The mechanism by which insulin stimulates glucose transport in the rat adipose cell has been shown to be a rapid, reversible, and energy-dependent process. Stimulation is achieved by the translocation of glucose transporters from an intracellular pool to the plasma membrane where their insertion is ultimately responsible for the increase in transport activity. The reversal of this process also occurs rapidly at 37 degrees C, with the transporters reappearing in the intracellular pool. The overall cycle thus appears as a reversible endocytic-exocytic process with the endocytic and exocytic steps showing markedly different kinetic properties. Studies of the effects of incubation temperature and TRIS confirm the existence of an intermediate state in which transporters are associated with the plasma membrane but incapable of transporting extracellular glucose. This suggests that insulin may act at the level of the plasma membrane at the step that results in the exposure of functional glucose transporters. The existence of a cAMP-mediated process capable of overriding the actions of insulin raises the possibility of a second level of control of glucose transport activity the significance of which remains to be assessed. Finally, a third control mechanism exists for regulating the absolute number of glucose transporters per cell that appears to be specifically affected in certain pathophysiological conditions in the rat.