Effect of glucocorticoids on the glucose transport system of isolated fat cells.

摘要: Glucocorticoids inhibit glucose utilization by fat cells. The possibility that this effect results from altered transport was investigated using an oil-centrifugation technique which allows a rapid (within 45 s) estimation of or 3-O-methylglucose uptake isolated At high concentration (greater than 25 muM), dexamethasone inhibited within 1 min its addition to Efflux also impaired 0.1 mM dexamethasone. However, diminished not specific glucocorticoids; concentrations (0.1 mM) 17beta-estradiol, progesterone, and deoxycorticosterone produced similar response in adipocytes. more physiologic steroid glucocorticoids time-dependent manner (maximum 2 hours). This for since, under these conditions, changed the non-glucocorticoid steroids. Lineweaver-Burk analysis showed muM treatment decrease Vmax but did change Ku. Hexokinase activity ATP levels were treatment, suggesting processes involved phosphorylation affected. Dexamethasone caused reduction when assayed low sugar mM). (10 mM), methyl only slightly less normal treated Stimulation insulin markedly enhanced both untreated hexose presence insulin, dexamethasone-treated cells control however completely overcome alteration larger sugars 5 used. There no detectable total protein synthesis during incubation with actinomycin C blocked inhibitory on uptake. Cycloheximide, small inhibition uptake, prevented full expression transport. These indicate alters facilitated and, secondly, suggest RNA is needed glucocorticoid action.