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Fatty Acid Oxidation and Ketogenesis in Transplantable Liver Tumors¹

(The Fels Research Institute, Temple University School of Medicine, Philadelphia, Pennsylvania, and The National Cancer Institute, Bethesda, Maryland)

Oxidation of butyric acid-¹⁴C and palmitic acid-¹⁴C to CO₂ and acetoacetic acid was studied in fortified homogenates of a variety of transplantable rat liver tumors. Both fatty acids were oxidized readily by the so-called "minimal deviation" hepatomas, the Morris 5123, 7793, and 7787 tumors, to a much lesser extent by the Reuber H-35 and Morris 7288C tumors, and hardly at all by the Morris 3924A and 3683 tumors and the Novikoff hepatoma. The ratio of fatty acid oxidation to CO₂ and to acetoacetate varied widely; for the most part, though, there was a resemblance to the pattern displayed by liver, in those tumors which oxidized the fatty acids. In general there was a reciprocal relationship between the ability to oxidize fatty acids and the ability to phosphorylate glucose. Those tumors which grew slowly and lacked the capability for glucose phosphorylation readily oxidized fatty acids, whereas the high glycolyzing tumors failed to oxidize fatty acids.

Randomization of ¹⁴C label from butyrate-3-¹⁴C into carbons 1 and 3 of acetoacetate occurred in all tumors that oxidized butyrate, pointing to the presence in these tumors of the same complex of enzymes for fatty acid oxidation as occurs in liver.

¹ This work was aided by a grant from the American Cancer Society (P 119) and by grants from the National Institutes of Health (AM-05487 and CA-07174).

² On leave from the Department of Experimental Medicine and Cancer Research, Hebrew University-Hadassah Medical School, Jerusalem, Israel.

³ This work will be included as part of a thesis, to be submitted by John Langan to the Graduate Council of Temple University in partial fulfillment of the requirements for the degree of Doctor of Philosophy.

Received 12/23/64.