Treatment of white fat cells with dexamethasone during a 1–2–hr isolation period inhibited the stimulatory effect of insulin on [l–14C]—D—glucose conversion to CO2 during a subsequent 1 hour incubation under the following two conditions: 1) Submaximal doses of insulin in the presence of 1 HIM glucose, and 2) A maximal dose of insulin and 0.05 mM or 0.1 mM glucose. Under conditions of high rates of labeled CO2 production which occur with a maximal dose of insulin and 1 mM or more glucose, dexamethasone was without effect on the response of white fat cell glucose oxidation to insulin. Isolation of fat cells in the presence of 8.1 X 10-8M dexamethasone followed by incubation with the glucocorticoid resulted in marked inhibition of the insulin—like effects of 1 mM cysteine and 2.8 X 10-7M prostaglandin E1 in the presence of 0.1 mM glucose. Cycloheximide mimicked the action of dexamethasone on labeled CO2 production in the absence or presence of insulin or cysteine when fat cells were incubated with 0.05 mM glucose. These results indicate that dexamethasone inhibits glucose oxidation in the presence and absence of insulin when transport of glucose into fat cells is rate—limiting. The data support the view that glucocorticoids alter fat cell glucose metabolism by inhibiting glucose transport. (Endocrinology91: 518, 1972)