(13-03-06) Glucagon response to hypoglycaemia tied to insulin secretion drop

NEW YORK (Reuters Health) - Increasing the drop in insulin secretion associated with the development of hypoglycemia leads to an increased glucagon response in advanced type 2 diabetes, researchers report in the November issue of Diabetes Care.

Dr. Christian Meyer of Hayden VA Medical Center, Phoenix, Arizona and colleagues note that in advanced beta-cell failure, a decrease in insulin secretion may prompt an increase in glucagon secretion during hypoglycemia. Thus, an absence or marked reduction in this decrease may help explain impaired glucagon responses seen in diabetes.
To investigate, the researchers studied 12 subjects with type 2 diabetes who were being treated with insulin.
Glucagon responses were examined during a 90-minute hypoglycemic clamp on two separate occasions. During one, the insulin secretagogue tolbutamide was infused for 2 hours before the clamp in order to raise insulin secretion, and thereby to artificially increase the decrement in insulin secretion during the subsequent hypoglycemic episode. On the other occasion, a control saline infusion was used.
Before the hypoglycemic clamp, the tolbutamide infusion almost doubled insulin secretion. However, after both tolbutamide and saline, during hypoglycemia, insulin secretion fell to similar levels, so the insulin "decrement was approximately twofold greater." Accordingly, during the subsequent hypoglycemic clamp, glucagon responses were more than twofold greater.
Moreover, on both occasions, plasma glucagon increased to similar levels in response to arginine given immediately after hypoglycemia, suggesting that tolbutamide had no residual effects.
Dr. Meyer told Reuters Health that these findings in humans and results of other studies indicate that "a decrease in insulin secretion is an important signal for increased secretion of glucagon during hypoglycemia."
"One may therefore postulate," he concluded, "that preserving beta-cell function in patients with diabetes may not only delay the onset of insulin requirement but also the defects in counterregulatory glucagon responses that are associated with severe insulin deficiency."

Source : Diabetes Care 2005;28:2691-2696.

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