AJP - Endocrinology and Metabolism, Vol 252, Issue 1 E1-E7, Copyright © 1987 by American Physiological Society
Pulsatile hyperglucagonemia fails to increase hepatic glucose production in normal man
G. Paolisso, A. J. Scheen, A. S. Luyckx and P. J. Lefebvre
To study the metabolic effects of pulsatile glucagon administration, six
male volunteers were submitted to a 260-min glucose-controlled glucose
intravenous infusion using the Biostator. The endogenous secretion of the
pancreatic hormones was inhibited by somatostatin (100 micrograms X h-1),
basal insulin secretion was replaced by a continuous insulin infusion (0.2
mU X kg-1 X min-1), and glucagon was infused intravenously in two
conditions at random: either continuously (125 ng X min-1) or
intermittently (812.5 ng X min-1, with a switching on/off length of 2/11
min). Blood glucose levels and glucose infusion rate were monitored
continuously by the Biostator, and classical methodology using a
D-[3-3H]glucose infusion allowed us to study glucose turnover. While basal
plasma glucagon levels were similar in both conditions (122 +/- 31 vs. 115
+/- 18 pg X ml-1), they plateaued at 189 +/- 38 pg X ml-1 during continuous
infusion and varied between 95 and 501 pg X ml-1 during pulsatile infusion.
When compared with continuous administration, pulsatile glucagon infusion
initially induced a similar increase in endogenous (hepatic) glucose
production and blood glucose, did not prevent the so-called "evanescent"
effect of glucagon on blood glucose, and after 3 h tended to reduce rather
than increase hepatic glucose production. In conclusion, in vivo pulsatile
hyperglucagonemia in normal man fails to increase hepatic glucose
production.
