Hepatoma 5123 as compared with liver showed a marked deficiency in incorporation of labeled carbon into glycogen, CO2, and fatty acids; however, lactate production was normal. The lesion in glycogenesis agrees with the decreased phosphoglucomutase activity of this tumor. Incubation of hepatoma slices with pyruvate showed markedly depressed glucose production, revealing a decrease in gluconeogenesis. This is in line with the decreased glucose-6-phosphatase and fructose-1,6-diphosphatase activities of this tumor. The preferential oxidation of carbon-1 of glucose in Morris tumor, as in normal liver, is compatible with the normal glucose-6-phosphate dehydrogenase activities of these tissues. Thus, the increase in the direct oxidative pathway and in glucose-6-phosphate dehydrogenase activity as well as the high lactate production of the Novikoff tumor were not present in Hepatoma 5123. However, the decreased glycogen synthesis and the depressed phosphoglucomutase activity occurred in both tumors to a similar extent. The gluconeogenic pathway which failed to operate in the Novikoff tumor, partly as a result of the absent specific phosphatases, was functioning in the Morris tumor, where part of the activities of these enzymes was retained.

The extent of the examined carbohydrate metabolic lesions may be correlated roughly with the growth rates of Morris and Novikoff hepatomas.


This work was supported in part by grants from the Damon Runyon Memorial Fund for Cancer Research, Inc. (DRG-542), American Cancer Society (No. E-254), and National Cancer Institute, National Institutes of Health, U.S. Public Health Service (CY-5034).

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