Effect of epinephrine on muscle glycogenolysis and insulin -stimulated muscle glycogen synthesis in man. Laurent, Didier, Kitt Falk Petersen, Raymond R. Russell, Gary W. Cline, Gerald I. Shulman. Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520 and the Howard Hughes Medical Institute
APStracts 4:0210E, 1997.
In order to examine the effects of a physiologic increase in plasma epinephrine concentration (800 pg/ml) on muscle glycogenolysis and insulin-stimulated glycogenesis, we infused epinephrine (1.2 [mu]g/[m2.min]) for 2 h, and monitored muscle glycogen and glucose-6 -phosphate (G-6-P) concentrations with 13C/31P NMR spectroscopy. Epinephrine caused an increase in plasma glucose (_80 mg/dl), lactate (_0.7 mM), free fatty acids (_1200 [mu]M at peak) and whole body glucose oxidation (_0.85mg/[kg.min]) compared to a group of control subjects (n=4) both in the presence of slight hyperinsulinemia (13 [mu]U/ml, n=8) or basal insulin (7 [mu]U/ml, n=7). However, epinephrine did not induce any detectable changes in glycogen or G-6 -P concentrations, whereas muscle inorganic phosphate (Pi) decreased by 35%. Epinephrine infusion during a euglycemic/hyperinsulinemic clamp (n=8) caused a 45% decrease in the glucose infusion rate which could be mostly attributed to a 73% decrease in muscle glycogen synthetic rate. After an initial increase to 160% of basal values, G -6-P levels decreased by 30% with initiation of the epinephrine infusion. We conclude that a physiologic increase in plasma epinephrine concentration: 1) has a negligible effect on muscle glycogenolysis at rest, 2) decreases muscle Pi which may maintain phosphorylase activity at a low level and, 3) causes a major impairment in insulin-stimulated muscle glycogen synthesis possibly due to inhibition of glucose transport/phosphorylation activity. 

Received 9 June 1997; accepted in final form 18 September 1997.
APS Manuscript Number E266-7.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 7 October 1997