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The present studies were undertaken to assess the mechanisms responsible for cortisol-induced insulin resistance in man. The insulin dose-response characteristics for suppression of glucose production and stimulation of glucose utilization and their relationship to monocyte and erythrocyte insulin receptor binding were determined in six normal volunteers after 24-h infusion of cortisol and 24-h infusion of saline. The infusion of cortisol (2 /µg kg^-1 min^-1) increased the plasma cortisol concentration approximately 4-fold (37 ± 3 us. 14 ± 1 µg/dl; P < 0.01) to values observed during moderately severe stress in man. This hypercortisolemia increased postabsorptive plasma glucose (126 ± 2 us. 97 ± 2 mg/dl; P < 0.01) and plasma insulin (16 ± 2 us. 10 ± 2 µU/ml; P < 0.01) concentrations and rates of glucose production (2.4 ± 0.1 us. 2.1 ± –0.1 mg kg^-1 min^-1; P < 0.01) and utilization (2.5 ± 0.1 us. 2.1 ± 0.1 mg kg^-1 min …