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

S.R. Gray, A. Ratkevicius, H. Wackerhage, P. Coats, M.A. Nimmo

Research output: Contribution to journalArticle

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Abstract

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.
Original languageEnglish
Pages (from-to)899-905
Number of pages7
JournalExperimental Physiology
Volume94
Issue number8
Early online date29 May 2009
DOIs
Publication statusPublished - 1 Aug 2009

Fingerprint

Interleukin-6 Receptors
Interleukin-6
Skeletal Muscle
Glucose
AMP-Activated Protein Kinases
Phosphorylation
Proto-Oncogene Proteins c-akt
Western Blotting
Insulin

Keywords

  • necrosis-factor-alpha
  • activated protein-kinase
  • subcutaneous adipose-tissue
  • insulin sensitivitiy
  • in-vitro
  • soluble receptors
  • lipid-metabolism
  • healthy-subjects
  • plasma il-6
  • resistance

Cite this

Gray, S.R. ; Ratkevicius, A. ; Wackerhage, H. ; Coats, P. ; Nimmo, M.A. / The effect of interleukin-6 and the interleukin-6 receptor on glucose transport in mouse skeletal muscle. In: Experimental Physiology. 2009 ; Vol. 94, No. 8. pp. 899-905.
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The effect of interleukin-6 and the interleukin-6 receptor on glucose transport in mouse skeletal muscle. / Gray, S.R.; Ratkevicius, A.; Wackerhage, H.; Coats, P.; Nimmo, M.A.

In: Experimental Physiology, Vol. 94, No. 8, 01.08.2009, p. 899-905.

Research output: Contribution to journalArticle

TY - JOUR

T1 - The effect of interleukin-6 and the interleukin-6 receptor on glucose transport in mouse skeletal muscle

AU - Gray, S.R.

AU - Ratkevicius, A.

AU - Wackerhage, H.

AU - Coats, P.

AU - Nimmo, M.A.

PY - 2009/8/1

Y1 - 2009/8/1

N2 - 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.

AB - 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.

KW - necrosis-factor-alpha

KW - activated protein-kinase

KW - subcutaneous adipose-tissue

KW - insulin sensitivitiy

KW - in-vitro

KW - soluble receptors

KW - lipid-metabolism

KW - healthy-subjects

KW - plasma il-6

KW - resistance

U2 - 10.1113/expphysiol.2009.048173

DO - 10.1113/expphysiol.2009.048173

M3 - Article

VL - 94

SP - 899

EP - 905

JO - Experimental Physiology

JF - Experimental Physiology

SN - 0958-0670

IS - 8

ER -