EPINEPHRINE-INDUCED IN-VIVO MUSCLE GLYCOGEN DEPLETION ENHANCES INSULIN SENSITIVITY OF GLUCOSE-TRANSPORT

Muscle glycogen depletion by means of exercise is associated with incr eased insulin-stimulated glucose transport activity. To determine whet her reduction in muscle glycogen content independent of muscle contrac tions would increase glucose transport activity, rats were injected wi th epinephrine (20 mu g/100 g body wt) or saline. Two hours later, epi trochlearis muscles were removed, washed thoroughly to remove epinephr ine, and assayed for glucose transport activity with 3-O-methyl-D-gluc ose (3-MG). Muscle adenosine 3',5'-cyclic monophosphate concentration was elevated 441% in muscles frozen immediately after removal from epi nephrine-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) mu mol glucose units/g wet wt] and a small increase in basal glucose t ransport activity (from 0.13 +/- 0.02 to 0.24 +/- 0.04 mu mol 3-MG . m l(-1) . 10 min(-1), P < 0.05). A submaximally effective insulin concen tration (30 mu U/ml) induced a 70% greater increase in 3-MG transport in epinephrine-treated muscles than in controls (0.57 +/- 0.09 and 0.3 4 +/- 0.04 mu mol . ml(-1) . 10 min(-1), respectively, P < 0.001). Res ponse to a maximally effective concentration of insulin was unaltered by prior exposure to epinephrine. When epinephrine-induced glycogen de pletion was prevented by prior injection with the beta-adrenergic anta gonist propranolol, glucose transport activity was no longer enhanced by epinephrine. In summary, depletion of skeletal muscle glycogen by p rior in vivo exposure to epinephrine is associated with an increase in basal glucose transport activity and an increase in sensitivity of th e glucose transport process to insulin.