Dynamic aspects of whole body glucose metabolism were assessed in ten young adult insulin-dependent (type I) diabetic men. Using a primed, continuous intravenous infusion of [6,6- 2H]glucose and [U- 13C]glucose, endogenous production, tissue uptake, carbon recycling, and oxidation of glucose were measured in the postabsorptive state. These studies were undertaken after blood glucose had been maintained overnight at 5.9 ± 0.4 mmol/L (n = 10), and on another night at 10.5 ± 0.4 mmol/L (n = 4) or 15.2 ± 0.6 mmol/L (n = 6). In the normoglycemic state, endogenous glucose production averaged 2.15 ± 0.13 mg × kg −1 × min −1. This value, as well as the rate of glucose carbon recycling (0.16 ± 0.04 mg × kg −1 × min −1) and glucose oxidation (1.52 ± 0.16 mg × kg −1 × min −1) are comparable to those found in nondiabetic controls. In the hyperglycemic states at 10 or 15 mmol/L, endogenous glucose production was increased by 11% ( P < .01) and 60% ( P < .01) compared to the normoglycemic states, respectively. Glucose carbon recycling contributed only a small percentage to this variation in glucose production (15% at the 15 mmol/L glucose level). This suggests that if gluconeogenesis participates in the increased glucose output, it is not dependent on a greater systemic supply of three-carbon precursors. The increased rate of glucose production in the hyperglycemic state was quantitatively offset by a rise in urinary glucose excretion. Glucose tissue uptake, as well as glucose oxidation, did not vary between normoglycemic and hyperglycemic states. Thus, insulin-deficiency does not markedly alter the overall kinetics and utilization of glucose in peripheral tissues during the postabsorptive state. Insulin-deficient hyperglycemia primarily depends on the balance between increased endogenous glucose production and glucose losses via the urine.