Why the study?
Does low-dose insulin infusion reveal defective glucagon release in insulin-requiring diabetics compared to normal subjects?
Does low-dose insulin infusion reveal defective glucagon release in insulin-requiring diabetics compared to normal subjects?
Insulin-requiring diabetics exhibit a defective glucagon response to hypoglycaemia, suggesting a selective form of autonomic neuropathy affecting vagal control.
Answers are grounded in this paper and cite their sources.
Indicates selective autonomic neuropathy in insulin-requiring diabetes; leaves open contribution to clinical hypoglycaemia risk.
Administration of a low-dose insulin infusion to normal subjects results in a mild drop in blood glucose concentration (1.1 mmol/1 (20 mg/100 ml)) and the resetting of the basal glucose at the lower concentration. Clinical hypoglycaemia does not develop, and there is a significant release of glucagon, growth hormone, and cortisol. A similar infusion in insulin-requiring diabetics results in hypoglycaemia accompanied by a release of growth hormone and cortisol but no significant release of glucagon. Subsequently giving arginine to these patients results in a significant release of glucagon, indicating that the alpha cell is intact and can respond to local, direct stimulation. In one patient the defect in glucagon response to impending hypoglycaemia developed after two years' insulin treatment. This type of dissociated response' of the alpha cell has been reported in animals after denervation of the pancreas, and insulin-requiring diabetics may develop a selective form of autonomic neuropathy affecting the vagal control of glucagon release.
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Campbell et al. (1977) studied this question.
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