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The effect of interleukin-6 and the interleukin-6 receptor on glucose transport in mouse skeletal muscle

journal contribution
posted on 09.07.2014, 12:18 by Stuart R. Gray, Aivaras Ratkevicius, Henning Wackerhage, Paul Coats, Myra A. Nimmo
Exercise results in an increase in interleukin-6 (IL-6), its receptor (IL-6R) and skeletal muscle glucose transport. Interleukin-6 has been found to have equivocal effects on glucose transport, with no studies, to our knowledge, investigating any potential role of IL-6R. In the present study, we hypothesized that a combined preparation of IL-6 and soluble IL-6R (sIL-6R) would stimulate glucose transport. Mouse soleus muscles were incubated with physiological and supraphysiological concentrations of IL-6 and a combination of IL-6 and sIL-6R. Total and phosphorylated AMP-activated protein kinase (AMPK) and Protein Kinase B (PKB/Akt) were also measured by Western blotting. Exposure to both physiological (80 pg ml−1) and supraphysiological IL-6 (120 ng ml−1) had no effect on glucose transport. At physiological levels, exposure to a combination of IL-6 and sIL-6R (32 ng ml−1) resulted in a 1.4-fold increase (P < 0.05) in basal glucose transport with no change to the phosphorylation of AMPK. Exposure to supraphysiological levels of IL-6 and sIL-6R (120 ng ml−1) resulted in an approximately twofold increase (P < 0.05) in basal glucose transport and an increase (P < 0.05) in AMPK phosphorylation. No effect of IL-6 or sIL-6R was observed on insulin-stimulated glucose transport. These findings demonstrate that, while IL-6 alone does not stimulate glucose transport in mouse soleus muscle, when sIL-6R is introduced glucose transport is directly stimulated, partly through AMPK-dependent signalling.

History

School

  • Sport, Exercise and Health Sciences

Published in

EXPERIMENTAL PHYSIOLOGY

Volume

94

Issue

8

Pages

899 - 905 (7)

Citation

GRAY, S.R. ... et al., 2009. The effect of interleukin-6 and the interleukin-6 receptor on glucose transport in mouse skeletal muscle. Experimental Physiology, 94 (8), pp. 899 - 905.

Publisher

© The Authors. Journal compilation © The Physiological Society

Version

VoR (Version of Record)

Publication date

2009

Notes

Closed access.

ISSN

0958-0670

Language

en

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Keywords

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