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 Vmax. 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.