Gluconeogenesis from14C- and3H-Labeled Substrates in Normal and Cortisone-Treated Rats

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Abstract
Treat-ment of rats for 4 days with cortisone acetate (20 nag/day) was followed by intraperitoneal injection in trace amount of one of the following pairs of compounds DL-alanine-2-C14, DL-lactic acid-2-H3; DL-malic acid-3-C14, DL-malic acid-2-H3; succinic acid-2,2[image]-c14, succinic acid-2,2[image]-H3; or glycerol-1,3-C14, glycerol-2-H3. Conversion of radioactivity to CO2, blood glucose and liver glycogen was studied. With all C14-labeled substrates t here was an increase of C14o2 after cortisone, which was partly due to an increased specific activity and partly to a general increase of respiration. Incorporation of C14 from alanine and malate into blood glucose was increased about 2-fold after cortisone, and there was no change in C14 from succinate or glycerol. Incorporation of tritium from lactate and malate into glucose was increased 4-fold and 5-fold, respectively, after cortisone, but there was no change in the amount of H3 transferred to glucose from suc-cinate or glycerol. Tracer incorporation into glycogen was increased markedly from alanine-C14, malate-C14, lactate-H3 and malate-H3, less markedly from guccinate-C14 and glycerol-C14, and there was no significant change with succinate-H3 or glycerol-H3. Though not increased by cortisone, the conversion of H3 to glucose and glycogen from succinate or glycerol was basically higher than from lactate or malate.