Seven fasted, healthy, anesthetized dogs were successively injected at a two-hour interval with guinea pig antiinsulin serum and with insulin. The dose of anti-insulin serum used had a total neutralizing potency of 2 U. insulin per kilogram body weight; the amount of insulin used was sufficient to restore normal blood glucose level. Glucose production was determined by hepatic catheterization; glucose tissue utilization by the study of the disappearance rate of a tracer dose of glucose l-C-14.

Anti-insulin serum induced hyperglycemia in five dogs and failed to provoke any change in blood glucose among the two others. This difference of behavior was probably related with differing sensitivity to the same fast.

In responders, hyperglycemia was accompanied by an increase in liver glucose output and by a reduction of tissue glucose utilization; insulin, when given in sufficient amount to restore normal blood glucose level, induced a decrease of glucose production and an increase in glucose utilization to basal values.

In the nonresponders, together with a slight decrease in glucose utilization, a tendency to reduced glucose production was noticed. The doses of insulin necessary to provoke hypoglycemia were three times more important than those used in the responders.

The action of insulin on liver glucose production observed in these acute deficiencies of insulin are discussed in relation to experiments previously carried out on normal dogs.

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