Abstract
Intracellular glucose concentrations in skeletal muscle have been measured in normal and injured rats individually infused with 51Cr-EDTA as an extracellular space marker. In normal rats, even when infused with glucose at a high rate, membrane transport appeared to be the rate-limiting step in glucose utilization by muscle. After injury the concentration of intracellular glucose was increased, and positively correlated with that in plasma, showing that the loss of sensitivity to insulin after injury is due to impairment of an intracellular metabolic step-