Contracting skeletal muscle releases IL-6, but not TNF-α, in healthy subjects and patients with type 2 diabetes

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University of York (2002) J Physiol 539P, S095

Communications: Contracting skeletal muscle releases IL-6, but not TNF-α, in healthy subjects and patients with type 2 diabetes

Adam Steensberg*, Rebecca L. Starkie†, Glenn K. McConell‡, Bronwyn A. Kingwellñ and Mark A. Febbraio*†

*Copenhagen Muscle Research Centre, Department of Infectious Diseases, Rigshospitalet, University of Copenhagen, †Exercise Physiology and Metabolism Laboratory, Department of Physiology, The University of Melbourne, Parkville, Australia, ‡Department of Physiology, Monash University, Clayton and ñBaker Medical Research Institute, Melbourne, Australia

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The evidence that insulin resistance in skeletal muscle is linked to tumour necrosis factor (TNF)-α is well established (Usal et al. 1997). In contrast, although the expression of interleukin (IL)-6 has been associated with insulin resistance (Kern et al. 2001), there is no evidence linking IL-6 in skeletal muscle with insulin resistance. On the contrary, IL-6 is produced by skeletal muscle during exercise when glucose uptake is markedly increased (Steensberg et al. 2001). In addition, incubating cultured 3T3-L1 adipocytes with IL-6 enhances both basal and insulin-stimulated glucose uptake (Stouthard et al. 1996). To examine the influence of type 2 diabetes on TNF-α and IL-6 release from the skeletal muscle at rest and during exercise, nine male type 2 diabetics (D) and nine age-, sex-, VO2,peak– and weight-matched control subjects (C) underwent 25 min of supine bicycle exercise at 60 % VO2,peak. The weight and body mass index for D were 88.3 ± 4.8 kg and 28.1 ± 1.4, and for C 85.5 ± 4.5 kg and 25.4 ± 1.0 (P > 0.05 comparing group). The study was approved by the local ethics committee in accordance with the Declaration of Helsinki. Blood samples were obtained from a femoral artery and vein from one limb before and after exercise and plasma was analysed for TNF-α and IL-6. Leg blood flow (LBF) was measured by thermodilution in the femoral vein, and net leg TNF-α and IL-6 balance were calculated as the product of LBF and femoral arterio-venous (fa-v) TNF-α and IL-6 difference. The data were statistically analysed by a two-way ANOVA. The results are summarised in Fig. 1. These data demonstrate that 25 min of supine bicycle exercise is sufficient to result in a net release of IL-6, but not TNF-α, from contracting muscle in both healthy control and diabetic subjects. In addition, these data suggest that the exercise-induced skeletal muscle IL-6 production may be augmented in type 2 diabetics. We hypothesise that the upregulation of IL-6 in type 2 diabetic contracting skeletal muscle is a consequence rather than a cause of insulin resistance and that the function is to enhance glucose uptake when the demand for glucose disposal is increased.

This work was supported, in part, by the National Health and Medical Research Council of Australia, and Diabetes Australia.


\"Figure 1. Arterial plasma IL-6 (top left) and TNF-α (bottom left), and net skeletal muscle IL-6 (top right) and TNF-α (bottom right) balance before and after supine bicycle exercise in type 2 diabetics (n = 9, filled bars) and healthy matched controls (n = 9, open bars). Data are expressed as means ± S.E.M. *Denotes difference (P < 0.05) from control at rest, # denotes main effect (P < 0.05) for exercise.\"
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\"Figure 1. Arterial plasma IL-6 (top left) and TNF-&alpha; (bottom left), and net skeletal muscle IL-6 (top right) and TNF-&alpha; (bottom right) balance before and after supine bicycle exercise in type 2 diabetics (n = 9, filled bars) and healthy matched controls (n = 9, open bars). Data are expressed as means &plusmn; S.E.M. *Denotes difference (P &lt; 0.05) from control at rest, # denotes main effect (P &lt; 0.05) for exercise.\"

Where applicable, experiments conform with Society ethical requirements.

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