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Discrepancy between GLUT4 translocation and glucose uptake after ischemia
Vlad Zaha1, Roland Nitschke, Heike Göbel
1Department of Cardiovascular Surgery, Albert-Ludwigs-University of Freiburg, Freiburg, Germany.
Molecular and Cellular Biochemistry
|September 24, 2005
Summary
Total ischemia in rat hearts did not increase glucose uptake despite GLUT4 transporter translocation. This suggests GLUT4 transporter inhibition in the plasma membrane may impair glucose uptake after ischemia.
Area of Science:
- Cardiovascular Physiology
- Metabolic Regulation
- Ischemic Heart Disease
Background:
- Low-flow ischemia typically increases glucose uptake due to glucose transporter (GLUT) translocation.
- However, studies on total ischemia have shown no corresponding increase in glucose uptake.
Purpose of the Study:
- To investigate the hypothesis that total ischemia leads to decreased activation of GLUT4, despite its translocation to the cell membrane.
- To explore the discrepancy between GLUT4 availability and actual glucose uptake after ischemic events.
Main Methods:
- Isolated working rat hearts (n=70) were perfused with either oleate or pyruvate, subjected to 15 minutes of total ischemia, followed by 35 minutes of reperfusion.
- Glucose uptake and intracellular free glucose (IFG) were measured using radiolabeled glucose and sucrose.
- GLUT4 distribution was assessed via immunofluorescence, examining colocalization with Na-K ATP-ase.
Main Results:
- Cardiac power and recovery rates were similar between the oleate and pyruvate groups post-ischemia.
- No significant increase in glucose uptake was observed during reperfusion in either group.
- While GLUT4 translocation was evident after reperfusion, intracellular free glucose levels did not increase, indicating a functional impairment.
Conclusions:
- A disconnect exists between the presence of GLUT4 transporters at the plasma membrane and their ability to facilitate glucose uptake following total ischemia.
- This suggests potential inhibition of GLUT4 transporter function in the plasma membrane as a key factor limiting glucose uptake after ischemic insult.