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1 Research Division, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02215; and 2 Copenhagen Muscle Research Centre, August Krogh Institute, University of Copenhagen, DK-2100 Copenhagen, Denmark
Exercise increases the rate of glucose uptake into the contracting skeletal muscles. This effect of exercise is similar to the action of insulin on glucose uptake, and the mechanism through which both stimuli increase skeletal muscle glucose uptake involves the translocation of GLUT-4 glucose transporters to the plasma membrane and transverse tubules. Most studies suggest that exercise and insulin recruit distinct GLUT-4-containing vesicles and/or mobilize different "pools" of GLUT-4 proteins originating from unique intracellular locations. There are different intracellular signaling pathways that lead to insulin- and exercise-stimulated GLUT-4 translocation. Insulin utilizes a phosphatidylinositol 3-kinase-dependent mechanism, whereas the exercise signal may be initiated by calcium release from the sarcoplasmic reticulum leading to the activation of other signaling intermediaries, and there is also evidence for autocrine- or paracrine-mediated activation of transport. The period after exercise is characterized by increased sensitivity of muscle glucose uptake to insulin, which can be substantially prolonged in the face of carbohydrate deprivation. The ability of exercise to utilize insulin-independent mechanisms to increase glucose uptake in skeletal muscle has important clinical implications, especially for patients with diseases that are associated with peripheral insulin resistance, such as non-insulin-dependent diabetes mellitus.
muscle contraction; glucose transporters; GLUT-4; calcium; insulin
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