Hepatic gluconeogenesis and glycogenesis in the starved, x-irradiated rat

body x-irradiation. The exposure to x-rays was preceded by intensive labeling of tissue proteins with alanine-UL-14C. Radioactivity and chemical analytical data on hepatic glycogen and free glucose as well as on plasma glucose indicate that 14C-alanyl 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 14C-alanyl 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 and 14C 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. 1 This paper is based on work performed under contract with the U.S. Atomic Energy Commission at the University of Rochester Atomic Energy Project and has been assigned Report No. UR-49-1224.