Post receptor insulin resistance has been demonstrated in insulin sensitive tissues from streptozotocin induced diabetic animals. Insulin deficiency itself or metabolic derangements of diabetes seem to contribute to this insulin resistant state. However, the mechanism is presently unknown. Using largely insulin insensitive rat thymocytes, we have studied glucose oxidation stimulated by agents that mimic insulin action but that work independently of the insulin receptor. Glucose oxidations stimulated by these agents were markedly diminished in the thymocytes from streptozotocin induced diabetic rats. These findings as well as our finding that the thymocytes from diabetic rats possess a normal complement of insulin receptor provide further evidence that post insulin receptor impairment of glucose metabolism occurs in streptozotocin diabetes. Thus although thymocytes are not sensitive to insulin, they are useful for the investigation of the impaired glucose metabolism.