Effect of Transient Ischemia on the Expression of Glucose Transporters GLUT-1 and GLUT-4 in Rat Myocardium
A number of observations indicate that myocardial glucose utilization is increased late during post-ischemic reperfusion. The present study was designed to examine whether transient ischemia elicits altered expression of glucose transporters GLUT-1 and GLUT-4. In rats, the left anterior descending c...
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Veröffentlicht in: | Journal of molecular and cellular cardiology 1999-05, Vol.31 (5), p.1143-1155 |
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Sprache: | eng |
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Zusammenfassung: | A number of observations indicate that myocardial glucose utilization is increased late during post-ischemic reperfusion. The present study was designed to examine whether transient ischemia elicits altered expression of glucose transporters GLUT-1 and GLUT-4. In rats, the left anterior descending coronary artery was occluded for 20 min followed by reperfusion for 1, 3 or 7 days. Regional myocardial uptake and phosphorylation of glucose was determined based on myocardial accumulation of 2-deoxy-D-[2,6-3H]glucose-6-phosphate. In hearts from fasted rats, after 3 days of reperfusion, myocardial uptake and phosphorylation of glucose was 48% higher in the reperfused region compared to a remote control region. No regional difference in myocardial glucose uptake and phosphorylation was detectable in hearts from fed rats. After 1 day of reperfusion, expression of myocardial glucose transporter GLUT-1 mRNA was increased to 195±24% (mean±SEM) of the value measured in the remote region and the expression of GLUT-4 mRNA was decreased to 58±7%. After 3 days of reperfusion both mRNA and protein of GLUT-1 were higher in the reperfused region, averaging 133±23% and 249±36%, respectively. The corresponding values for GLUT-4 mRNA and protein were 77±7% and 62±6%, respectively. The results indicate that a short period of ischemia alters the expression of glucose transporter isoforms GLUT-1 and GLUT-4. Observed changes may be involved in the mechanisms underlying late changes of substrate metabolism during reperfusion. |
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ISSN: | 0022-2828 1095-8584 |
DOI: | 10.1006/jmcc.1999.0952 |