Prevention of human diabetic ketoacidosis by somatostatin: evidence for an essential role of glucagon
JE Gerich, M Lorenzi, DM Bier… - … England Journal of …, 1975 - Mass Medical Soc
JE Gerich, M Lorenzi, DM Bier, V Schneider, E Tsalikian, JH Karam, PH Forsham
New England Journal of Medicine, 1975•Mass Medical SocTo evaluate the role of glucagon in the pathogenesis of diabetic ketoacidosis in man, we
studied the effect of suppression of glucagon secretion by somatostatin on changes in
plasma β-hydroxybutyrate and glucose concentrations (as well as changes in their
precursors) after acute withdrawal of insulin from seven patients with juvenile-type diabetes.
Suppression of glucagon secretion prevented the development of ketoacidosis for 18 hours
after acute insulin withdrawal, whereas in control studies mild ketoacidosis occurred 10 …
studied the effect of suppression of glucagon secretion by somatostatin on changes in
plasma β-hydroxybutyrate and glucose concentrations (as well as changes in their
precursors) after acute withdrawal of insulin from seven patients with juvenile-type diabetes.
Suppression of glucagon secretion prevented the development of ketoacidosis for 18 hours
after acute insulin withdrawal, whereas in control studies mild ketoacidosis occurred 10 …
Abstract
To evaluate the role of glucagon in the pathogenesis of diabetic ketoacidosis in man, we studied the effect of suppression of glucagon secretion by somatostatin on changes in plasma β-hydroxybutyrate and glucose concentrations (as well as changes in their precursors) after acute withdrawal of insulin from seven patients with juvenile-type diabetes.
Suppression of glucagon secretion prevented the development of ketoacidosis for 18 hours after acute insulin withdrawal, whereas in control studies mild ketoacidosis occurred 10 hours after insulin was stopped. Plasma β-hydroxybutyrate, glucose, free fatty acid, and glycerol levels were all markedly lower during suppression of glucagon secretion (p < 0.001), whereas plasma alanine levels were higher (P<0.001).
These studies indicate that insulin lack per se does not lead to fulminant diabetic ketoacidosis in man and that glucagon, by means of its gluconeogenic, ketogenic, and lipolytic actions, is a prerequisite to the development of this condition. (N Engl J Med 292:985–989,1975)
The New England Journal Of Medicine