Muscle-Derived IL-6 Is Not Regulated by IL-1 during Exercise. A Double Blind, Placebo-Controlled, Randomized Crossover Study.
- Nordmann TM Clinic of Endocrinology, Diabetes and Metabolism University Hospital Basel, and Department Biomedicine. University of Basel, 4031 Basel, Switzerland.
- Seelig E Clinic of Endocrinology, Diabetes and Metabolism University Hospital Basel, and Department Biomedicine. University of Basel, 4031 Basel, Switzerland.
- Timper K Clinic of Endocrinology, Diabetes and Metabolism University Hospital Basel, and Department Biomedicine. University of Basel, 4031 Basel, Switzerland.
- Cordes M Division of Sports and Exercise Medicine, Department of Sport, Exercise and Health, Medical Faculty, University of Basel, Basel, Switzerland.
- Coslovsky M Clinical Trial Unit, University Hospital Basel, 4031 Basel, Switzerland.
- Hanssen H Division of Sports and Exercise Medicine, Department of Sport, Exercise and Health, Medical Faculty, University of Basel, Basel, Switzerland.
- Schmidt-Trucksäss A Division of Sports and Exercise Medicine, Department of Sport, Exercise and Health, Medical Faculty, University of Basel, Basel, Switzerland.
- Donath MY Clinic of Endocrinology, Diabetes and Metabolism University Hospital Basel, and Department Biomedicine. University of Basel, 4031 Basel, Switzerland.
- 2015-10-09
Published in:
- PloS one. - 2015
Adult
C-Reactive Protein
Cell Line
Chemokines
Cross-Over Studies
Diabetes Mellitus, Type 2
Double-Blind Method
Exercise
Humans
Insulin-Secreting Cells
Interleukin-1beta
Interleukin-6
Interleukin-8
Male
Middle Aged
Muscle, Skeletal
Placebo Effect
Receptors, Interleukin-1
Recombinant Proteins
Serum
English
UNLABELLED
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.
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.
- Language
-
- English
- Open access status
- gold
- Identifiers
-
- DOI 10.1371/journal.pone.0139662
- PMID 26448147
- Persistent URL
- https://sonar.ch/global/documents/232285
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