L-Amino acids, when administered intra-peritoneally either individually or as mixtures to fasted rats, blocked the epinephrine-induced hyperglycemic response. The injection of 2.5 mmoles/kg of either arginine, lysine, leucine, isoleucine, threonine, or tryptophan inhibited epinephrine-induced hyperglycemia 76–89%. The same dosage of methionine or valine had less effect on the hyperglycemic response (42 and 32% respectively). By contrast phenylalanine and histidine did not exhibit significant inhibitory actions (4 and 6% respectively) at the same dosages. Equivalent amounts of bovine serum albumin, casein hydrolysate, or a mixture of 10 essential amino acids were no more inhibitory than either valine or methionine alone. In addition the non-metabolizable amino acids, α-aminoisobutyric acid and 1-aminocyclo-pentanecarboxylic acid are about as potent as methionine and valine in blocking epinephrine hyperglycemia. Several metabolites of tryptophan, namely indole-3-acetic acid, quinolinic acid, and hydroxyanthranilic acid blocked epinephrine hyperglycemia 87–99%. Xanthurenic acid, kynurenic acid, and serotonin inhibit the response 48–65%. DL-Kynurenine was the least potent exhibiting a 24-percent inhibition. In addition the tryptophan analogue, DL-α-methyltryptophan produced an 47-percent inhibition. The fact that no correlation could be found between the capacities of the amino acids to produce hypoglycemia and their capacity to inhibit epinephrine-induced hyperglycemia suggests than insulin is not involved in preventing the hyperglycemic response. This idea is supported by the observation that tryptophan inhibits epinephrine-induced hyperglycemia to the same extent in both intact and diabetic rats.

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The injection of epinephrine (1.0 mg/kg) into alloxan-diabetic, fasted rats depressed the serum concentration of previously administered α-aminoisobutyric acid (AIB) and 1-aminocyclopentanecarboxylic acid (ACPC) within 2 h and simultaneously increased the concentration of these amino acids in the liver. The increase of ACPC and AIB concentrations in the liver following epinephrine injection was nearly 3 times as great in the alloxan-diabetic rats as in normal intact rats. The levels of the two amino acids in skeletal muscle, heart, and diaphragm of the alloxanized rats were unchanged following epinephrine injection, but the distribution ratios in these tissues were raised because the serum concentration decreased 20%.Further studies were carried out employing rats that were treated 1 h before epinephrine injection, with mannoheptulose, a compound which blocks insulin release. The concentration of ACPC and AIB in the serum 2 h after epinephrine injection were lowered. At the same time the concentrations of ACPC in liver and heart were raised, as was the concentration of AIB in heart. The levels of the two amino acids in skeletal muscle and diaphragm were unaltered. However, distribution ratios were raised in the four tissues. These results demonstrate that epinephrine enhances AIB and ACPC transport into the tissues of the insulin-deficient rats in vivo and suggest that epinephrine-stimulated amino acid transport is not due indirectly to insulin.

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