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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%), 
  
     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. 
  
  
  
    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
  
    16 drogenase complex activation, acetyl-CoA and acetylcarnitine by approximately 20-fold (P < 0.01), app
  
    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
  
  
    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.
  
  
    31  quantitative determination of carnitine and acetylcarnitine in analytical standard solutions as well
  
  
  
    35 14C]acetyl-CoA, which is converted to [2-14C]acetylcarnitine in the presence of excess L-carnitine an
  
  
  
    39 The positively charged radiolabeled product, acetylcarnitine, is separated from negatively charged ex
  
  
  
  
    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
  
  
    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
  
  
    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
  
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