Abstract
Background: In hyperthyroidism, tissue glucose disposal is increased to adapt to high energy
demand. Our aim was to examine the glucose transporter isoforms involved in this process
and their regulation through insulin in monocytes from subjects with hyperthyroidism.
Methods: Blood (20 ml) was withdrawn from 12 healthy and 12 hyperthyroid subjects. The abundance
of glucose transporter isoforms (GLUT) on the monocyte surface membrane was determined
in the absence and presence of insulin (10 - 100 mU/l) using flow cytometry. Anti-CD14-PE
monoclonal antibody was used for monocyte gating. GLUT isoforms were determined after
staining the cells with specific antisera to GLUT1, GLUT3 and GLUT4. Results: Hyperthyroidism increased basal monocyte-surface GLUT1, GLUT3 and GLUT4 transporters.
In these cells, insulin had a marginal effect on GLUT4 translocation (25 %, p < 0.02)
and a more significant effect on GLUT3 translocation (45 %, p < 0.001) on plasma membrane.
Conclusions: In the hyperthyroid state, (1) basal abundance of GLUT1, GLUT3 and GLUT4 transporters
on the cell surface is increased; (2) insulin mainly increases the recruitment of
GLUT3 and, to a lesser extent, GLUT4 glucose transporters on the plasma membrane.
These findings may provide a mechanism to explain the increment of glucose disposal
in peripheral tissues in hyperthyroidism.
Key words
Monocytes - Cytometry - Insulin - Glucose transporters - GLUT3 - GLUT4 - GLUT1 - Thyroxin
- Hyperthyroidism
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George Dimitriadis, M. D., DPhil
2nd Department of Internal Medicine, Research Institute and Diabetes Center, University
General Hospital ‘Attikon’
1 Rimini Street · 12462-Haidari · Greece
Phone: +30 (210) 5831152
Fax: +30 (210) 5326454
Email: gdim@internet.gr