Acute exercise, epinephrine, and diabetes enhance insulin binding to skeletal muscle.

We measured insulin binding to crude membranes from rat skeletal muscle, with binding expressed relative to the sarcolemmal marker, cholesterol ester (CE). The amount of CE in the sarcolemma remained constant after streptozotocin-induced diabetes and acute exercise (swam for 90 min). Soleus (predominantly slow-twitch fibers) had higher insulin binding capacity than extensor digitorum longus (predominantly fast twitch). Both diabetes and acute exercise enhanced insulin binding. The shape of the enhanced insulin binding curve differed, however, between diabetes and acute exercise. Diabetes elicited a uniform increase in binding across the insulin concentrations measured (0.04-166 nM); acute exercise elicited the largest increase at the lower concentrations, suggesting different mechanisms cause the enhanced binding. Addition of 13.1 nM epinephrine to the perfusate in a rat hindlimb preparation increased insulin binding in a pattern similar to acute exercise. In contrast, muscular contraction stimulated by the sciatic nerve (1 Hz) or reduction of perfusate insulin from 100 to 40 pM, two additional correlates of acute exercise, had no effect. The increased insulin binding after acute exercise, therefore, appears to be mediated through elevated levels of catecholamines and not upregulation of the insulin receptor.