The inability of the embryo to utilize glucose as a fuel before compaction has been an area of much speculation. It is suggested that limitations in glucose transporter processes are the prime reasons for this. The recent identification of GLUT3 as the transporter responsible for the uptake of maternal glucose after compaction may provide the missing link in this puzzle. Furthermore, the coincidence of its expression with the onset of embryonic glucose utilization suggests that GLUT3 may be involved in the determination of metabolic priorities of the embryo. A model for the uptake of glucose by the blastocyst based on the function of two facilitative glucose transporters, GLUT3 and GLUT1, is proposed which can accommodate growth factor regulation of embryonic processes and is consistent with both the well established biochemical characteristics of GLUT proteins and the physiology of the embryo.