BLOOD GLUCOSE LEVEL IN MICE.

Abstract

ABSTRACT Using serial sampling (25 μl) the blood glucose level in individual mice was followed during the induction of and during the steady state of alloxan diabetes. It was found that 70 mg/kg body weight of alloxan, given intravenously to female NMRI mice, caused 1) a rapid blood glucose level increase to 300–400 mg/100 ml within 45 minutes (initial hyperglycaemia), the increase being highly significant after 10 minutes; 2) a subsequent fall in blood glucose (hypoglycaemic phase) to levels of about 50 mg/100 ml measured from 4–8 hours following alloxan injection, sometimes associated with convulsions and death; 3) permanently elevated blood sugar levels from 12–48 hours after alloxan injection (final hyperglycaemia). Permanently diabetic mice still possess a blood sugar level homeostatic mechanism as shown by relatively constant individual blood glucose levels in a population with large differences between animals. This mechanism is highly sensitive to external influences such as handling and blood sampling. A second dose of alloxan, diabetogenic in normal mice, was completely ineffective in diabetic mice irrespective of their degree of hyperglycaemia. Insulin administration or hypophysectomy abolished the initial hyperglycaemia following alloxan injection. Adrenalectomy greatly reduced but failed to abolish the initial hyperglycaemic phase. Alloxan injection into hypophysectomized or adrenalectomized animals resulted in fatal hypoglycaemia. Alloxan diabetic mice responded to hypophysectomy by a total disappearance of hyperglycaemia within 24 hours and death in severe hypoglycaemia within one week. Liver glycogen levels were decreased during the initial hyperglycaemic phase. The hypothesis is put forward that the liver glycogen level at the time of alloxan injection may play a role in the occurrence and intensity of the initial hyperglycaemic phase.