GLUCAGON AND DIABETES.

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Abstract
In order to determine whether glucagon levels of diabetic subjects are suppressible, .alpha.- cell responsiveness to acute insulin administration (0.1 units/kg i.v.) was determined in 14 juvenile onset, healthy diabetic and 8 control subjects. In the diabetics, insulin produced a significant but slow fall in blood glucose over 60 min (P < 0.01). Glucagon levels fell dramatically in all diabetics to undetectable levels (P < 0.001). Only 1 diabetic became hypoglycemic, and he alone showed a rebound rise of glucagon at 60 min. The rate of fall of blood glucose in the diabetic subjects was not influenced by the basal glucagon level (r = 0.13) or the rate of fall of plasma glucagon (r = 0.04). The glucose and glucagon responses of control subjects to insulin administration were in sharp contrast to the diabetics: blood glucose levels fell rapidly to hypoglycemic levels and were associated with a major rise in glucagon levles (mean rise 116 pmol/l, P < 0.001). .alpha.-Cell hyperfunction in human diabetes can be completely suppressed by insulin administration and is therefore not autonomous. The slow rate of fall of blood glucose following insulin administration in diabetics is not secondary to glucagon excess.