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Cited by 28Thyroid Disorders and TreatmentsMetabolism, Diabetes, and CancerPancreatic function and diabetes

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

Dimitriadis, G., Maratou, E., Alevizaki, M., Boutati, E., Psara, K., Papasteriades, C., Raptis, S. A.·2005·Hormone and Metabolic Research
DOI 10.1055/s-2005-861026
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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 METHODS: Blood (20 ml) was withdrawn from 12 healthy and 12 hyperthyroid subjects.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.

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Authors
Dimitriadis, G., Maratou, E., Alevizaki, M., Boutati, E., Psara, K., Papasteriades, C., & Raptis, S. A.
Affiliations
  • National and Kapodistrian University of Athens (GR)
  • Evangelismos Hospital (GR)
ORCID
Venue
Hormone and Metabolic Research
Publisher
Georg Thieme Verlag KG
Published
2005-01
Volume
37
Issue
1
Pages
15-20
ISSN
  • 0018-5043 (ISSN-L)
  • 1439-4286
DOI
10.1055/s-2005-861026
OpenAlex
W2066786247
Cited by
28
References
0
Citations by year
2026: 1 · 2022: 2 · 2017: 4 · 2016: 1 · 2015: 1 · 2014: 4 · 2013: 1 · 2012: 1
FWCI
1.03
Type
journal article
Language
de
Open access
closed
Locations
  • Hormone and Metabolic Research (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
Keywords
hyperthyroidism, thyroid hormone excess, glucose transporters, GLUT3, GLUT4, GLUT1, monocytes, insulin-stimulated glucose transport, glucose transporter translocation
MeSH terms
Adult, Humans, Hyperthyroidism, Insulin, Monocytes, Monosaccharide Transport Proteins, Muscle Proteins, Nerve Tissue Proteins, Thyroid Hormones, Protein Isoforms, Glucose Transporter Type 1, Glucose Transporter Type 3, Glucose Transporter Type 4, In Vitro Techniques

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