Molecular mechanisms of enhanced [18F] fluorodeoxy glucose (FDG) uptake in isochemically injured myocardium: the role of glucose transporter and hexokinase expression. Final technical report for period August 1, 1993--November 30, 1997

摘要

We determined that there were no regional differences in GLUT1 or GLUT4 expression in normal dog heart. We demonstrated that glucose uptake was relatively enhanced in regions of severe ischemia in this model. We showed that GLUT1 mRNA and polypeptide expression but not GLUT4 expression were substantially and significantly increased in both ischemic and nonischemic myocardial regions after 6 hours. We also found that GLUT4 translocation and glucose uptake induced by ischemia in perfused rat hearts were not inhibited by Wortmannin, a PI3 kinase inhibitor, whereas insulin-stimulatd increases in GLUT4 translocation and glucose uptake were inhibited. To determine whether some of the same phenomena occurred in humans with chronic myocardial ischemia, we investigated myocardial GLUT mRNA expression in 11 patients who underwent coronary artery bypass surgery. We have cultured neonatal rat cardiomyocytes and tested the effects of several factors including hypoxia and insulin.