Glucose transporter 2 concentrations in hyper- and hypothyroid rat livers
| Autor: | Hiroaki Kakizawa, M Kotake, Akio Nagasaka, R Hayashi, A. Nakai, Naohisa Oda, Y Sawai, Nobuki Hayakawa, Masaki Makino, T Mokuno, Keiko Uchimura, Mitsuyasu Itoh, Mutsuko Nagata |
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| Rok vydání: | 1999 |
| Předmět: |
Male
endocrine system medicine.medical_specialty endocrine system diseases Monosaccharide Transport Proteins Endocrinology Diabetes and Metabolism Blotting Western Carbohydrate metabolism Hyperthyroidism Impaired glucose tolerance Endocrinology Hypothyroidism Internal medicine medicine Animals Euthyroid Rats Wistar Glucose Transporter Type 2 biology Thyroid Cell Membrane Glucose transporter Metabolism medicine.disease Thyroid Diseases Rats medicine.anatomical_structure Liver Hepatocyte biology.protein GLUT2 hormones hormone substitutes and hormone antagonists |
| Zdroj: | The Journal of endocrinology. 160(2) |
| ISSN: | 0022-0795 |
| Popis: | The deterioration of glucose metabolism frequently observed in hyperthyroidism may be due in part to increased gluconeogenesis in the liver and glucose efflux through hepatocyte plasma membranes. Glucose transporter 2 (GLUT 2), a facilitative glucose transporter localized to the liver and pancreas, may play a role in this distorted glucose metabolism. We examined changes in the levels of GLUT 2 in livers from rats with l-thyroxine-induced hyperthyroidism or methimazole-induced hypothyroidism by using Western blotting to detect GLUT 2. An oral glucose tolerance test revealed an oxyhyperglycemic curve (impaired glucose tolerance) in hyperthyroid rats (n=7) and a flattened curve in hypothyroid rats (n=7). GLUT 2 levels in hepatocyte plasma membranes were significantly increased in hyperthyroid rats and were not decreased in hypothyroid rats compared with euthyroid rats. The same results were obtained with a densitometric assay. These findings suggest that changes in the liver GLUT 2 concentration may contribute to abnormal glucose metabolism in thyroid disorders. |
| Databáze: | OpenAIRE |
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