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J Appl Physiol 83: 1623-1629, 1997;
8750-7587/97 $5.00
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Vol. 83, Issue 5, 1623-1629, 1997

Glucose transporter content and enzymes of metabolism in nerve-repair grafted muscle of aging Fischer 344 rats

Lisa Larkin1, Eric R. Leiendecker1, Mark Supiano1,2,3, and Jeffrey Halter1,2,3

1 Division of Geriatric Medicine, Department of Internal Medicine, and 2 Institute of Gerontology, University of Michigan; and 3 Geriatric Research, Education, and Clinical Center, Department of Veterans Affairs Medical Center, Ann Arbor, Michigan 48109

Received 4 April 1997; accepted in final form 8 July 1997.

Larkin, Lisa, Eric R. Leiendecker, Mark Supiano, and Jeffrey Halter. Glucose transporter content and enzymes of metabolism in nerve-repair grafted muscle of aging Fischer 344 rats. J. Appl. Physiol. 83(5): 1623-1629, 1997.---Aging and grafting are associated with decreased ability of muscle to sustain power, likely reflecting diminished fuel availability. To assess mechanisms that may contribute to availability of glucose, we studied GLUT-1 and GLUT-4 protein as well as mRNA contents and enzymes of glucose metabolism in grafted and control medial gastrocnemius (MG) muscles of 6-, 12-, and 24-mo-old male Fischer 344 rats. There was no effect of age or grafting on MG GLUT-4 content. There was both an age- and graft-associated increase in GLUT-1 content (P = 0.0044 and 0.0063, respectively). There was no effect of aging or grafting on hexokinase and phosphofructokinase activity or on protein and glycogen content. Muscle mass and citrate synthase activity were significantly diminished with grafting. Citrate synthase activity was significantly greater in the 12-mo-old compared with the 6- and 24-mo-old animals. Grafting in combination with aging had no impact on any of the parameters measured. We conclude that diminished glucose transporter expression cannot explain the decreased ability of aged muscle to sustain power. In addition, we conclude that the diminished ability of the grafted MG muscle to sustain power may be explained, in part, by a decrease in energy available from oxidative metabolism.

glucose transporter protein; messenger ribonuclease content; muscle regeneration





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