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.
- AMP-activated protein kinases
- biological transport
- mice, inbred BALB C
- muscle, skeletal
- proto-oncogene proteins c-akt
- receptors, interleukin-6