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GLUCAGON AND DIABETES
Author(s) -
WARNE G. L.,
ALFORD F. P.,
CHISHOLM D. J.,
COURT J.
Publication year - 1977
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.1977.tb02012.x
Subject(s) - glucagon , medicine , endocrinology , insulin , basal (medicine) , diabetes mellitus , hypoglycemia
SUMMARY In order to determine whether glucagon levels of diabetic subjects are suppressible, alpha cell responsiveness to acute insulin administration (0.1 units/kg intravenously) was determined in fourteen juvenile onset, healthy diabetic and eight control subjects. In the diabetics, insulin produced a significant but slow fall in blood glucose over 60 min ( P <0.01). On the other hand, glucagon levels fell dramatically in all diabetics to undetectable levels ( P <0.001). Only one diabetic became hypoglycaemic 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 hypoglycaemic levels and were associated with a major rise in glucagon levels (mean rise 116 pmol/1, P <0.001). We conclude that alpha cell hyperfunction in human diabetes can be completely suppressed by insulin administrtion and is therefore not autonomous, and that the slow rate of fall of blood glucose following insulin administration in diabetics is not secondary to glucagon excess.