Insulin and nonhydrolyzable GTP analogs induce translocation of GLUT 4 to the plasma membrane in α-toxin-permeabilized rat adipose cells

Rat adipose cells treated with Staphylococcus aureus α-toxin are permeable and retain their ability to respond to insulin after hormone treatment. The GLUT 4 glucose transporter isoform, specific to fat and muscle cells, is translocated normally from low density microsomes to the plasma membrane in permeabilized cells. Addition of guanosine 5′-O-(3-thiotriphosphate), guanylyl imidodiphosphate, or guanylyl β,γ-methylenediphosphate to permeabilized adipocytes induces an insulin-like translocation of GLUT 4 to the plasma membrane; GTP or adenosine 5′-(β,γ-imino)triphosphate has no effect. No translocation of GLUT 4 is observed when GTP analogs are added to intact adipocytes. These results suggest the involvement of a GTP-binding protein in insulin-triggered recruitment of GLUT 4 to the cell surface.