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IL-6 directly increases glucose metabolism in resting human skeletal muscle

¹Department of Molecular Medicine and Surgery, Section for Integrative Physiology, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden
²Department of Physiology and Pharmacology, Section for Integrative Physiology, Karolinska Institutet, Stockholm, Sweden
³Department of Molecular Medicine and Surgery, Section for Clinical Physiology, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden
⁴Helsinki University Central Hospital and Biomedicum, Helsinki, Finland

Correspondence: anna.krook{at}ki.se

Objective:: IL-6 is a pro-inflammatory cytokine shown to modify insulin sensitivity. Elevated plasma levels of IL-6 are observed in insulin resistant states. Interestingly, plasma IL-6 levels also increase during exercise, with skeletal muscle being the predominant source. Thus, IL-6 has also been suggested to promote insulin-mediated glucose utilization. We determined the direct effects of IL-6 on glucose transport and signal transduction in human skeletal muscle.

Research Design and Methods:: Skeletal muscle strips were prepared from vastus lateralis biopsies obtained from 22 healthy men. Muscle strips were incubated with or without IL-6 (120 ng/ml).

Results:: IL-6 increased glucose transport in human skeletal muscle 1.3 fold (P<0.05). A 30 min pre-exposure to IL-6 did not affect insulin-stimulated glucose transport. IL-6 also increased skeletal muscle glucose incorporation into glycogen, and glucose oxidation (1.5 fold and 1.3 fold, respectively, P<0.05). IL-6 increased phosphorylation of STAT3 (P<0.05), AMPK (P=0.063), and p38 MAPK (P<0.05), and reduced phosphorylation of S6 ribosomal protein (P<0.05). In contrast, phosphorylation of PKB/Akt, AS160, GSK3/ß, as well as IRS1-associated PI 3-kinase activity was unaltered.

Conclusion:: Acute IL-6 exposure increases glucose metabolism in resting human skeletal muscle. Insulin-stimulated glucose transport and insulin signaling were unchanged following IL-6 exposure.

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