GSBS Student Publications

Title

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

GSBS Program

Biochemistry & Molecular Pharmacology

UMMS Affiliation

Graduate School of Biomedical Sciences; Department of Biochemistry and Molecular Pharmacology

Date

3-25-1993

Document Type

Article

Medical Subject Headings

3-O-Methylglucose; Animals; Binding Sites; Biological Transport; Blotting, Western; *Carbohydrate Metabolism; Columbidae; Enzyme-Linked Immunosorbent Assay; Erythrocytes; Glucose Transporter Type 1; Humans; Insulin; Ligands; Methylglucosides; Monosaccharide Transport Proteins

Disciplines

Life Sciences | Medicine and Health Sciences

Abstract

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

Rights and Permissions

Citation: J Biol Chem. 1993 Mar 25;268(9):6437-44.

Related Resources

Link to article in PubMed

Journal Title

The Journal of biological chemistry

PubMed ID

8454616