A study of glucose utilization in the Morris 5123 hepatomas indicates that these tumors have a low capability for glucose uptake and for conversion of glucose to lactate and CO2. Whole homogenates of these tumors exhibit a high respiration when fortified with nicotinamide adenine dinucleotide and adenosine triphosphate but utilize little glucose. On addition of crystalline yeast hexokinase, lactic acid production is increased from five- to twentyfold and oxidation to CO2 is increased two- to fivefold. Lactate production was as rapid from glucose-6-phosphate or fructose-1,6-diphosphate as from glucose and hexokinase. However, oxygen uptake was unchanged, with or without glucose, or hexokinase, or the hexose phosphates. The data point to a deficiency of glucokinase in these tumors, and this assumption was borne out by independent glucokinase assays, which indicate that this enzyme is present in quantities approximately one-third to one-fifth that of normal liver, and are of the order of one-tenth those of highglycolyzing tumors. In a study of a variety of other hepatomas a wide diversity in glucose utilization was observed, which was dependent on glucokinase levels. Those tumors which glycolyze slowly and have low glucokinase activity grow slowly and require more than 2 months to reach detectable size, whereas the highly glycolyzing hepatomas, with high glucokinase activity, grow to large size in less than 2 weeks.


This work was aided by grants from the American Cancer Society and the National Cancer Institute, National Institutes of Health.

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