Cortisol-Induced Insulin Resistance in Man: Impaired Suppression of Glucose Production and Stimulation of Glucose Utilization due to a Postreceptor Defect of Insulin Action

TLDR: The results indicate that the cortisol-induced insulin resistance in man is due to the decrease in both hepatic and extrahepatic sensitivity to insulin.

Abstract: 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 < 001) to values observed during moderately severe stress in man This hypercortisolemia increased postabsorptive plasma glucose (126 ± 2 us 97 ± 2 mg/dl; P < 001) and plasma insulin (16 ± 2 us 10 ± 2 µU/ml; P < 001) concentrations and rates of glucose production (24 ± 01 us 21 ± –01 mg kg-1 min-1; P < 001) and utilization (25 ± 01 us 21 ± 01 mg kg-1 min-1; P < 001) Insulin dose-response curves for both suppression of glucose production (half-