agent in heart disease.

Animals↗
PubMed2001

Creatine transporter and mitochondrial creatine kinase protein content in myopathies.

Total creatine or phosphocreatine, or both, are reduced in the skeletal muscle of patients with inflammatory myopathy, mitochondrial myopathy, and muscular dystrophy/congenital myopathy. We used Western blotting techniques to measure skeletal muscle creatine transporter protein and sarcomeric mitochondrial creatine kinase (mtCK) protein content in patients with inflammatory myopathy (N = 8), mitochondrial myopathy (N = 5), muscular dystrophy (N = 7), and congenital myopathy (N = 3), as compared to a control group without a neuromuscular diagnosis (N = 8). Creatine transporter protein content was lower for all groups compared to control subjects (P < 0.05; P < 0.01 for congenital myopathy). Mitochondrial CK (mtCK) was lower for inflammatory myopathy (P < 0.05), higher for mitochondrial myopathy (P < 0.05), not different for muscular dystrophy, and markedly lower for the congenital myopathy group (P < 0.01), compared to control subjects. Together, these data suggest that the reduction in total creatine or phosphocreatine in patients with certain myopathies is correlated with creatine transporter and not mtCK protein content. This further supports the belief that creatine monohydrate supplementation may benefit patients with low muscle creatine stores, although the reduction in creatine transporter protein may have implications for dosing.

Adult↗
PubMed2003

Creatine transporter activity and content in the rat heart supplemented by and depleted of creatine.

The intracellular creatine concentration is an important bioenergetic parameter in cardiac muscle. Although creatine uptake is known to be via a NaCl-dependent creatine transporter (CrT), its localization and regulation are poorly understood. We investigated CrT kinetics in isolated perfused hearts and, by using cardiomyocytes, measured CrT content at the plasma membrane or in total lysates. Rats were fed control diet or diet supplemented with creatine or the creatine analog beta-guanidinopropionic acid (beta-GPA). Creatine transport in control hearts followed saturation kinetics with a K(m) of 70 +/- 13 mM and a V(max) of 3.7 +/- 0.07 nmol x min(-1) x g wet wt(-1). Creatine supplementation significantly decreased the V(max) of the CrT (2.7 +/- 0.17 nmol x min(-1) x g wet wt(-1)). This was matched by an approximately 35% decrease in the plasma membrane CrT; the total CrT pool was unchanged. Rats fed beta-GPA exhibited a >80% decrease in tissue creatine and increase in beta-GPA(total). The V(max) of the CrT was increased (6.0 +/- 0.25 nmol x min(-1) x g wet wt(-1)) and the K(m) decreased (39.8 +/- 3.0 mM). The plasma membrane CrT increased about fivefold, whereas the total CrT pool remained unchanged. We conclude that, in heart, creatine transport is determined by the content of a plasma membrane isoform of the CrT but not by the total cellular CrT pool.

Adenosine Triphosphate↗
PubMed1995

Time changes of creatine kinase and creatine kinase-MB isoenzyme versus discrimination values in the diagnosis of acute myocardial infarction: what is the optimal method for displaying the data?

We wanted to determine the optimal method for displaying data for the clinical evaluation of patients with possible acute myocardial infarction. Our primary question was, are the time changes (slopes) of the enzyme tests better predictors of disease than the discrimination values, i.e., the cut-off points? We studied 152 patients with and 114 without a diagnosis of acute myocardial infarction in their medical records. For patients with acute myocardial infarction, we found the most discriminating tests, in decreasing order of the area of the ROC curves, to be the creatine kinase-MB slope at 0 to 12 hours, the creatine kinase-MB slope at 12 to 24 hours, the creatine kinase-MB values between 12 and 24 hours, and the creatine kinase-MB values between 0 and 12 hours. Decreasing values of creatine kinase-MB in the first tests after admission were only slightly less discriminating than increasing ones. At 12 to 24 hours after admission, the total creatine kinase as a value or slope, or the "relative index" (a ratio of the creatine kinase-MB in microgram/l [times 100] to the total creatine kinase) as a value or slope were inferior to creatine kinase-MB presentations. From the data for 44 patients with acute myocardial infarction and a known time of onset of symptoms, we were able to estimate an approximate onset time in patients where this was not available.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical Enzyme Tests↗
PubMed1976

Mechanism of thyroid-induced creatinuria in rat, with special reference to creatine synthesis in liver and creatine loss from skeletal muscle.

Mechanism of thyroid-induced creatinuria was investigated in rats. The rats were injected with triiodothyronine (T3) (100 mug/100g, sc) at 9.00 hr. Oxygen consumption increased 12 hr after T3 injection, reaching peak value 48 hr after the injection and decreasing to the pre-injection level at 96 hr. Urinary creatine excretion also increased during the first 10 hr after the injection, approaching maximal value 34-48 hr after the injection, and decreasing to the pre-injection level 72-82 hr after the injection. Throughout the experimental period, urinary creatinine decreased with time after the injection, although the difference between the groups was not significant. A decreased creatine tolerance was also observed after T3 injection. Beta-Guanidinopropionic acid (beta-GPA), a competitive inhibitor of creatine transport into skeletal muscle, as well as partial hepatectomy, caasing inhibition of creatine synthesis, were without effect on the difference in urinary creatine excretion between T3-treated and control animals. T3 increased the plasma creatine level both in bilateral nephrectomized and in bilateral nephrectomized plus beta-GPA administrated groups. These results suggest that increased creatine loss from skeletal muscle in addition to decreased creatine uptake of skeletal muscle rather than increased hepatic synthesis of creatine play an important role in T3-induced creatinuria.

Animals↗
PubMed1999

The effect of longer-term creatine supplementation on elite swimming performance after an acute creatine loading.

We investigated the effect of an acute creatine loading (25 g per day for 4 days) and longer-term creatine supplementation (5 g of creatine or 5 g of placebo per day for 2 months) on the performance of 22 elite swimmers during maximal interval sessions. After the acute creatine loading, the mean of the average interval swim times for all swimmers (n = 22) improved (44.3+/-16.5 s before vs. 43.7+/-16.3 s after supplementation; P<0.01). Three of the 22 swimmers did not respond positively to supplementation. After 2 months of longer-term creatine supplementation or placebo, neither group showed a significant change in swimming performance (38.7+/-13.5 s before vs. 38.7+/-14.1 s after for the creatine group; 48.7+/-18.0 s before vs. 48.7+/-18.1 s after for the placebo group). We conclude that, in elite swimmers, 4 days of acute creatine loading improves swimming performance significantly when assessed by maximal interval sessions. However, longer-term supplementation for 2 months (5 g of creatine per day) did not benefit significantly the creatine group compared with the placebo group.

Adult↗
PubMed2001

Soluble interleukin-2 receptor and interleukin-8 plasma levels during and after cardiopulmonary bypass: correlations with creatine kinase and creatine kinase MB.

In this study, soluble receptor of interleukin-2, interleukin-8, creatine kinase, and creatine kinase MB isoenzyme levels were determined serially before, during, and after cardiopulmonary bypass in blood samples of 24 patients. Interleukin-2 receptor levels were 683+/-80 U/ml in the preoperative period and 640+/-60 U/ml during hypothermia. Subsequently, these levels increased significantly at the end of the procedure (791+/-70 U/ml, P<0.01), remaining elevated 1 h after (882+/-92 U/ml, P<0.001) and reaching peak values 24 h postoperatively (1,752+/-200 U/ml, P<0.001). Preoperative plasma values of interleukin-8 were 230+/-43 pg/ml. Interleukin-8 concentrations were 185+/-25 pg/ml during hypothermia. The peak interleukin-8 levels were observed at the end of cardiopulmonary bypass (754+/-94 pg/ml, P<0.001) and tended to decrease 1 h after the procedure (643+/-76 pg/ml, P<0.001), declining to preoperative values, 24 h postoperatively (273+/-41 pg/ml). Interleukin-2 receptor levels correlated well with creatine kinase levels during the procedure. Furthermore, creatine kinase MB levels were correlated with interleukin-2 receptor values only at the end and 1 h after completion of cardiopulmonary bypass. We concluded that interleukin-8 and Interleukin-2 receptor levels are elevated after cardiopulmonary bypass and may contribute to myocardial injury as reflected by increased levels of creatine kinase and creatine kinase MB and correlations between interleukin-2 receptor and both creatine kinase and creatine kinase MB levels.

Adult↗
PubMedDate not supplied

[Role of calcium in the regulation of syncytial formation and the formation of creatine kinase during the development of muscle in the absence of creatine].

1. It is demonstrated for the first time that typically elongated chick myotubes, with more than 20 nuclei per fiber and creatine kinase, appear in cultures fed all time with partially defined auto-conditioned medium. 2. It was found that the skeletal muscle enzyme of the chick embryo is independent of the presence of creatine and consequently is another constitutive enzyme like the creatine kinase of the early embryonic chick heart. 3. Calcium elicited the activity of the enzyme and promoted fusion of myoblasts in a creatine-free partially defined medium, in the absence of embryo extract. 4. It is suggested that creatine kinase is a dual molecule, working as an ATPasa in the absence of creatine with H2O as the nucleophilic reagent. 5. Alternatively, it is possible that creatine kinase can be synthesized and localized in advance to the advent of creatine in myocardial and skeletal muscle cells.

Animals↗
PubMed2003

Validation of a simple liquid chromatography assay for creatine suitable for pharmacokinetic applications, determination of plasma protein binding and verification of percent labeled claim of various creatine products.

Creatine has been quantified in various tissues by a range of methodologies. This paper reports on the development and validation of a simplified HPLC assay to determine plasma creatine, plasma protein binding of creatine, creatine in microdialysate and creatine in over-the-counter products. An isocratic, reversed-phase (C(18)) HPLC assay, using potassium phosphate monobasic (pH 4) as a mobile phase, was validated in human plasma and microdialysis perfusion fluid (normal saline). The lower limit of quantification for the assay was 1 mg l(-1) in saline and 5 mg l(-1) in plasma. The RSD was below 6% and accuracy was below 12% in both matrices. Protein binding in human plasma was found to be negligible (<10%). Over-the-counter creatine monohydrate products tested contained 100% creatine monohydrate. This assay was found to be suitable for pharmacokinetic studies and the assessment of plasma creatine and skeletal muscle microdialysate.

Chromatography, High Pressure Liquid↗
PubMed2006

Determination of creatine in commercial creatine powder with new potentiometric and amperometric biosensors.

New potentiometric and amperometric biosensors were developed for the determination of creatine. The potentiometric creatine biosensor was prepared by immobilizing urease and creatinase on poly(vinylchloride) (PVC) ammonium membrane electrode containing palmitic acid prepared by using nonactine as an ammonium-ionophore. The linear working range of the biosensor was 1.0 x 10(-5) - 1.0 x 10(-3) M and the response time was about 60 s. The optimum pH, temperature, and buffer concentration were found to be 7.0, 20 degrees C, and 5 mM, respectively. The slope of the electrode was 49.2 mV/p[creatine]. The storage stabilization of the biosensor was investigated and 40-45% decrease in the response was detected after 2 months. The amperometric creatine biosensor was prepared by immobilizing creatinase (CI) and sarcosine oxidase (SO) in a poly(vinylferrocenium) matrix onto the surface of a platinum working electrode by crosslinking with glutaraldehyde (GA) and bovine serum albumine (BSA). Determination of creatine was performed by the oxidation of enzymatically generated H2O2 at +0.7 V vs. Ag/AgCl. The linear working range of the biosensor was 2.0 x 10(-5) - 3.2 x 10(-4) M and the response time was about 50 s. The effects of pH, temperature, enzyme ratio and buffer concentration were investigated and optimum parameters were found to be 7.5, 37 degrees C, 2.5:1 (CI:SO) and 0.05 M, respectively. The determination of creatine in commercial creatine powder was successfully carried out with these creatine biosensors by using the standard addition and calibration curve methods. The results were in good agreement with those obtained from Jaffé method at 95% confidence level.

Biosensing Techniques↗
PubMed2002

The blood-brain barrier creatine transporter is a major pathway for supplying creatine to the brain.

Although creatine plays a pivotal role in the storage of phosphate-bound energy in the brain, the source of cerebral creatine is still unclear. The authors examined the contribution made by the creatine transporter (CRT) at the blood-brain barrier in supplying creatine to the brain from blood. An intravenous administration study suggested that creatine is continuously transported from the blood to the brain against the creatine concentration gradient that exists between brain and blood. Conditionally immortalized mouse brain capillary endothelial cells (TM-BBB) exhibited creatine uptake, which is Na+ and Cl- dependent and inhibited by CRT inhibitors, such as beta-guanidinopropionate and guanidinoacetate. Northern blot and immunoblot analyses demonstrated that CRT is expressed in TM-BBB cells and isolated mouse brain microvessels. Moreover, high expression of CRT was observed in the mouse brain capillaries by confocal immunofluorescent microscopy. These results suggest that CRT plays an important role in supplying creatine to the brain via the blood-brain barrier.

Amino Acid Sequence↗