Open AccessMuscle-Derived IL-6 Is Not Regulated by IL-1 during Exercise. A Double Blind, Placebo-Controlled, Randomized Crossover Study
Author(s) -
Thierry M. Nordmann,
Eleonora Seelig,
Katharina Timper,
Mareike Cordes,
Michael Coslovsky,
Henner Hanssen,
Arno SchmidtTrucksäss,
Marc Y. Donath
Publication year - 2015
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0139662
Subject(s) - anakinra , medicine , placebo , crossover study , endocrinology , inflammation , interleukin , antagonist , receptor antagonist , antagonism , interleukin 1 receptor antagonist , randomized controlled trial , receptor , cytokine , pathology , alternative medicine , disease
Exercise increases muscle derived Interleukin–6 (IL–6) leading to insulin secretion via glucagon-like peptide–1. IL–1 antagonism improves glycemia and decreases systemic inflammation including IL–6 in patients with type 2 diabetes. However, it is not known whether physiological, exercise-induced muscle-derived IL–6 is also regulated by the IL–1 system. Therefore we conducted a double blind, crossover study in 17 healthy male subjects randomized to receive either the IL–1 receptor antagonist IL-1Ra (anakinra) or placebo prior to an acute treadmill exercise. Muscle activity led to a 2–3 fold increase in serum IL–6 concentrations but anakinra had no effect on this exercise-induced IL–6. Furthermore, the IL–1 responsive inflammatory markers CRP, cortisol and MCP–1 remained largely unaffected by exercise and anakinra. We conclude that the beneficial effect of muscle-induced IL–6 is not meaningfully affected by IL–1 antagonism. Trial Registration ClinicalTrials.gov NCT01771445