Abstract

1. 1. Male buffalo rats, with and without Morris Hepatoma 7787, were adapted to a schedule of 4 hr feeding-20 hr fasting for at least 3 weeks before the experiments. 2. 2. Livers and hepatomas were taken from anaesthetized rats by freeze-clamping. 3. 3. In normal animals, liver glycogen rose 34-fold, peaking 12 hr after feeding. At this time, the stomach retained about 40% of its immediately post-prandial contents. 4. 4. In 3 hr, glucose 6-phosphate rose from 0.11 to 0.35 mM, and uridine-diphosphate glucose from 0.28 to 0.39 mM. 5. 5. The injection of radioactive fructose was used to determine the rate of glycogen synthesis 6 hr after the onset of feeding in normal liver, in Hepatoma 7787, and the liver of the tumor-bearing rat (host liver). 6. 6. The rates were 0.27, 0.006 and 0.033 mM glucose equivalents/min, respectively. The isotopic labelling pattern suggested that glycogen was compartmented into “active” and “inactive” portions. 7. 7. The uridine-diphosphate glucose of all three tissues was highly labelled in 20–40 min, indicating that Hepatoma 7787 has no impairment of fructose metabolism. 8. 8. The data obtained are used in the accompanying paper to construct models of glycogen metabolism for each tissue.

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