Modulation of glucose transport in skeletal muscle by reactive oxygen species

2007 ◽  
Vol 102 (4) ◽  
pp. 1671-1676 ◽  
Author(s):  
Abram Katz

Glucose transport is an essential physiological process that is characteristic of all eukaryotic cells, including skeletal muscle. In skeletal muscle, glucose transport is mediated by the GLUT-4 protein under conditions of increased carbohydrate utilization. The three major physiological stimuli of glucose transport in muscle are insulin, exercise/contraction, and hypoxia. Here, the role of reactive oxygen species (ROS) in modulating glucose transport in skeletal muscle is reviewed. Convincing evidence for ROS involvement in insulin- and hypoxia-mediated transport in muscle is lacking. Recent experiments, based on pharmacological and genetic approaches, support a role for ROS in contraction-mediated glucose transport. During contraction, endogenously produced ROS appear to mediate their effects on glucose transport via AMP-activated protein kinase.

2006 ◽  
Vol 575 (1) ◽  
pp. 251-262 ◽  
Author(s):  
Marie E. Sandström ◽  
Shi-Jin Zhang ◽  
Joseph Bruton ◽  
José P. Silva ◽  
Michael B. Reid ◽  
...  

2000 ◽  
Vol 33 (3) ◽  
pp. 287-293 ◽  
Author(s):  
O. Pansarasa ◽  
L. Castagna ◽  
B. Colombi ◽  
J. Vecchiet ◽  
G. Felzani ◽  
...  

2013 ◽  
Vol 304 (11) ◽  
pp. R1009-R1016 ◽  
Author(s):  
Li Zuo ◽  
Amy Shiah ◽  
William J. Roberts ◽  
Michael T. Chien ◽  
Peter D. Wagner ◽  
...  

Contractions in whole skeletal muscle during hypoxia are known to generate reactive oxygen species (ROS); however, identification of real-time ROS formation within isolated single skeletal muscle fibers has been challenging. Consequently, there is no convincing evidence showing increased ROS production in intact contracting fibers under low Po2 conditions. Therefore, we hypothesized that intracellular ROS generation in single contracting skeletal myofibers increases during low Po2 compared with a value approximating normal resting Po2. Dihydrofluorescein was loaded into single frog ( Xenopus) fibers, and fluorescence was used to monitor ROS using confocal microscopy. Myofibers were exposed to two maximal tetanic contractile periods (1 contraction/3 s for 2 min, separated by a 60-min rest period), each consisting of one of the following treatments: high Po2 (30 Torr), low Po2 (3–5 Torr), high Po2 with ebselen (antioxidant), or low Po2 with ebselen. Ebselen (10 μM) was administered before the designated contractile period. ROS formation during low Po2 treatment was greater than during high Po2 treatment, and ebselen decreased ROS generation in both low- and high-Po2 conditions ( P < 0.05). ROS accumulated at a faster rate in low vs. high Po2. Force was reduced >30% for each condition except low Po2 with ebselen, which only decreased ∼15%. We concluded that single myofibers under low Po2 conditions develop accelerated and more oxidative stress than at Po2 = 30 Torr (normal human resting Po2). Ebselen decreases ROS formation in both low and high Po2, but only mitigates skeletal muscle fatigue during reduced Po2 conditions.


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