Rats were starved for 24 hours before and 72 hours after 750 R total body x-irradiation. The exposure to x-rays was preceded by intensive labeling of tissue proteins with <tex-math>$\text{alanine-}{\rm UL}\text{-}{}^{14}{\rm C}$</tex-math>. Radioactivity and chemical analytical data on hepatic glycogen and "free" glucose as well as on plasma glucose indicate that <tex-math>${}^{14}{\rm C}\text{-alanyl}$</tex-math> residues derived from degraded tissue proteins contribute significantly to the pool which serves as a source of carbon atoms for the radiation-induced increase in hepatic gluconeogenesis and glycogenesis. Specific inhibitors of gluconeogenesis provided further evidence for the utilization of <tex-math>${}^{14}{\rm C}\text{-alanyl}$</tex-math> residues of proteins for gluconeogenesis and glycogenesis via the pathway of "reverse glycolysis." The most potent of the three inhibitors used in this study, namely, quinaldate, caused a reduction of the hepatic glycogen content and14 C activity as well as increase in plasma glucose in x- and sham-irradiated rats, whereas L-tryptophan and quinolinate had no effect on hepatic glycogen metabolism or plasma glucose in sham-irradiated rats. The results obtained with inhibitors suggest that glycerol can be excluded as an important source of carbon atoms of gluconeogenesis and glycogenesis in livers of x-irradiated rats. It appears unlikely that a radiation-induced decrease of glycogenolysis plays an important role as a contributing factor in the accumulation of hepatic glycogen during the first 48 hours when glycogen deposition attains maximal values in livers of starved, x-irradiated rats.

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