SLC2A4 and Insulin resistance: Taken together with numerous reports demonstrating that acutely increasing circulating NEFA concentrations causes skeletal muscle insulin resistance, and that insulin resistance has plateaued by 24 hours of forearm immobilisation [11], this would suggest that acutely increasing circulating NEFA causes insulin resistance via a different, albeit transient, mechanism to a lack of contraction per se (e.g. Randle Cycle vs reduced GLUT4 translocation, respectively [13, 34]) during disuse.