TY - JOUR
T1 - Interleukin-6 modifies mRNA expression in mouse skeletal muscle
AU - Hassing, Helle Adser
AU - Wojtaszewski, Jørgen
AU - Jakobsen, Anne Hviid
AU - Kiilerich, Kristian
AU - Hidalgo, J
AU - Pilegaard, Henriette
N1 - CURIS 2011 5200 028
PY - 2011/6
Y1 - 2011/6
N2 - 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.
AB - 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.
U2 - 10.1111/j.1748-1716.2011.02269.x
DO - 10.1111/j.1748-1716.2011.02269.x
M3 - Journal article
C2 - 21352507
SN - 1748-1716
VL - 202
SP - 165
EP - 173
JO - Acta Physiologica
JF - Acta Physiologica
IS - 2
ER -