ライフサイエンスコーパス: acetylcarnitine

1 ductions in acylcarnitines and elevations in acetylcarnitine.

2 2 of beta-hydroxybutyrate, malonyl-CoA, and acetylcarnitine.

3 e conversion of acetyl-coenzyme A (CoA) into acetylcarnitine.

4 was no detectable current in the presence of acetylcarnitine.

5 transport carnitine, propionylcarnitine and acetylcarnitine.

6 anges in [(13)C]bicarbonate (-48%), [1-(13)C]acetylcarnitine (+113%), and [5-(13)C]glutamate (-63%),

7 creased muscle PDC activity (130%) and flux (acetylcarnitine 130%) and decreased inhibitory phosphory

8 The observed enrichment of (13)C in acetylcarnitine (19%), M+6 stearoylcarnitine (16.2%), an

9 ce of M+2 myristoylcarnitine (95.7%) and M+2 acetylcarnitine (19.4%) is evidence for beta-oxidation o

10 ylglycine, 1-methylnicotinamide, methionine, acetylcarnitine, 2-oxoglutarate, choline, and creatine.

11 Treatment with acetylcarnitine (AcCN) increases the activity of cytochr

12 Whereas (+)-acetylcarnitine also failed to influence CACT, both (+)-

13 release of 2 specific acylcarnitine species, acetylcarnitine and 3-hydroxybutyryl-carnitine.

14 s on the abundance of two polar metabolites (acetylcarnitine and cytidine-5-diphosphocholine) during

15 eased tissue efflux and urinary excretion of acetylcarnitine and improvement of whole body glucose to

16 Because of this channeling, the labeling of acetylcarnitine and ketone bodies released by the heart

17 the release of small excess acetyl groups as acetylcarnitine and ketone bodies, and (iii) the channel

18 The association between plasma acetylcarnitine and multiple organ dysfunction severity,

19 This included acetylcarnitine and ornithine, which are considered part

20 human kidney tissue, such as argininic acid, acetylcarnitine, and choline that localize to the cortex

21 Cycling of acetyl-CoA through acetylcarnitine appears key to matching instantaneous ac

22 cetylornithine, D-glucose, putrescine, and L-acetylcarnitine are consumed in relatively large amounts

23 The data define acetylcarnitine as an ACLY- and ACSS2-independent precur

24 drogenase complex activation, acetyl-CoA and acetylcarnitine by approximately 20-fold (P < 0.01), app

25 ine and higher long-chain acylcarnitines and acetylcarnitine (C2) but lower palmitoylcarnitine (C16)-

26 Acetylcarnitine (C2), showing a late response pattern an

27 s like propionylcarnitine (C3), its ratio to acetylcarnitine (C3/C2) and palmitoylcarnitine (C3/C16).

28 oduction of [5-(13)C]glutamate and [1-(13)C] acetylcarnitine can be observed real time in vivo.

29 We confirm that plasma acetylcarnitine can reflect the severity of organ dysfun

30 enzymatic conversion of pyruvate to lactate, acetylcarnitine, citrate, and glutamate with 1 s tempora

31 ne, acetone, leucine, quinolinate, valine, O-acetylcarnitine, citrate, and trigonelline.

32 (P < 0.01), when there was a 47% decrease in acetylcarnitine concentration (P < 0.05), and a 24-fold

33 showed a reciprocal distribution, with mean acetylcarnitine concentration correlating with mean insu

34 Skeletal muscle acetylcarnitine concentration showed a reciprocal distri

35 omic analysis showed a 2.2 times increase in acetylcarnitine concentrations (p=0.002).

36 nterest, noninvasive alternatives to measure acetylcarnitine concentrations could facilitate our unde

37 Interestingly, acetylcarnitine concentrations in skeletal muscle were i

38 troscopy (1H-MRS) to measure skeletal muscle acetylcarnitine concentrations on a clinical 3T scanner.

39 min of passive recovery, muscle lactate and acetylcarnitine concentrations were elevated above basal

40 These results demonstrate that measuring acetylcarnitine concentrations with 1H-MRS is feasible o

41 ate dehydrogenase complex (PDC) activity and acetylcarnitine content at rest, it has also been establ

42 chenodesoxycholic acid and lower levels of L-acetylcarnitine, creatinine, L-asparagine, L-glutamine,

43 irst 3 min of infusion, the concentration of acetylcarnitine declined (pre-infusion = 3.8 +/- 0.3 vs.

44 derivatives, rose from virtual absence, and acetylcarnitines fell.

45 GCBCs generate most of their acetyl-CoA and acetylcarnitine from FAs.

46 Patients with high plasma acetylcarnitine (>= 6,000 ng/mL) had significantly incre

47 The effect on each of (+)-acetylcarnitine, (+)-hexanoylcarnitine, (+)-octanoylcarn

48 quantitative determination of carnitine and acetylcarnitine in analytical standard solutions as well

49 We applied long-TE 1H-MRS to measure acetylcarnitine in endurance-trained athletes, lean and

50 ategy to the quantification of carnitine and acetylcarnitine in rat liver is shown.

51 umulation of glucose-6-phosphate (G-6-P) and acetylcarnitine in resting canine skeletal muscle.

52 14C]acetyl-CoA, which is converted to [2-14C]acetylcarnitine in the presence of excess L-carnitine an

53 for successful detection of skeletal muscle acetylcarnitine in these individuals.

54 Because current methods to detect acetylcarnitine involve biopsy of the tissue of interest

55 Acetylcarnitine is produced by the mitochondrial matrix

56 However, acetylcarnitine is the only acylcarnitine significantly

57 The positively charged radiolabeled product, acetylcarnitine, is separated from negatively charged ex

58 The acetylating agent L-acetylcarnitine (LAC), a well-tolerated drug, behaves as

59 ay mortality compared with those with plasma acetylcarnitine less than 6,000 ng/mL (52.6% vs 13.9%; h

60 e NAD+ metabolites, affected skeletal muscle acetylcarnitine metabolism, and induced minor changes in

61 production by 35% and increased the overall acetylcarnitine pool size by 33%.

62 arnitine production by 37% and decreased the acetylcarnitine pool size by 40%.

63 between pyruvate-derived acetyl-CoA and the acetylcarnitine pool.

64 re characterized by a decreased formation of acetylcarnitine, possibly underlying decreased insulin s

65 chloroacetate increased the rate of [1-(13)C]acetylcarnitine production by 35% and increased the over

66 Dobutamine decreased the rate of [1-(13)C]acetylcarnitine production by 37% and decreased the acet

67 Animal models suggest that acetylcarnitine production is essential for maintaining

68 Carnosine and 3 acylcarnitines (acetylcarnitine, propionylcarnitine, and 2-methylbutyryl

69 tic resonance spectroscopy has revealed that acetylcarnitine provides a route of disposal for excess

70 zed [2-(13)C]pyruvate infusion, the [1-(13)C]acetylcarnitine resonance was saturated with a radiofreq

71 In the perfused heart, [1-(13)C]acetylcarnitine saturation reduced the [1-(13)C]citrate

72 5% decrease in short-chain acylcarnitine and acetylcarnitine secretion.

73 ndent histone acetylation required an intact acetylcarnitine shuttle.

74 nd histone acetylation in DKO cells and that acetylcarnitine shuttling can transfer two-carbon units

75 , with strong trends for both acetyl-CoA and acetylcarnitine to actually decline (indicating the exis

76 y weight, P = 0.04) and the capacity to form acetylcarnitine upon exercise was higher in NR than in p

77 levated compared to controls, while [1-(13)C]acetylcarnitine was not different.

78 13)C-label flux into citrate, glutamate, and acetylcarnitine, which correlated with the degree of car

79 ous distribution of 1-methylnicotinamide and acetylcarnitine, which mostly colocalized with hypoxic t

80 esulted in the biphasic changes in G-6-P and acetylcarnitine with infusion time.