We are interested in understanding how insulin stimulates glucose transport into fat and muscle cells, and how this process breaks down in disease. Impaired insulin-stimulated glucose transport in muscle and fat is a major contributor to whole body insulin resistance, the key pathophysiological mechanism underlying type 2 diabetes. There is currently no consensus on the molecular basis for impaired insulin responses in these tissues. We aim to address this knowledge gap to identify how the insulin signalling network and GLUT4 trafficking apparatus are altered in insulin resistance.