Metabolic control of sugar transport by derepression of cell surface glucose transporters. An insulin-independent recruitment-independent mechanism of regulation.

摘要: Protein-mediated sugar transport is nominally absent in normoxic pigeon erythrocytes. Following exposure to metabolic inhibitors (cyanide or carbonyl-cyanide-p-trifluoromethoxyphenylhydrazone), red cells sugars by a saturable stereoselective pathway that inhibited cytochalasin B forskolin. The capacity of fully poisoned consistent with transporter density approximately 30 carriers/erythrocyte. Immunoblot analyses and competition enzyme-linked immunosorbent assay indicate contain 200 copies an integral plasma membrane protein immunologically related the glucose isoform GLUT1. GLUT1 quantitatively restricted at all times. Pigeon brain lack proteins isoforms GLUT3 GLUT4. Specific immunodepletion cell content results subsequent loss reconstitutable protein-mediated transport. These findings demonstrate avian erythrocyte mediated GLUT1-like stimulation depletion from derepression surface proteins.