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Glucose Transporter 4 (GLUT4) is Not the Only GLUT Responsible for Ca2+/Calmodulin‐Dependent Protein Kinase Kinase α (CaMKKα)‐Induced Glucose Uptake in Mouse Skeletal Muscle

Chronic activation of Ca2+/calmodulin‐dependent protein kinase kinase α (CaMKKα) signaling for 2 weeks stimulates skeletal muscle glucose uptake in both insulin‐sensitive and insulin‐resistant mice; yet surprisingly the glucose transporter(s) that mediate this effect are currently unknown. The goal of this study was to determine if glucose transporter 4 (GLUT4) is the main glucose transporter responsible for CaMKKα‐induced muscle glucose uptake. To stimulate CaMKKα signaling, muscles from 13‐14 week old, male, wild‐type/control, muscle‐specific GLUT4 heterozygous and muscle‐specific GLUT4 knockout mice were transfected with plasmid DNA containing constitutively active CaMKKα or empty vector by in vivo electroporation. After 2 weeks, active CaMKKα protein levels were robustly increased and were not different between groups. In vivo muscle [3H]‐2‐deoxyglucose uptake was examined in the absence of insulin stimulation. Constitutively active CaMKKα increased glucose uptake ~250% in wild‐type/control mice, ~100% in GLUT4 heterozygous mice, and ~60% in GLUT4 knockout mice. Collectively, these results show that activation of CaMKKα signaling primarily stimulates glucose uptake via GLUT4, but suggest that another glucose transporter is also involved. SUPPORT: NIH R00AR056298, ECU start‐up funds.