Pancreatic glucagon secretion in normal and diabetic subjects.

Availability of a relatively specific antiserum to glucagon has made possible studies of alpha cell function in man. In healthy volunteers fasting plasma glucagon averaged 13G μμg/ml (SEM ± 20); in genetic diabetics, despite their hyperglycemia, glucagon averaged 150 μμg/ml (± 26). In all normal subjects and genetic diabetics arginine infusion elicited significant increases in plasma glucagon within five minutes, with a peak at 40 minutes. The mean maximal increment of glucagon was 270 μμg/ml (± 30) in normals and 340 μμg/ml (± 60) in diabetics. In a patient with severe pancreatitis, however, glucagon was zero throughout the entire experiment. In normals the mean maximal glucose rise during arginine infusion was 16 mg7, while in genetic diabetics it was 48 mg7. It is concluded, first, that arginine induces hyperglucagonemia in normals and in presumably genetic diabetics, and that in diabetics hyperglucagoncmia, unaccompanied by proportional hyperinsulinemia, may contribute to the greater hyperglycemia; second, in genetic diabetes byperglycemia fails to reduce either the fasting glucagon concentration or the glucagon response to arginine, suggesting hypo-suppressibility of the α cell; and third, in juvenile diabetes, the α cells' capacity to synthesize hormone remains intact long after that of the cell is completely lost, suggesting an isolated α cell lesion, rather than diffuse involvement of the islet, as in the patient with severe pancreatitis.