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Effect of Acylcarnitines on Pyruvate Metabolism in Liver Mitochondria from Thiamin-deficient Rats1

R. J. Paquet, M. A. Mehlman, R. B. Tobin and E. M. Sporn2

Department of Biochemistry, University of Nebraska, College of Medicine, Omaha, Nebraska 68105, and Veterans Administration Hospital, Omaha, Nebraska 68105

The effect of acylcarnitines on pyruvate metabolism was compared in liver mitochondria from thiamin-deficient and pair-fed rats. Respiration and oxidative phosphorylation were investigated with pyruvate, succinate, {alpha}-ketoglutarate or {alpha}-glycerophosphate as substrate. The respiratory rate was significantly decreased in state 4 when {alpha}-glycerophosphate was used as substrate (P < 0.001). In state 3, the respiratory rates in the presence of {alpha}-ketoglutarate, pyruvate or {alpha}-glycerophosphate were significantly decreased (P < 0.05). The ratio of ADP to oxygen was decreased when {alpha}-ketoglutarate was used as substrate (P < 0.025). Pyruvate utilization by liver mitochondria from thiamin-deficient rats was markedly decreased but the percentages of pyruvate carboxylation and oxidation were not altered. Acylcarnitines stimulated pyruvate carboxylation more in deficient mitochondria than in mitochondria from pair-fed controls. Maximum stimulation in the percentage carboxylation of pyruvate was obtained in the presence of 0.83 mM L-octanoylcarnitine. Pyruvate oxidation was greatly reduced by the addition of acylcarnitines. These experiments indicate that the ability of fatty acids to alleviate the symptoms of thiamin deficiency may be related to their effect on the regulation of pyruvate carboxylase, a key enzyme in the pathway of gluconeogenesis.

1 Supported by Army Research Grant no. DAHC 1968 G0039, and National Institutes of Health Grant no. AM 13782-02.

2 Present address: Life Science Division, Army Research Office, 3045 Columbia Pike, Arlington, Virginia 22204.

Manuscript received 27 March 1970.




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