Decreasing rations of dietary carbohydrate to fat in young, lean rats are accompanied by a decreasing ability of insulin to stimulate glucose transport activity in the adipose cell and a decreasing capacity of this cell to metabolize glucose. The mechanism of the former alteration has been examined by measuring the number of functional glucose transport systems with an equilibrium 3H-cytochalasin B binding assay in the purified plasma membranes of basal and insulin-stimulated isolated adipose cells from rats raised on diets differing only in their ratio of carbohydrate to fat. While the number of functional glucose transport systems/mg plasma membrane protein in the basal state remains constant, the number of insulin-stimulatable systems decreases with decreasing dietary carbohydrate in proportion to insulin's decreasing ability to stimulate transport activity in the intact cell. The mechanism of the latter alteration has been examined by estimating the activities of the specific pathways for glucose carbon metabolism in intact adipose cells from rats raised on the same diets through the use of increasing concentrations of differentially radiolabeled glucose in the presence of increasing insulin concentrations. Decreasing dietary carbohydrate is accompanied by markedly decreasing de novo fatty acid synthesis and hexose monophosphate shunt activity.