Issue 127 Item 15 Autonomic Defect At Root Of Low Glucagon Response In Type 1 Di

“Residual insulin secretion is not coupled to a maintained glucagon response to hypoglycemia in long-term type 1 diabetes.” Autonomic nervous dysfunction is the most likely cause of defective glucagon secretory response to hypoglycemia in type 1 diabetes.

Dr S Sjoberg and coworkers from the Departments of Medicine Huddinge University Hospital, Karolinska Instituetet, Stockholm, and at Lund University, Lund, Sweden, came to this conclusion as a result of a study they undertook on 18 type 1 diabetics of long duration (nine of whom had residual insulin secretion) and 12 healthy subjects. The purpose of the study was to evaluate the influence of residual beta-cell function on glucagon secretion and glucose counter-regulation following hypoglycemia in the type 1 diabetics.

While the hypoglycemic nadirs were similar in all groups, the recovery of plasma glucose levels was delayed in the diabetic groups. Plasma glucagon in the control subjects increased by about 50 percent. In contrast, no glucagon response occurred in the two diabetic groups. The peak values of plasma adrenaline and pancreatic polypeptide response to hypoglycemia (markers of autonomic function) were similar in the two diabetic groups but were lower in the healthy control subjects.

The researchers concluded, "Residual beta-cell function in patients with long-term type 1 diabetes is not accompanied by preservation of the glucagon response to hypoglycemia".

They added that since the markers of autonomic function were reduced in the two diabetic groups in a similar manner, it is likely that the defective glucagon response to hypoglycemia is because of autonomic nervous dysfunction.
J Intern Med 2002;252(4):342-51