Summary
In order to study whether or not exogenous and/or endogenous glucocorticoids affect the glucose transport rate in human cells, we examined the transport rate of a non-metabolizable hexose analogue, 3-O-methyl-D-glucose, in polymorphonuclear leukocytes from patients with hypercortisolism. The mean glucose transport rate was prominently decreased in 5 patients with Cushing's syndrome compared with 29 healthy controls (5.4±1.8 vs 10.4±2.5 fl/cell · sec, mean±SD, p<0.001) and the transport rate returned to normal range after adenoma resection in 2 of them. In 10 patients with nephrotic syndrome treated with prednisolone, a significant negative correlation was found between transport rates and daily prednisolone doses. When prednisolone of 40 mg/day was administered to a diabetic patient and the dose was gradually reduced, glucose transport rate was transiently decreased during the initial period. In an in vitro study, a synthetic glucocorticoid, dexamethasone, directly inhibited glucose transport rate in those cells in time- and concentration-dependent manners by mainly reducing max. These results suggest that either exogenous or endogenous hypercortisolism in humans is associated with a decrease in glucose transport rate in polymorphonuclear leukocytes, and that the direct effect of glucocorticoids accounts at least in part for the decreased glucose transport rates found in those cells.
Key words
Glucose Transport - Polymorphonuclear Leukocytes - Hypercortisolism - Glucocorticoids
