Members of the solute carrier family 2 are classified as facilitative glucose transporters (GLUTs), which transport glucose into most cells. SLC2A2/GLUT2 is predominantly expressed in the liver and weakly expressed in the kidney and small intestine. Mice in which the slc2a2 gene is deleted are hyperglycemic and hypoinsulinemic; they have elevated plasma levels of glucagons, free fatty acids, and -hydroxybutyrate. Truncated forms of SLC2A2/GLUT2 that result from gene mutation are detected in patients with Fanconi-Bickel syndrome; this condition is characterized by hepatorenal glycogen accumulation, proximal renal tubular dysfunction, and impaired carbohydrate metabolism, possibly caused by dysfunction of the truncated SLC2A2/GLUT2.