<P> During fasting, some GLUT4 transporters will be expressed at the surface of the cell . However, most will be found in cytoplasmic vesicles within the cell . After a meal and at the binding of insulin (released from the islets of Langerhans) to receptors on the cell surface, a signalling cascade begins by activating phosphatidylinositolkinase activity which culminates in the movement of the cytoplasmic vesicles toward the cell surface membrane . Upon reaching the plasmalemma, the vesicles fuse with the membrane, increasing the number of GLUT4 transporters expressed at the cell surface, and hence increasing glucose uptake . </P> <P> Facilitated diffusion can occur between the bloodstream and cells as the concentration gradient between the extracellular and intracellular environments is such that no ATP hydrolysis is required . </P> <P> However, in the kidney, glucose is reabsorbed from the filtrate in the tubule lumen, where it is at a relatively low concentration, passes through the simple cuboidal epithelia lining the kidney tubule, and into the bloodstream where glucose is at a comparatively high concentration . Therefore, the concentration gradient of glucose opposes its reabsorption, and energy is required for its transport . </P> <P> The secondary active transport of glucose in the kidney is Na linked; therefore an Na gradient must be established . This is achieved through the action of the Na / K pump, the energy for which is provided through the hydrolysis of ATP . Three Na ions are extruded from the cell in exchange for two K ions entering through the intramembrane enzyme Na+ / K+ - ATPase; this leaves a relative deficiency of Na in the intracellular compartment . Na ions diffuse down their concentration gradient into the columnar epithelia, co-transporting glucose . Once inside the epithelial cells, glucose reenters the bloodstream through facilitated diffusion through GLUT2 transporters . </P>

Glucose entry into gut absorbing cells from the lumen is by co-transport with