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1 Department of Medicine, Case Western Reserve University, Cleveland, OH, USA
2 Department of Medicine, Case Western Reserve University, Cleveland, OH, USA; Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, OH, USA
* To whom correspondence should be addressed. E-mail: fxi2{at}cwru.edu.
Glucose transport is stimulated in a variety of cells and tissues in response to inhibition of oxidative phosphorylation. However, the underlying mechanisms and mediating steps remain largely unknown. In the present study we first tested whether a decrease in the redox state of the cell per se and the resultant increase in generation of reactive oxygen species (ROS) leads to stimulation of glucose transport. Clone 9 cells (expressing the Glut1 isoform of facilitative glucose transporters) were exposed to azide, lactate, and ethanol for 1 h. While all three agents stimulated glucose transport and increased cell NADH/NAD+ ratio and phospho-ERK1/2 signifying increased ROS generation, the response to the stimuli was not blocked by N-acetylcysteine (an agent that counteracts ROS); moreover, the response to azide was not blocked by diamide (an intracellular sulfydryl oxidizing agent). We then found that cell AMP/ATP and ADP/ATP ratio was increased and 5[[rad]]-AMP-activated protein kinase (AMPK) was stimulated by all three agents, as evidenced by increased phosphorylation of AMPK and acetyl CoA carboxylase. We conclude that while azide, lactate, and ethanol increase NADH/NAD+ ratios and ROS production, their stimulatory effect on glucose transport is not mediated by increased ROS generation. However, all three agents increased cell AMP/ATP ratio and stimulated AMPK, making it likely that the latter pathway plays an important role in the glucose transport response.
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