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

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)