Glucose transporters in the thyroid

• Published in: Thyroid (New York, N.Y.) Vol. 15; no. 6; p. 545
• Main Authors: Matsuzu, Kenichi, Segade, Fernando, Wong, Mariwil, Clark, Orlo H, Perrier, Nancy D, Bowden, Donald W
• Format: Journal Article
• Language: English
• Published: United States 01.06.2005
• Subjects: Glucose Transport Proteins, Facilitative - metabolism; Humans; Thyroid Gland - metabolism
• ISSN: 1050-7256
• DOI: 10.1089/thy.2005.15.545

Glucose transport, mediated by proteins expressed from the glucose transporter genes, plays an essential role in cellular metabolism. Increased uptake of glucose compared to cells in normal tissue is a defining characteristic of malignant cells. This has been the basis for positron emission tomography imaging of thyroid tumor metastases using fluorodeoxyglucose uptake. Despite this key difference between tumor and normal cells, the mechanism which mediates increased glucose uptake is poorly understood. Several research studies have assessed the expression of different glucose transporter (GLUT) proteins and expression of the genes which code for them in thyroid tissues. While no consensus exists on the specifics of which GLUT genes or proteins are expressed, a picture has emerged that a single specific transporter, GLUT1, is expressed at higher levels in thyroid carcinomas compared to a variety of normal and nonmalignant forms of thyroid disease. Greater levels of GLUT1 expression may be associated with poorer prognosis. Experiments in established thyroid carcinoma cells lines may provide useful insights into glucose transport in the thyroid. Thyroid cells show increased glucose uptake in response to thyroid-stimulating hormone (TSH), but expression of GLUT genes does not appear to be significantly affected by TSH suggesting TSH affects glucose uptake by affecting GLUT localization/ translocation rather than through increased GLUT gene expression. Improving technologies are providing a stronger foundation for detailed analyses of glucose transporters in thyroid to better elucidate the mechanisms by which these genes and proteins are regulated in normal and pathogenic tissue.