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Interleukin-6 Markedly Decreases Skeletal Muscle Protein Turnover and Increases Nonmuscle Amino Acid Utilization in Healthy Individuals

The Centre of Inflammation and Metabolism at Department of Infectious Diseases Rigshospitalet (G.v.H., A.S., C.F., C.K., K.M., P.M., B.K.P.), Faculty of Health Sciences, and Department of Biomedical Sciences (G.v.H.), University of Copenhagen, DK-1017 Copenhagen, Denmark; and Copenhagen Muscle Research Centre (G.v.H., A.S., C.F., C.K., K.M.), Rigshospitalet, DK-2100 Copenhagen, Denmark

Address all correspondence and requests for reprints to: G. van Hall, Copenhagen Muscle Research Centre, Rigshospitalet, section 7652, 9 Blegdamsvej, DK-2100, Copenhagen Ø, Denmark. E-mail: gvhall{at}cmrc.dk.

Context: IL-6 is a key modulator of immune function and suggested to be involved in skeletal muscle wasting as seen in sepsis.

Objective: Our objective was to determine the role of IL-6 in human in vivo systemic and skeletal muscle amino acid metabolism and protein turnover.

Subjects and Methods: There were 12 healthy men infused for 3 h with saline (saline, n = 6) or recombinant human IL (rhIL)-6 (n = 6). Systemic and muscle protein turnover was determined with a combination of tracer dilution methodology, primed constant infusion of L-[ring-²H₅]phenylalanine, and femoral arterial-venous blood differences and m. vastus lateralis biopsies after 2-h basal, 3-h infusion, and 3 h after infusion.

Results: The IL-6 concentration after 30-min infusion was approximately 4 (saline) and 140 pg/ml (rhIL-6). Three-hour rhIL-6 infusion caused an approximate 50% decrease in muscle protein turnover, albeit synthesis was more suppressed than breakdown, causing a small increase in net muscle protein breakdown. Furthermore, rhIL-6 decreased arterial amino acid concentration with 20–40%, despite the increase net release from muscle.

Conclusions: We demonstrated that IL-6 profoundly alters amino acid turnover. A substantial decrease in plasma amino acids was observed with a concomitant 50% decrease in muscle protein turnover, however, modest increase in net muscle degradation. We hypothesize that the profound reduction in muscle protein turnover and modest increase in net degradation are primarily caused by the reduced plasma amino acid availability and not directly mediated by IL-6.

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