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Interleukin-6 modifies mRNA expression in mouse skeletal muscle.
H Adser1, J F P Wojtaszewski, A H Jakobsen
1Centre of Inflammation and Metabolism, Copenhagen, Denmark.
Acta Physiologica (Oxford, England)
|March 1, 2011
Summary
Interleukin-6 (IL-6) influences how mouse skeletal muscle uses glycogen and responds to exercise. IL-6 impacts AMP-activated protein kinase (AMPK) signaling and tumor necrosis factor-alpha (TNF-α) mRNA production after exercise.
Area of Science:
- Exercise physiology
- Molecular biology
- Muscle metabolism
Background:
- Interleukin-6 (IL-6) is a cytokine with known roles in inflammation and immune responses.
- Its specific role in skeletal muscle adaptations to exercise, particularly concerning key metabolic and signaling pathways, requires further elucidation.
Purpose of the Study:
- To investigate the role of IL-6 in exercise-induced changes in peroxisome proliferator-activated receptor gamma coactivator (PGC)-1α and tumor necrosis factor (TNF)-α mRNA expression in skeletal muscle.
- To examine the potential regulation of AMP-activated protein kinase (AMPK) signaling by IL-6 during exercise.
Main Methods:
- Comparison of exercise responses between IL-6 knockout (KO) mice and wildtype (WT) mice.
- Treadmill exercise protocol (1 hour) followed by immediate or 4-hour post-exercise muscle tissue collection (white gastrocnemius and quadriceps).
- Analysis of muscle glycogen concentration, AMPK and Acetyl CoA carboxylase (ACC) phosphorylation, and PGC-1α and TNF-α mRNA levels.
Main Results:
- Exercise reduced muscle glycogen significantly in WT mice, but not in IL-6 KO mice.
- AMPK and ACC phosphorylation increased post-exercise in WT mice, with no change observed in IL-6 KO mice.
- IL-6 influenced PGC-1α mRNA expression and TNF-α mRNA responses to exercise, with distinct patterns observed between WT and IL-6 KO mice.
Conclusions:
- IL-6 plays a significant role in modulating exercise-induced changes in skeletal muscle.
- The findings highlight IL-6's involvement in regulating glycogen utilization, AMPK signaling pathways, and TNF-α mRNA expression in response to physical activity.
