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Skeletal muscle glucose uptake can be regulated in response to different stimuli, with insulin and contraction being central. While the processes underlying insulin-induced glucose uptake have been extensively characterized, the processes underlying contraction-induced glucose uptake remain elusive. In this issue of Diabetes , Sylow et al. (1) provide another piece to this puzzle. They report that Rac1 is essential for contraction-induced GLUT4 translocation.Contraction induces glucose uptake in skeletal muscle both independently (2) and synergistically (3) with insulin. Several different mechanisms have been proposed, which appear to be activated in parallel following muscle contraction (Fig. 1). Key pathways include activation of the AMP-sensitive protein kinase (AMPK) through changes in the AMP:ATP ratio in response to increasing energy demands (4). Increased Ca2+/calmodulin-dependent protein kinase I (CaMKI) influx during muscle depolarization results in activation of calcium signaling cascades via CaMKI (5) and protein kinase C (PKC) (6). Downstream candidates include the Rab-GTPase-activating protein TBC1D1 (7), and evidence supports a role of increased free radical content in contraction-mediated glucose uptake …

ContRac1ion-Mediated Glucose Uptake: A Central Role for Rac1