The role of glucagon, catecholamines and cortisol in counterregulation of insulin-induced hypoglycemia in normal man

• Published in: Acta medica Scandinavica Vol. 220; no. 1; p. 39
• Main Authors: Lins, P E, Adamson, U, Clausen, N, Hamberger, B, Efendić, S
• Format: Journal Article
• Language: English
• Published: Sweden 01.01.1986
• Subjects: Adult; Epinephrine - blood; Glucagon - pharmacology; Humans; Hydrocortisone - blood; Hypoglycemia - blood; Hypoglycemia - chemically induced; Insulin - administration & dosage; Insulin Antagonists - pharmacology; Male; Norepinephrine - blood; Somatostatin - pharmacology
• ISSN: 0001-6101
• DOI: 10.1111/j.0954-6820.1986.tb02728.x

To study the response of glucose counterregulation to insulin-induced hypoglycemia, six normals were given a 4-hour infusion of insulin (2.4 U/h) +/- somatostatin (50 micrograms/h). Supplementary glucagon (1.5 or 3.0 ng/kg/min) was given in additional experiments. In a separate study, glucagon was supplemented for 4 hours as a constant rate infusion (3.25 ng/kg/min) or at rates stepwise increasing from 1.5 to 5.0 ng/kg/min. Insulin decreased blood glucose by 1.5 mmol/l and simultaneous suppression of glucagon resulted in a more pronounced hypoglycemia enhancing the adrenaline and cortisol responses. The hyperglycemic effect of glucagon substitution (3 ng/kg/min) faded out after about 2 hours, whereafter exaggerated adrenaline and cortisol responses to hypoglycemia were seen. A comparison between the effects of steady state hyperglucagonemia and gradually appearing hyperglucagonemia on the counterregulation of hypoglycemia revealed no significant differences in glucose, adrenaline and cortisol responses to insulin. It is concluded that the glycemic effect of glucagon is transient in the hypoglycemic state. When the hepatic responsiveness to this hormone is decreased during hypoglycemia, adrenaline becomes the essential protective factor.