Aim: The aim of this study was to test the hypothesis that interleukin (IL)-6 plays a role in exercise-induced peroxisome proliferator-activated receptor γ co-activator (PGC)-1α and tumor necrosis factor (TNF)-α mRNA responses in skeletal muscle and to examine the potential IL-6-mediated AMP-activated protein kinase (AMPK) regulation in these responses. Methods: Whole body IL-6 knockout (KO) and wildtype (WT) male mice (4months of age) performed 1h treadmill exercise. White gastrocnemius (WG) and quadriceps (Quad) muscles were removed immediately (0') or 4h after exercise and from mice not run acutely. Results: Acute exercise reduced only in WT muscle glycogen concentration to 55 and 35% (P<0.05) of resting level in Quad and WG respectively. While AMPK and Acetyl CoA carboxylase (ACC) phosphorylation increased 1.3-fold (P<0.05) in WG and twofold in Quad immediately after exercise in WT mice, no change was detected in WG in IL-6 KO mice. The PGC-1α mRNA content was in resting WG 1.8-fold higher (P<0.05) in WT mice than in IL-6 KO mice. Exercise induced a delayed PGC-1α mRNA increase in Quad in IL-6 KO mice (12-fold at 4h) relative to WT mice (fivefold at 0'). The TNF-α mRNA content was in resting Quad twofold higher (P<0.05) in IL-6 KO than in WT, and WG TNF-α mRNA increased twofold (P<0.05) immediately after exercise only in IL-6 KO. Conclusion: In conclusion, IL-6 affects exercise-induced glycogen use, AMPK signalling and TNF-α mRNA responses in mouse skeletal muscle. © 2011 The Authors. Acta Physiologica © 2011 Scandinavian Physiological Society.
|Publication status||Published - 1 Jun 2011|
- AMP activated protein kinase
- Skeletal muscle
- Tumor necrosis factor α