1. The significant reduction of the concentration of ascorbic acid in adrenals in normal rats 2 hours after the exposure to cold stress (O°C, 30 minutes) was observed. Normal rats showed the slight hyperglycemia just after the exposure, but the blood sugar returned soon to initial level and held the normal level during 10 hours. In adrenalectomized rats, the blood sugar fell just after the exposure, then turned to upward during 2 hours but did not return to the initial level even after 10 hours.
2. Although the ascorbic acid concentration in adrenals in rats showed a significant reduction when 1 or 2 mg. of ACTH was given, the fasting blood sugar did not show any changes. So the hyperactivity of pituitary adrenocortical system which is. produced by the alloxan can not be the single cause of the initial hyperglycemia.
3. The diabetogenic action of alloxan disappears within 5 minutes after the time of injection, without any possible involvement of the liver.
4. In normal rabbits which were injected alloxan in dose of, 100mg. per kg. of body weight, the response is the typical triphasic reaction of the blood sugar followed by permanent diabetes. However, when. the liver is stunted from the blood stream for 5 minutes after the injection of alloxan by temporary ligation of hepatic artery and portal vein, the alloxan initial hyperglycemia is completely gone or at least markedly repressed. As the influence of operative procedure can entirely be excluded, it is suggested that alloxan has an action to the liver and produces the mobilization of liver glycogen.
5. These observations and discussions in all lead to a conclusion that the alloxan initial hyperglycemia is probably produced by the hyperactivity of pituitary adrenocortical system on one hand, and by the mobilization of liver glycogen by the effect of alloxan on the liver on the other hand.
The author acknowledges with deep appreciation the kind advices and helps given to him by Prof. Shigeo Okinaka and Instructor Nobusada Kuzuya.