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GLUT2 and glucokinase expression is coordinately regulated by sulfonylurea
O Porzio1, L N Marlier, M Federici
1Department of Internal Medicine, University of Rome Tor Vergata, Italy.
Molecular and Cellular Endocrinology
|August 25, 1999
Summary
Sulfonylurea initially boosts glucose transporter (GLUT2) and glucokinase (GK) expression, but prolonged use reduces them. This dual effect impacts glucose sensing and insulin secretion.
Area of Science:
- Endocrinology
- Cell Biology
Background:
- Sulfonylureas are widely used to manage type 2 diabetes.
- Understanding their molecular mechanisms on glucose sensing is crucial.
Purpose of the Study:
- To investigate the effect of sulfonylurea on glucose transporter 2 (GLUT2) and glucokinase (GK) expression.
- To analyze sulfonylurea's impact on glucose-responsiveness and sensitivity in betaTC6-F7 cells.
Main Methods:
- Treatment of betaTC6-F7 cells with varying doses and durations of sulfonylurea.
- Quantitative analysis of GLUT2 and GK mRNA and protein expression.
- Assessment of glucose-induced insulin release and glucose sensitivity.
Main Results:
- Short-term sulfonylurea exposure (24h) dose-dependently increased GLUT2 and GK mRNA and protein.
- Long-term exposure (48-72h) time-dependently decreased GLUT2 and GK mRNA and protein.
- Sulfonylurea enhanced glucose-induced insulin release and glucose sensitivity.
Conclusions:
- GLUT2 and GK are coordinately regulated by sulfonylurea through a likely common mechanism.
- Short-term sulfonylurea treatment upregulates glucose sensing elements, while long-term treatment downregulates them.
- The long-term inhibitory effect may explain reduced insulin secretion observed with chronic sulfonylurea use.