Role of hepatic [alpha] and [beta] adrenergic receptor stimulation
on hepatic glucose production during heavy exercise.
Coker, Robert H., Mahesh G. Krishna, D. Brooks Lacy, Deanna P. Bracy,
and David H. Wasserman.
Department of Molecular Physiology and Biophysics and Diabetes
Research and Training Center, Vanderbilt University School of
Medicine, Nashville, TN 37232
APStracts 4:0153E, 1997.
The role of catecholamines in control of hepatic glucose production
was studied during heavy exercise in dogs using a technique to
selectively block hepatic [alpha]- and [beta]-adrenergic receptors.
Surgery was done >16 days prior to study at which time catheters
were implanted in the carotid artery, portal vein and hepatic vein
for sampling and the portal vein and vena cava for infusions. In
addition, flow probes were implanted on the portal vein and hepatic
artery. Each study consisted of a 100 min equilibration, 30 min
basal, 20 min heavy exercise (85% HRmax), 30 min recovery and a 30
min adrenergic blockade test period. Either saline (CONT; n=7) or
[alpha] - (phentolamine) and [beta] - (propranolol) adrenergic
blockers (BLK; n=6) were infused in the portal vein. In both groups
epinephrine (EPI) and norepinephrine (NE) were infused in the portal
vein during the blockade test period to create supraphysiological
levels at the liver. Isotope (3-3H glucose) dilution and
arteriovenous differences were used to assess hepatic function.
Arterial EPI, NE, glucagon and insulin levels were similar during
exercise in both groups. Endogenous glucose production (Ra) rose
similarly during exercise to 7.9+/-1.2 mg/kg x min and 7.5+/-2.0
mg/kg x min in CON and BLK at t=20 min. Net hepatic glucose output
also rose to a similar rate in CONT and BLK with exercise. During the
blockade test period arterial plasma glucose and Ra rose to 164+/-5
mg/dl and 12.0+/-1.4 mg/kg x min, but was essentially unchanged in
BLK. The attentuated response to catecholamine infusion in BLK
substantiates the effectiveness of the hepatic adrenergic blockade.
In conclusion, these results show that direct hepatic adrenergic
stimulation does not participate in the increase in Ra even during
the exaggerated sympathetic response to heavy exercise.
Received 11 March 1997; accepted in final form 7 July 1997.
APS Manuscript Number E106-7.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 24 July 1997