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1 lites (i.e., choline, N-acetylaspartate, and creatine).
2 lutamate, glutamine, myo-inositol, and total creatine).
3 to 28% in samples containing high amounts of creatine.
4 is is down-regulated by dietary/supplemental creatine.
5 oforms, citrate synthase activity, and total creatine.
6 to a diverse set of regulatory functions for creatine.
7 amic acid, alanine, glycine, pyrimidine, and creatine.
8 ed by nutritional factors such as folate and creatine.
9 mino acids, neurotransmitters, osmolytes, or creatine.
10 ntly higher intracellular diffusion of total creatine (0.202 +/- 0.032 mum(2)/ms, P = 0.018) and tota
11 Participants were randomized to placebo or creatine (10 g/d) monohydrate for a minimum of 5 years (
12 mized to receive 400 mug FA, 800 mug FA, 3 g creatine, 3 g creatine+400 mug FA, or placebo daily.
15 ter the RG diet, whereas melatonin, betaine, creatine, acetylcholine, aspartate, hydroxyproline, meth
18 ages/microglia into lesions, suggesting that creatine affects oligodendrocyte survival independently
25 measurement of the isotopic distribution of creatine and creatinine by liquid chromatography-tandem
26 y be affected by the interconversion between creatine and creatinine during sample preparation or by
27 rations of glutamate, taurine, myo-inositol, creatine and inosine were present in aqueous extracts an
28 anglia) N-acetylaspartate (NAA)/Choline, NAA/Creatine and myo-inositol/Creatine ratios were measured.
29 ifteen healthy adults were supplemented with creatine and placebo treatments for 7 d, which increased
30 coveries of other BAT futile cycles based on creatine and succinate have provided additional targets.
31 inositol (mI) and metabolic changes in total creatine and taurine previously reported to be associate
34 tions in creatine phosphate/ATP ratio, total creatine, and ATP-mirror changes observed in failing hea
35 , total choline-containing compounds (tCho), creatine, and glutamine and glutamate complex were estim
36 ict myocardial ATP, ADP, creatine phosphate, creatine, and inorganic phosphate concentrations as func
38 ntrations of cytoplasmic adenine nucleotide, creatine, and phosphate pools that occur with aging impa
40 fusivities of choline compounds and of total creatine are potentially unique markers for glial reacti
41 for the first time in humans, the utility of creatine as a dietary supplement to protect against ener
44 umaric acid, inosine, inosine monophosphate, creatine, betaine, carnosine and hypoxanthine) out of ei
45 Herein, we highlight the latest advances in creatine biology in tissues and cell types that have his
48 e (GATM) catalyzes the rate-limiting step of creatine biosynthesis: the transfer of an amidino group
49 tients, levels were modestly lower for GABA+/creatine but did not differ for GABA+/water compared wit
52 Patients in ARISTOTLE without severe renal (creatine clearance <=30 mL/min) or liver disease were in
53 function was the highest for RCV (0.58 with creatine clearance, 0.54 with estimated glomerular filtr
54 partate (NAA), choline-containing compounds, creatine-containing compounds (Cr), myo-inositol (mI), a
57 age diffusivities of total choline and total creatine, correlate with systemic lupus erythematosus ac
58 n SAM-dependent metabolism of polyamines and creatine could not be directly attributed to alterations
59 te plus N-acetyl-aspartyl-glutamate (NAA) to creatine (Cr) and choline compounds (Cho) to Cr in wides
60 t this, we measured RSFC with fMRI and GABA+/Creatine (Cr) concentrations with proton magnetic resona
61 uronal mitochondrial function, normalized to creatine (Cr) levels were measured from the motor cortex
64 e ratios (citrate [Cit], spermine [Spm], and creatine [Cr] to choline [Cho] and Cho to Cr plus Spm) w
66 od capable of correcting and quantifying the creatine-creatinine interconversion occurring during the
67 s of real serum samples by GC-MS showed that creatine-creatinine separation by SPE can be a nonquanti
68 s, four metabolites significantly increased: creatine, dehydroascorbate, fumarate, and succinate in t
70 ermally stable but less soluble comparing to creatine due to a self-aggregation process that occurs a
71 nation.SIGNIFICANCE STATEMENT We report that creatine enhances oligodendrocyte mitochondrial function
72 beige adipose signature and demonstrate that creatine enhances respiration in beige-fat mitochondria
74 itamin D, with positive isolated studies for creatine, folinic acid, and an amino acid combination.
77 N-acetylaspartate, choline, myo-inositol and creatine) group contrasts from all individual voxels tha
79 spectroscopic findings of N-acetylaspartate/creatine in frontal gray matter (r = -0.40; P = .03), fr
80 ncover a previously uncharacterized role for creatine in macrophage polarization by modulating cellul
81 our results demonstrate a novel function for creatine in promoting oligodendrocyte viability during C
85 gyri (16 voxels, CCLAV = 0.04) and increased creatine in two clusters involving left temporal, pariet
87 monohydrate supplementation augments neural creatine, increases corticomotor excitability, and preve
95 hypothesized that ATP transfer rate through creatine kinase (CK) (k(f)(CKrest)) would be increased,
98 We investigate the hypothesis that reduced creatine kinase (CK) capacity and flux is associated wit
99 a 2-tiered approach to NBS with screening by creatine kinase (CK) levels in dried blood spots followe
102 iation of a recently reported variant in the creatine kinase (CK) muscle gene, CKM Glu83Gly (rs115590
103 lationship between cTnT, cardiac troponin I, creatine kinase (CK), CK-myocardial band levels, and ske
104 erase (AST), lactate dehydrogenase (LDH) and creatine kinase (CK), which cardiac troponins being the
106 re we report cryo-EM data for the substrate, creatine kinase (CKB) bound to ASB9-ELOB/C, and for full
107 common grade 3-4 adverse events were raised creatine kinase (five [6%] in the 200 mg group vs 19 [13
108 inol-binding protein (hRBP) under the muscle creatine kinase (MCK) promoter (MCKhRBP) with the PKCdel
109 o proceeded directly to phase B for elevated creatine kinase (N = 218, with 73 randomized to ezetimib
110 95% CI 1.34, 13.71; p = 0.014), and elevated creatine kinase (OR 3.79; 95% CI 1.06, 13.51; p = 0.04),
111 nfarction </=1 flow, there was reduced serum creatine kinase (P=0.030) and a 19% reduction in cardiac
113 fat, cold exposure stimulates mitochondrial creatine kinase activity and induces coordinated express
114 further explore the effect of calmodulin on creatine kinase activity and show that it is increased b
115 f differentiation, demonstrated by increased creatine kinase activity, fusion index and myotube diame
116 ne blood chemistry was normal, as were serum creatine kinase and aldolase levels and thyroid, hepatic
118 boratory analysis showed alteration of serum creatine kinase and creatinine in the Leu389Ser ALS4 coh
121 Of the 1,800 patients enrolled, 1,652 with creatine kinase and/or creatine kinase-myocardial band (
122 terquartile range, 14-42; P<0.01) and median creatine kinase areas under the curve were 22 000 and 38
123 variability compared with the commonly used creatine kinase assay, and correlated better with the re
124 y plus rifaximin group showed an increase in creatine kinase at the end of treatment compared with pa
128 identified the ATP-buffering, mitochondrial creatine kinase CKMT1 as necessary for survival of EVI1-
129 e dye uptake into muscle and increased serum creatine kinase compared to the 129T2/SvEmsJ background.
130 he most common adverse event was an elevated creatine kinase concentration to more than ten times the
133 3 and miR-551a expression, which derepresses creatine kinase expression and allows energy to be captu
135 nally, these mice exhibited increased plasma creatine kinase following exhaustive exercise when unfed
136 ne kinase reaction, we have now measured the creatine kinase forward reaction rate constant in BD.
138 hy control participants at 4T and quantified creatine kinase forward reaction rate constant using (31
140 on by OXPHOS (vOX), anaerobic glycolysis and creatine kinase in moderate and severe intensity exercis
145 = 0.45; I2 = 0%), and increases in the serum creatine kinase level were reduced (OR, 0.72 [CI, 0.54 t
152 distribution and significantly reduced serum creatine kinase levels, but had limited effect on muscle
153 ut without an earlier onset, increased serum creatine kinase levels, or decreased muscle strength.
156 Fractional synthesis rate (FSR) of plasma creatine kinase M-type (CK-M) and carbonic anhydrase 3 (
157 NAME induced elevation of cardiac output and Creatine Kinase Muscle-Brain (CKMB), but had no signific
158 ts, there was a reduction in serum levels of creatine kinase muscle-brain isoenzyme, a myocardial-spe
159 ted by targeted replacement of mitochondrial creatine kinase or mitochondrial-targeted CaMKII inhibit
161 e overexpressing PGC-1alpha under the muscle creatine kinase promoter (MPGC-1alphaTG mice) displayed
162 is replenished from phosphocreatine via the creatine kinase reaction, we have now measured the creat
164 y (31)P nuclear MR spectroscopy, lactate and creatine kinase release spectrophotometrically, and hypo
165 ed muscle degeneration and fibrosis, reduced creatine kinase serum levels, restored running capacity
166 Diagnosis using the classic blood marker creatine kinase sometimes yields unsatisfactory results
167 olipoprotein A1 (apoA1), apoE, mitochondrial creatine kinase U-type, beta-synuclein, synaptogyrin-3,
171 tions of serum transaminases, bilirubin, and creatine kinase were infrequent and similar between grou
172 catalytic site of bound hexokinase or bound creatine kinase without ATP dilution in the cytosol.
173 h large increases in blood concentrations of creatine kinase), new-onset diabetes mellitus, and, prob
174 ased lactate dehydrogenase, pyruvate kinase, creatine kinase, and cytochrome c oxidase activities, an
175 derived from lactate dehydrogenase, one from creatine kinase, and four from serum albumin protein.
177 size distribution, centralized nuclei, serum creatine kinase, and quantitative histopathology scores.
178 f such therapy, the levels of troponin T and creatine kinase, and the rates of bleeding and stroke di
179 e levels of creatine kinase, MB isoenzyme of creatine kinase, blood urea nitrogen, creatinine, K(+) i
181 ants or isoforms of tropomyosin, arginine or creatine kinase, glyceraldehyde-3-phosphate dehydrogenas
182 ice exhibited progressive MD, elevated serum creatine kinase, heart dilation, blood vessel irregulari
183 ved hemodynamics and decreased the levels of creatine kinase, MB isoenzyme of creatine kinase, blood
184 st notably the regions harboring CKMT2 gene (creatine kinase, mitochondrial 2) and RASGRF2 gene (Ras
185 arkers included high-sensitivity troponin T, creatine kinase, myoglobin, N-terminal B-type natriureti
186 intra- and intermolecular cross-links within creatine kinase, then to map the interaction surfaces be
187 erize the interaction between calmodulin and creatine kinase, which we identify as a novel calmodulin
189 MI (PMI(Prot)) required a large elevation of creatine kinase-MB (CK-MB), with identical threshold for
190 rocedural MI, the primary MI definition used creatine kinase-MB as the preferred biomarker, whereas t
192 enrolled, 1,652 with creatine kinase and/or creatine kinase-myocardial band (CK-MB) post-procedure w
200 but not pravastatin, induced elevated serum creatine kinase; swollen, misaligned, size-variable, and
202 ir of high-energy phosphate (HEP) bonds, and creatine kinases (CK) catalyze the transfer of HEP from
203 istidine, xanthurenate, isovalerylcarnitine, creatine, kynurenate, 1-(1-enyl-palmitoyl)-2-arachidonoy
205 and -1.6 ppm, likely arising from changes in creatine level and nuclear overhauser effects, which wer
208 erformance liquid chromatography (to measure creatine levels), qRT-PCR, transepithelial electrical re
210 al excretion of guanidinoacetate, but normal creatine levels, suggesting that MCT12 may function as a
212 S metabolite peak-area ratios (n=160) of NAA-creatine (<1.29) had an AUC of 0.79 (0.72-0.85), of NAA-
223 domized placebo-controlled clinical trial of creatine monohydrate (10 g/d) that was performed at 45 s
224 nd treated Parkinson disease, treatment with creatine monohydrate for at least 5 years, compared with
225 These findings do not support the use of creatine monohydrate in patients with Parkinson disease.
227 ical shift imaging (CSI) was used to explore creatine-normalized measures of other metabolites in bas
229 ed proteins or macromolecules) referenced to creatine or water were studied with J-edited proton spec
232 to receive FA (400 or 800 mug per day), 3 g creatine per day, 400 mug FA + 3 g creatine per day, or
235 l energetics to predict myocardial ATP, ADP, creatine phosphate, creatine, and inorganic phosphate co
236 ergetics associated with aging-reductions in creatine phosphate/ATP ratio, total creatine, and ATP-mi
239 of N-acetyl compounds, glutamate+glutamine, creatine+phosphocreatine, and choline compounds in 78 ch
240 of N-acetyl compounds, glutamate+glutamine, creatine+phosphocreatine, or choline compounds measured
241 of 179), anaemia (ten [6%]), increased blood creatine phosphokinase (12 [7%]), and fatigue (eight [4%
242 ty population in either group were increased creatine phosphokinase (52 [19%] of 269 patients in the
243 CKM Glu83Gly (rs11559024) with constitutive creatine phosphokinase (CK) levels, CK variation, and in
245 vent in the upadacitinib group was increased creatine phosphokinase (eight [9%] of 93 patients in the
246 rade 3 or worse adverse events were elevated creatine phosphokinase (five [10%]) and maculopapular ra
248 h autoimmune disorder (n=3), increased blood creatine phosphokinase (n=2), and increased aspartate am
249 [11%] in treatment group B), increased blood creatine phosphokinase (one [1%] vs four [4%]), and hypo
250 laboratory values, including increased blood creatine phosphokinase (seven [8%]), increased alanine a
251 ffect was an asymptomatic increase in plasma creatine phosphokinase concentration (200 mg, n=5; 400 m
252 (6.8%) and included asthenia, AST elevation, creatine phosphokinase elevation, and decreased appetite
253 es were uncommon, except for 15 increases in creatine phosphokinase in 14 participants (three partici
254 and one patient at 20 mg/kg, increased blood creatine phosphokinase in two patients at 20 mg/kg, and
255 in the placebo and vemurafenib group), blood creatine phosphokinase increase (30 [12%] vs one [<1%]),
256 patients: lymphopenia in two patients, blood creatine phosphokinase increase in one patient, aminotra
257 or diarrhea; an asymptomatic increase in the creatine phosphokinase level; acneiform rash; and parony
258 ete blood count and electrolyte, creatinine, creatine phosphokinase, and troponin T levels were norma
259 dividuals had eye defects or elevated muscle creatine phosphokinase, separating the TMTC3 COB phenoty
262 cetylaspartate and N-acetylaspartylglutamate/creatine ratio (NAA/Cr) in a group of 89 women with CFS.
263 ptimized MEGA-PRESS editing sequence and GSH/creatine ratios were calculated for DLPFC (SZ: n = 33, H
266 ic, and immunological analyses revealed that creatine reprogrammed macrophage polarization by suppres
269 the placebo group at wk 6 and 12 (P < 0.05); creatine supplementation did not affect change in %InAs
271 o determine whether 400 or 800 mug FA and/or creatine supplementation lowers bAs in an As-exposed Ban
272 is study was to assess the influence of oral creatine supplementation on the neurophysiological and n
273 igated the effects of folic acid (FA) and/or creatine supplementation on the proportion of As metabol
274 cell immunity, underscoring the potential of creatine supplementation to improve T cell-based cancer
275 e mouse tumor models, and the combination of creatine supplementation with a PD-1/PD-L1 blockade trea
276 pacity, were restored when participants were creatine supplemented, and corticomotor excitability inc
277 Although the reasons for this are unclear, creatine synthesis is a major consumer of methyl donors,
278 iated demyelination in mice deficient in the creatine-synthesizing enzyme guanidinoacetate-methyltran
279 (8.1 +/- 0.2 vs 9.4 +/- 0.4; P < .01), total creatine (tCr) (7.5 +/- 0.2 vs 8.3 +/- 0.3; P < .01), an
280 for mIns in hippocampus and thalamus, total creatine (tCr) and tCho in ACC and hippocampus; lower le
282 ch is mainly localized in neurons, and total creatine (tCr), an energy metabolite, in 19 BD patients
283 olic fate of L-arginine is the generation of creatine that acts as a key source of cellular energy re
284 13)C analogues ((13)C1-creatinine and (13)C2-creatine), the measurement of the isotopic distribution
287 MCT12 (also known as SLC16A12) that mediates creatine transport was recently identified as the cause
290 of intracellular creatine by ablation of the creatine transporter Slc6a8 altered macrophage-mediated
294 Using CrT knockout mice, we showed that creatine uptake deficiency severely impaired antitumor T
299 neurochemical measure, myo-inositol+glycine/creatine, was consistently increased in each brain regio
300 the distribution indicates that supplemented creatine would be widely taken up by brain cells, althou