The direct effects of catecholamines on hepatic glucose production
in the conscious dog are solely attributable to glycogenolysis.
Chu, Chang An, Dana K. Sindelar, Doss W. Neal, and Alan D.
Cherrington.
Department of Molecular Physiology and Biophysics, Vanderbilt,
University School of Medicine, Nashville, Tennessee 37232-0615
APStracts 3:0049E, 1996.
The effects of catecholamines (CATS) infused into the hepatic portal
vein were studied in ten 18-hour fasted conscious dogs. Glucose
production (GP) and gluconeogenesis (GNG) were assessed using tracer
(3H glucose, 14C alanine) and arteriovenous difference techniques.
Each experiment consisted of a 100 min. equilibration, a 40 min.
basal and two 90 min. test periods. A pancreatic clamp (somatostatin
+ basal portal insulin and glucagon) was used to fix insulin and
glucagon at basal levels. Propranolol (1 [mu]g/kg.min.) and
phentolamine (2 [mu]g/kg.min.) were infused intraportally during both
test periods of the blockade group while a carrier solution was
infused in the control group. Norepinephrine (NE) (100 ng/kg.min.)
and epinephrine (EPI) (40 ng/kg.min.) were infused intraportally
during the second test period of both protocols. Portal NE (70 +/- 46
to 8404 +/- 674 and 162 +/- 57 to 6530 +/- 624 pg/ml respectively)
and portal EPI (21 +/- 11 to 3587 +/- 309 and 29 +/- 6 to 2989 +/-
406 pg/ml respectively) rose in the control and adrenergic blockade
groups respectively. The increases in arterial NE and EPI were modest
in both groups. Intraportal infusion of CATS increased GP from 2.1
+/- 0.2 to 6.2 +/- 1.0 mg/kg.min. in control group but did not change
it (2.7 +/- 0.4 to 2.7 +/- 0.3 mg/kg.min.) in the blockade group.
Portal CATS had no effect on GNG in the presence or absence of
adrenergic blockade (GNG rose from 0.7 +/- 0.2 to 0.9 +/- 0.2 and 0.8
+/- 0.2 to 1.0 +/- 0.2 mg/kg.min. in the control and blockade groups
respectively). In conclusion, portal infusion of catecholamines
significantly augmented GP by selectively stimulating glycogenolysis.
The increase in hepatic glucose production could be completely
inhibited by intraportal adrenergic blockade.
Received 20 November 1995; accepted in final form 20 February
1996.
APS Manuscript Number E550-5.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 March 96