![]() More recent studies have shown that hypoxia causes the translocation of the GLUT-4 transporter to the sarcolemma in L6 muscle cells 12 and perfused rat hearts. 8 9 Early in vitro studies demonstrated that hypoxia increases the number of glucose transporters present in the sarcolemma in both heart 10 and skeletal muscle, 11 as assessed by cytochalasin B binding, but did not clearly identify the specific transporters involved. ![]() 5 Insulin-stimulated heart glucose uptake involves translocation of GLUT-4 from an intracellular membrane pool to the sarcolemma, 6 7 where it is thought to account for insulin-mediated increases in glucose transport rates. Of the seven reported members of the facilitative glucose transporter family, GLUT-4 and GLUT-1 are the primary forms expressed in adult mammalian heart muscle. However, the mechanisms responsible in vivo for increased heart glucose transport with ischemia are not yet defined. 1 2 The ischemia-mediated increase in glucose utilization is characterized by enhanced rates of exogenous glucose uptake in vivo, 3 4 which requires greater rates of transport across the plasma membrane. Ischemia induces many changes in heart metabolism, including shifts from aerobic fatty acid metabolism to anaerobic glycolysis, which provides energy for critical myocardial cellular function. These results indicate that both GLUT-1 and GLUT-4 are important in ischemia-mediated myocardial glucose uptake in vivo. GLUT-1 is also present in an intracellular storage pool from which it undergoes translocation to the sarcolemma in response to ischemia. However, significant GLUT-4 surface labeling was found in the ischemic region.Ĭonclusions Translocation of the insulin-responsive GLUT-4 transporter from an intracellular storage pool to the sarcolemma occurs in vivo during acute low-flow ischemia. GLUT-1 had a more prominent cell surface pattern than GLUT-4, which was primarily intracellular in the nonischemic region. Immunofluorescence demonstrated the presence of both GLUT-4 and GLUT-1 on cardiac myocytes. Ischemia led to an increase in the sarcolemma content of both GLUT-4 (15☒% to 30☓%, P<.02) and GLUT-1 (41±4% to 58☓%, P<.03) compared with the nonischemic region and to a parallel decrease in their intracellular contents. In vivo glucose extraction increased fivefold ( P<.001) and was associated with net lactate release in the ischemic region. Methods and Results In a canine model, we evaluated myocardial glucose metabolism in vivo and the distribution of GLUT-4 and GLUT-1 by use of immunoblotting of sarcolemma and intracellular membranes and immunofluorescence localization with confocal microscopy. However, whether low-flow ischemia leads to the translocation of glucose transporter (GLUT)-4 and/or GLUT-1 to the sarcolemma in vivo is unknown. Customer Service and Ordering Informationīackground Myocardial ischemia increases heart glucose utilization in vivo.Stroke: Vascular and Interventional Neurology.Journal of the American Heart Association (JAHA).Circ: Cardiovascular Quality & Outcomes.Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB).
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