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1 The Copenhagen Muscle Research Centre and The Department of Infectious Diseases, Rigshospitalet, Copenhagen, Denmark
* To whom correspondence should be addressed. E-mail: bkp{at}rh.dk.
High circulating levels of interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha) are found in patients with hyperinsulinemia. Insulin stimulates release of IL-6 from adipocyte cultures and insulin stimulates IL-6 gene expression in insulin-resistant, but not control, rat skeletal muscle. In addition, TNF-alpha may be involved in the pathogenesis of insulin resistance. Therefore, we studied the effect of insulin on IL-6 and TNF-alpha gene expression in human skeletal muscle and adipose tissue. Nine healthy young volunteers participated in the study. They underwent six hours of hyperinsulinemic euglycemic clamping at a fixed insulin infusion rate, with blood glucose clamped at fasting level. Blood samples, drawn at time points 0, 1, 2, 3, 4, 5, and 6 hours, were analyzed for IL-6 and TNF-alpha. Muscle and fat biopsies, obtained at time points 0, 2, 4 and 6 hours, were analyzed for IL-6 and TNF-alpha mRNA using real-time PCR. IL-6 mRNA increased 11, 3 and 5 fold at 2, 4 and 6 hours, respectively, in adipose tissue, (ANOVA p=0.027), whereas there was no significant effect of insulin on skeletal muscles. Plasma-IL-6 increased during insulin stimulation. TNF-alpha mRNA increased 2.4, 1.4 and 2.2 fold in adipose tissue (ANOVA p=0.001) and decreased 0.74, 0.64 and 0.68 fold in muscle tissue (ANOVA p=0.04). Plasma levels of TNF-alpha were constant. In conclusion, the finding that insulin stimulates IL-6 and TNF-alpha gene expression in adipose tissue, only, and inhibits the TNF-alpha production in skeletal muscles, suggests a differential regulation of muscle- and adipose tissue-derived IL-6 and TNF-alpha.
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