Horm Metab Res 2005; 37(1): 15-20
DOI: 10.1055/s-2005-861026
Original Basic
© Georg Thieme Verlag KG Stuttgart · New York

Thyroid Hormone Excess Increases Basal and Insulin-stimulated Recruitment of GLUT3 Glucose Transporters on Cell Surface

G.  Dimitriadis1 , E.  Maratou2 , M.  Alevizaki3 , E.  Boutati1 , K.  Psara4 , C.  Papasteriades4 , S.  A.  Raptis1, 2
  • 12nd Department of Internal Medicine, Research Institute and Diabetes Center, Athens University, University General Hospital - Attikon, Greece
  • 2Hellenic National Center for Research, Prevention and Treatment of Diabetes, Athens, Greece
  • 3Department of Therapeutics, Athens University, Greece
  • 4Department of Immunology and Histocompatibility, Evangelismos General Hospital, Athens, Greece
Further Information

Publication History

Received 30 March 2004

Accepted after Revision 26 July 2004

Publication Date:
09 February 2005 (online)

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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 Methods: Blood (20 ml) was withdrawn from 12 healthy and 12 hyperthyroid subjects.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.

References

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