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Interleukin‐6 modifies mRNA expression in mouse skeletal muscle
Author(s) -
Adser H.,
Wojtaszewski J. F. P.,
Jakobsen A. H.,
Kiilerich K.,
Hidalgo J.,
Pilegaard H.
Publication year - 2011
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/j.1748-1716.2011.02269.x
Subject(s) - endocrinology , medicine , skeletal muscle , ampk , messenger rna , glycogen , chemistry , tumor necrosis factor alpha , gastrocnemius muscle , biology , kinase , protein kinase a , biochemistry , gene
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 (4 months of age) performed 1 h treadmill exercise. White gastrocnemius (WG) and quadriceps (Quad) muscles were removed immediately (0′) or 4 h 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 4 h) 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.