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J Appl Physiol 95: 1908-1916, 2003. First published July 25, 2003; doi:10.1152/japplphysiol.00909.2002
8750-7587/03 $5.00
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Octanoate oxidation measured by 13C-NMR spectroscopy in rat skeletal muscle, heart, and liver

Marlei E. Walton,1 Douglas Ebert,1 and Ronald G. Haller1,2,3

1Department of Veterans Affairs North Texas Health Care System, Dallas 75216; 2Department of Neurology, University of Texas Southwestern Medical Center, Dallas 75235; and 3Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, Dallas, Texas 75231

Submitted 2 October 2002 ; accepted in final form 22 July 2003

Contribution of octanoate to the oxidative metabolism of the major sites of fatty acid oxidation (heart, liver, and resting and contracting skeletal muscle) was assessed in the intact rat with 13C-NMR spectroscopy. Under inhalation anesthesia, [2,4,6,8-13C4]octanoate was infused into the jugular vein and the sciatic nerve of one limb was stimulated for 1 h. Octanoate was a principal contributor to the acetyl-CoA pool in all tissues examined, with highest oxidation occurring in heart and soleus muscle followed by predominantly red portion of gastrocnemius muscle (RG), liver, and then white portion of gastrocnemius muscle (WG). Fractional contribution of 13C-labeled octanoate to the acetyl-CoA pool (Fc2) was 0.563 ± 0.066 for heart and 0.367 ± 0.054 for liver. Significant differences were observed between each of the muscle types during both rest and contraction. In muscle, Fc2 was highest in soleus (0.565 ± 0.089 rested, 0.564 ± 0.096 contracted), followed by RG (0.470 ± 0.092 rested, 0.438 ± 0.072 contracted), and lowest in WG (0.340 ± 0.081 rested, 0.272 ± 0.065 contracted). Our findings demonstrate that the fractional contribution of octanoate to oxidative metabolism correlates with oxidative capacity of the tissue and that octanoate metabolism increases in contracted muscle in proportion to the overall increase in oxidative rate.

13C isotopomer analysis; metabolism; nuclear magnetic resonance; fiber type



Address for reprint requests and other correspondence: M. E. Walton, Veterans Affairs North Texas Health Care System, 4500 South Lancaster Road (151), Dallas, TX 75216 (E-mail: mwde{at}swbell.net).







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