Streptozotocin-treated rats were diabetic, as assessed by blood glucose and plasma insulin values, while vanadate treatment restored blood glucose values to normal. Immunoblot analysis using a monoclonal antibody to the insulin-responsive glucose transporter demonstrated a 70% decline in transporter expression in skeletal muscle of diabetic rats. Subsequent treatment of diabetic animals with vanadate resulted in renewed expression of the transporter to 87% of control levels. Northern blot analysis of total skeletal muscle RNA from diabetic animals revealed a 55% decline in the steady state level of muscle glucose transporter mRNA, while vanadate treatment led to a 187% increase in transporter mRNA over normal levels. These results support the conclusion that vanadate acts to relieve diabetic hyperglycemia by inducing expression of the insulin-responsive glucose transporter at the pretranslational level.