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1 e conversion of acetyl-coenzyme A (CoA) into acetylcarnitine.
2  2 of beta-hydroxybutyrate, malonyl-CoA, and acetylcarnitine.
3 was no detectable current in the presence of acetylcarnitine.
4  transport carnitine, propionylcarnitine and acetylcarnitine.
5 anges in [(13)C]bicarbonate (-48%), [1-(13)C]acetylcarnitine (+113%), and [5-(13)C]glutamate (-63%),
6          The observed enrichment of (13)C in acetylcarnitine (19%), M+6 stearoylcarnitine (16.2%), an
7 ce of M+2 myristoylcarnitine (95.7%) and M+2 acetylcarnitine (19.4%) is evidence for beta-oxidation o
8 ylglycine, 1-methylnicotinamide, methionine, acetylcarnitine, 2-oxoglutarate, choline, and creatine.
9                               Treatment with acetylcarnitine (AcCN) increases the activity of cytochr
10                                  Whereas (+)-acetylcarnitine also failed to influence CACT, both (+)-
11 release of 2 specific acylcarnitine species, acetylcarnitine and 3-hydroxybutyryl-carnitine.
12 eased tissue efflux and urinary excretion of acetylcarnitine and improvement of whole body glucose to
13  Because of this channeling, the labeling of acetylcarnitine and ketone bodies released by the heart
14 the release of small excess acetyl groups as acetylcarnitine and ketone bodies, and (iii) the channel
15                Cycling of acetyl-CoA through acetylcarnitine appears key to matching instantaneous ac
16 drogenase complex activation, acetyl-CoA and acetylcarnitine by approximately 20-fold (P < 0.01), app
17                                              Acetylcarnitine (C2), showing a late response pattern an
18 enzymatic conversion of pyruvate to lactate, acetylcarnitine, citrate, and glutamate with 1 s tempora
19 (P < 0.01), when there was a 47% decrease in acetylcarnitine concentration (P < 0.05), and a 24-fold
20  showed a reciprocal distribution, with mean acetylcarnitine concentration correlating with mean insu
21                              Skeletal muscle acetylcarnitine concentration showed a reciprocal distri
22 omic analysis showed a 2.2 times increase in acetylcarnitine concentrations (p=0.002).
23 nterest, noninvasive alternatives to measure acetylcarnitine concentrations could facilitate our unde
24 troscopy (1H-MRS) to measure skeletal muscle acetylcarnitine concentrations on a clinical 3T scanner.
25  min of passive recovery, muscle lactate and acetylcarnitine concentrations were elevated above basal
26     These results demonstrate that measuring acetylcarnitine concentrations with 1H-MRS is feasible o
27 ate dehydrogenase complex (PDC) activity and acetylcarnitine content at rest, it has also been establ
28 irst 3 min of infusion, the concentration of acetylcarnitine declined (pre-infusion = 3.8 +/- 0.3 vs.
29  derivatives, rose from virtual absence, and acetylcarnitines fell.
30                    The effect on each of (+)-acetylcarnitine, (+)-hexanoylcarnitine, (+)-octanoylcarn
31  quantitative determination of carnitine and acetylcarnitine in analytical standard solutions as well
32         We applied long-TE 1H-MRS to measure acetylcarnitine in endurance-trained athletes, lean and
33 ategy to the quantification of carnitine and acetylcarnitine in rat liver is shown.
34 umulation of glucose-6-phosphate (G-6-P) and acetylcarnitine in resting canine skeletal muscle.
35 14C]acetyl-CoA, which is converted to [2-14C]acetylcarnitine in the presence of excess L-carnitine an
36  for successful detection of skeletal muscle acetylcarnitine in these individuals.
37            Because current methods to detect acetylcarnitine involve biopsy of the tissue of interest
38                                              Acetylcarnitine is produced by the mitochondrial matrix
39 The positively charged radiolabeled product, acetylcarnitine, is separated from negatively charged ex
40                      The acetylating agent L-acetylcarnitine (LAC), a well-tolerated drug, behaves as
41  production by 35% and increased the overall acetylcarnitine pool size by 33%.
42 arnitine production by 37% and decreased the acetylcarnitine pool size by 40%.
43  between pyruvate-derived acetyl-CoA and the acetylcarnitine pool.
44 re characterized by a decreased formation of acetylcarnitine, possibly underlying decreased insulin s
45 chloroacetate increased the rate of [1-(13)C]acetylcarnitine production by 35% and increased the over
46    Dobutamine decreased the rate of [1-(13)C]acetylcarnitine production by 37% and decreased the acet
47                   Animal models suggest that acetylcarnitine production is essential for maintaining
48              Carnosine and 3 acylcarnitines (acetylcarnitine, propionylcarnitine, and 2-methylbutyryl
49 tic resonance spectroscopy has revealed that acetylcarnitine provides a route of disposal for excess
50 zed [2-(13)C]pyruvate infusion, the [1-(13)C]acetylcarnitine resonance was saturated with a radiofreq
51              In the perfused heart, [1-(13)C]acetylcarnitine saturation reduced the [1-(13)C]citrate
52 5% decrease in short-chain acylcarnitine and acetylcarnitine secretion.
53 , with strong trends for both acetyl-CoA and acetylcarnitine to actually decline (indicating the exis
54 13)C-label flux into citrate, glutamate, and acetylcarnitine, which correlated with the degree of car
55 ous distribution of 1-methylnicotinamide and acetylcarnitine, which mostly colocalized with hypoxic t
56 esulted in the biphasic changes in G-6-P and acetylcarnitine with infusion time.

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