Glucose Suppression of Glucagon: Relationship to Pancreatic Beta Cell Function?

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Abstract
Plasma insulin and glucagon responses during 4h, 50 g oral glucose tolerance tests were assessed in 35 adults subdivided into four groups: weight-matched obese control and obese diabetic; lean control and lean, insulin-requiring diabetic subjects. Average basal glucagon levels were not significantly different among the four groups despite relative fasting hyperinsulinemia in obese subjects. Patterns of plasma glucagon suppression and plasma insulin excursions after oral glucose loading differentiated the four groups from one another. In obese controls, brisk hyperinsulinemia was associated with sustained suppression of glucagon from 60 through 240 min. In lean controls, significant glucagon suppression also occurred at 60 min but was not sustained. Subnormal plasma insulin increments during the initial 60 min of the test in obese diabetic subjects was attended by a delayed onset of glucagon suppression at 90 min which was also unsustained. In lean diabetic subjects no suppression of glucagon was observed at any time interval, and this corresponded to a markedly attenuated plasma insulin increment. Total plasma glucagon suppression during the 4 h procedure related better to initial 30 min plasma insulin increments than to the total 240 min insulin response curve. We conclude that there is an association between the degree of plasma glucagon suppression after oral glucose loads and the briskness and magnitude of the plasma insulin response. Resistance to suppression in diabetes relates to the degree of insulin deficiency. Accentuated glucagon suppression in obese nondiabetic subjects follows exaggerated postchallenge hyperinsulinemia.