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Calcineurin does not mediate exercise-induced increase in muscle GLUT4
Pablo M Garcia-Roves1, Terry E Jones, Kenichi Otani
1Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Diabetes
|March 1, 2005
Summary
Exercise increases glucose transporter type 4 (GLUT4) in skeletal muscle. This study found that calcineurin inhibition did not affect exercise-induced GLUT4 adaptation, suggesting calcineurin is not the mediator.
Area of Science:
- Exercise physiology
- Molecular biology
- Skeletal muscle adaptation
Background:
- Exercise rapidly increases glucose transporter type 4 (GLUT4) in skeletal muscle.
- Cytosolic Ca(2+) and calcineurin are implicated in mediating this exercise adaptation.
- An alternative pathway involving Ca(2+)-calmodulin-dependent protein kinase has been suggested.
Purpose of the Study:
- To test the hypothesis that calcineurin mediates exercise-induced increases in GLUT4 expression in skeletal muscle.
Main Methods:
- Rats underwent a 5-day swimming exercise protocol.
- One group received cyclosporin (a calcineurin inhibitor) before exercise; a control group received vehicle.
- Expression of GLUT4, MEF2A, and hexokinase II was measured post-exercise.
Main Results:
- Exercise increased GLUT4 protein and mRNA, MEF2A, and hexokinase II.
- Cyclosporin completely inhibited calcineurin activity.
- Calcineurin inhibition did not affect the exercise-induced increases in GLUT4, MEF2A, or hexokinase II.
Conclusions:
- Calcineurin activation is not the mediator of exercise-induced adaptive increases in GLUT4 expression in skeletal muscle.
- The findings challenge the proposed role of calcineurin in this specific adaptive response.