Glucose counterregulation in diabetes secondary to chronic pancreatitis

• Published in: Metabolism, clinical and experimental Vol. 39; no. 2; p. 138
• Main Authors: Larsen, S, Hilsted, J, Philipsen, E K, Tronier, B, Christensen, N J, Damkjaer Nielsen, M, Worning, H
• Format: Journal Article
• Language: English
• Published: United States 01.02.1990
• Subjects: Adrenergic beta-Antagonists - administration & dosage; Blood Glucose - analysis; Blood Pressure - drug effects; Diabetes Mellitus - blood; Diabetes Mellitus - drug therapy; Diabetes Mellitus - etiology; Diabetes Mellitus, Type 1 - blood; Diabetes Mellitus, Type 1 - drug therapy; Female; Glucagon - blood; Glycerol - blood; Heart Rate - drug effects; Hormones - blood; Humans; Hydroxybutyrates - blood; Hypoglycemia - chemically induced; Hypoglycemia - metabolism; Insulin - administration & dosage; Insulin - physiology; Lactates - blood; Male; Middle Aged; Pancreatic Polypeptide - blood; Pancreatitis - complications
• ISSN: 0026-0495
• DOI: 10.1016/0026-0495(90)90066-L

Glucose counterregulation and hormonal responses after insulin-induced hypoglycemia were investigated in six patients with diabetes mellitus secondary to chronic pancreatitis, in seven with insulin-dependent (type I) diabetes mellitus, and in seven healthy subjects. Glucose counterregulation was identical in type I patients and in the patients with chronic pancreatitis, whereas both groups had impaired glucose recovery compared with the healthy subjects. The patients with chronic pancreatitis had no glucagon response to hypoglycemia, whereas epinephrine increased significantly. In an additional experiment, glucose recovery did not occur after hypoglycemia during concomitant beta-adrenoceptor blockade in these patients. In conclusion, glucose counterregulation is preserved but slightly impaired in patients with diabetes secondary to chronic pancreatitis, and the combination of total glucagon deficiency and pharmacological blockade of the metabolic actions of circulating epinephrine abolishes glucose counterregulation after hypoglycemia.