Glycogen metabolism in Novikoff ascites-hepatoma cells

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Abstract
A study of the enzymes of the glycogen pathway in Novikoff ascites hepatoma shows that glycogen synthetase has the lowest activity and that the tumour contains no high-Km soluble glucokinase. However, incubation of tumour cells with metabolizable sugars in vitro, or intraperitoneal administration of glucose into the tumour-bearing rat, results in glycogen accumulation by the tumour cells. Glycogen synthesis in the tumour is supported by aerobically produced ATP but is decreased anaerobicially and by uncouplers of oxidative phosphorylation. Absence of P1 from the intubation medium increases glycogen synthesis arid decreases glycolysis. The optimum temperature for glycogen synthesis is 37[degree]. The capacity of the intact tumour cell to degrade deposited glycogen is low, but is accelerated by 2, 4-dinitrophenol. Tumour homogenates prepared after osmotic shock do not incorporate [14C]glucose into glycogen. The glucose moiety of glucose 1-phosphate, and of UDP uridine diphosphate glucose is incorporated into glycogen by the homogenates and the incorporation of glucose 1-phosphate is greatly enhanced by AMP (adenosine monophosphate). Glucose 6-phosphate is a poor precursor of glycogen in the homogenate system, probably because it inhibits activation of phosphorylase b by AMP.