Cytosolic ROS production by NADPH oxidase 2 regulates muscle glucose uptake during exercise

Carlos Henríquez-Olguin, Jonas R. Knudsen, Steffen H. Raun, Zhencheng Li, Emilie Dalbram, Jonas T. Treebak, Lykke Sylow, Rikard Holmdahl, Erik A. Richter, Enrique Jaimovich and Thomas E. Jensen ()
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Carlos Henríquez-Olguin: University of Copenhagen
Jonas R. Knudsen: University of Copenhagen
Steffen H. Raun: University of Copenhagen
Zhencheng Li: University of Copenhagen
Emilie Dalbram: University of Copenhagen
Jonas T. Treebak: University of Copenhagen
Lykke Sylow: University of Copenhagen
Rikard Holmdahl: Karolinska Institute
Erik A. Richter: University of Copenhagen
Enrique Jaimovich: Universidad de Chile
Thomas E. Jensen: University of Copenhagen

Nature Communications, 2019, vol. 10, issue 1, 1-11

Abstract: Abstract Reactive oxygen species (ROS) act as intracellular compartmentalized second messengers, mediating metabolic stress-adaptation. In skeletal muscle fibers, ROS have been suggested to stimulate glucose transporter 4 (GLUT4)-dependent glucose transport during artificially evoked contraction ex vivo, but whether myocellular ROS production is stimulated by in vivo exercise to control metabolism is unclear. Here, we combined exercise in humans and mice with fluorescent dyes, genetically-encoded biosensors, and NADPH oxidase 2 (NOX2) loss-of-function models to demonstrate that NOX2 is the main source of cytosolic ROS during moderate-intensity exercise in skeletal muscle. Furthermore, two NOX2 loss-of-function mouse models lacking either p47phox or Rac1 presented striking phenotypic similarities, including greatly reduced exercise-stimulated glucose uptake and GLUT4 translocation. These findings indicate that NOX2 is a major myocellular ROS source, regulating glucose transport capacity during moderate-intensity exercise.

Date: 2019
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DOI: 10.1038/s41467-019-12523-9

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