One of the major physiological functions of insulin is to promote the disposal of glucose during the post-prandial state into skeletal muscle and fat. The principal mechanism by which the hormone achieves this is through the acute stimulation of glucose transport across the plasma membrane of these tissues. This stimulation is due largely to the insulin mediated translocation of the GLUT4 glucose transporter from its intracellular storage compartment to the cell surface. The increase in plasma membrane GLUT4 abundance is primarily responsible for bringing about an increase in glucose uptake. The precise mechanism(s) by which insulin triggers the translocation of GLUT4 still remain unclear, but recent advances have enabled some progress to be made with respect to our understanding of the early signalling events participating in the hormonal regulation of glucose transport. This review focuses on the potential role of the serine/threonine kinase. Protein Kinase B (PKB) as an insulin signalling intermediate regulating glucose transport. We discuss how impaired PKB activation may be involved in the dysregulation of glucose transport during insulin resistance, and how PKB may control other important cellular processes.