Journal of Applied Physiology, Vol 76, Issue 5 2054-2058, Copyright © 1994 by American Physiological Society

ARTICLES

Epinephrine-induced in vivo muscle glycogen depletion enhances insulin sensitivity of glucose transport

L. A. Nolte, E. A. Gulve and J. O. Holloszy
Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri 63110.

Muscle glycogen depletion by means of exercise is associated with increased insulin-stimulated glucose transport activity. To determine whether reduction in muscle glycogen content independent of muscle contractions would increase glucose transport activity, rats were injected with epinephrine (20 micrograms/100 g body wt) or saline. Two hours later, epitrochlearis muscles were removed, washed thoroughly to remove epinephrine, and assayed for glucose transport activity with 3-O-methyl-D-glucose (3-MG). Muscle adenosine 3',5'-cyclic monophosphate concentration was elevated 441% in muscles frozen immediately after removal from epinephrine-injected rats but had returned to control levels by the time 3-MG transport was measured. Prior exposure to epinephrine resulted in depletion of muscle glycogen [from 18.6 +/- 1.4 to 11.0 +/- 0.1 (SE) mumol glucose units/g wet wt] and a small increase in basal glucose transport activity (from 0.13 +/- 0.02 to 0.24 +/- 0.04 mumol 3-MG.ml-1 x 10 min-1, P < 0.05). A submaximally effective insulin concentration (30 microU/ml) induced a 70% greater increase in 3-MG transport in epinephrine-treated muscles than in controls (0.57 +/- 0.09 and 0.34 +/- 0.04 mumol.ml-1 x 10 min-1, respectively, P < 0.001). Response to a maximally effective concentration of insulin was unaltered by prior exposure to epinephrine. When epinephrine-induced glycogen depletion was prevented by prior injection with the beta-adrenergic antagonist propranolol, glucose transport activity was no longer enhanced by epinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)

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