Pulsatile hyperglucagonemia fails to increase hepatic glucose production in normal man
Paolisso, G.; Scheen, A.J.; Luyckx, A.S.; Lefebvre, P.J.
American Journal of Physiology 252(1 Pt 1): E1-E7
1987
ISSN/ISBN: 0002-9513 PMID: 3544860 Document Number: 298718
To study the metabolic effects of pulsatile glucagon administration, 6 men had a 260-min glucose-controlled glucose intravenous infusion using the Biostator. The endogenous secretion of the pancreatic hormones was inhibited by somatostatin 100 mu g/h, basal insulin secretion was replaced by a continuous insulin infusion 0.2 mU/kg min, and glucagon was infused intravenously in 2 conditions at random: continuously (125 ng/min) or intermittently (812.5 ng/min, with a switching on/off length of 2/11 min). Blood glucose and glucose infusion rate were monitored continuously by the Biostator, and a D-[3-superscript 3H]glucose infusion was used to study glucose turnover. Whereas basal plasma glucagon was similar in both conditions (122 +or- 31 and 115 +or- 18 pg/ml), values plateaued at 189 +or- 38 pg/ml during continuous infusion and varied between 95 and 501 pg/ml 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.