The Role of GLUT1 in the Sugar-Induced Dielectric Response of Human Erythrocytes

We propose a key role for the glucose transporter 1 (GLUT1) in mediating the observed changes in the dielectric properties of human erythrocyte membranes as determined by dielectric spectroscopy. Cytochalasin B, a GLUT1 transport inhibitor, abolished the membrane capacitance changes in glucose-expos...

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Veröffentlicht in:The journal of physical chemistry. B 2009-02, Vol.113 (7), p.2212-2220
Hauptverfasser: Livshits, Leonid, Caduff, Andreas, Talary, Mark S, Lutz, Hans U, Hayashi, Yoshihito, Puzenko, Alexander, Shendrik, Andrey, Feldman, Yuri
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Sprache:eng
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Zusammenfassung:We propose a key role for the glucose transporter 1 (GLUT1) in mediating the observed changes in the dielectric properties of human erythrocyte membranes as determined by dielectric spectroscopy. Cytochalasin B, a GLUT1 transport inhibitor, abolished the membrane capacitance changes in glucose-exposed red cells. Surprisingly, d-fructose, known to be transported primarily by GLUT5, exerted similar membrane capacitance changes at increasing d-fructose concentrations. In order to evaluate whether the glucose-mediated membrane capacitance changes originated directly from intracellularly bound adenosine triphosphate (ATP) or other components of the glycolysis process, we studied the dielectric responses of swollen erythrocytes with a decreased ATP content and of nucleotide-filled ghosts. Resealed ghosts containing physiological concentrations of ATP yielded the same glucose-dependent capacitance changes as biconcave intact red blood cells, further supporting the finding that ATP is the effector of the glucose-mediated dielectric response where the ATP concentration is also the mediating factor in swollen red blood cells. The results suggest that ATP binding to GLUT1 elicits a membrane capacitance change that increases with the applied concentration gradient of d-glucose. A simplified model of the membrane capacitance alteration with glucose uptake is proposed.
ISSN:1520-6106
1520-5207
DOI:10.1021/jp808721w