Activation of glucose transport in diabetic muscle: responses to contraction and insulin.

The purpose of this study was to evaluate the effect of insulin deficiency on the ability of muscle contraction to activate glucose transport. Rats were made severely diabetic by injection of streptozotocin (SZ; 125 mg/kg body wt). Only those diabetic rats in which plasma insulin was too low to measure 3 days after SZ injection were included in this study. Glucose transport activity was evaluated by measuring 3-O-methylglucose uptake in epitrochlearis muscles in vitro. Contractile activity induced a 2.8-fold increase in 3-O-methylglucose uptake rate in epitrochlearis muscles of diabetic rats (P less than 0.01) even after the muscles had been thoroughly washed to remove any traces of insulin remaining in the extracellular fluid. However, this increase in sugar uptake was less than 50% as great as that seen in normal controls. This reduced ability to activate glucose transport was not limited to the effect of contractile activity, as the increase in sugar uptake rate in response to a maximal concentration of insulin was similarly reduced in the diabetic muscles. Thus it appears that contractile activity can accelerate glucose transport in insulin-deficient muscle; however, the maximal capacity to activate glucose transport is decreased in skeletal muscle after sustained insulin deficiency.