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Interleukin-6 contributes to hepcidin mRNA increase in response to exercise
Sébastien Banzet1, Hervé Sanchez, Rachel Chapot
1Institut de Recherche Biomédicale des Armées, Brétigny-sur-Orge 91223, France. sbanzet@crssa.net
Cytokine
|February 14, 2012
Summary
Exercise increases hepcidin, a hormone linked to iron deficiency. This study shows that interleukin-6 (IL-6) plays a key role in exercise-induced hepcidin gene expression in rodents.
Area of Science:
- Exercise Physiology
- Molecular Biology
- Endocrinology
Background:
- Hepcidin, an iron regulatory hormone, is implicated in training-induced iron deficiency.
- Prolonged exercise elevates plasma hepcidin and interleukin-6 (IL-6).
- IL-6 is known to activate hepcidin transcription during inflammation.
Purpose of the Study:
- To investigate the role of IL-6 in hepatic hepcidin mRNA expression during and after exercise.
- To determine if IL-6 mediates the exercise-induced increase in hepcidin.
Main Methods:
- Rodent model of exhaustive running exercise.
- Treatment with cyclosporin A (CsA) to inhibit IL-6 production.
- Measurement of plasma IL-6, hepatic IL-6 responsive genes (SOCS3, IL-6 receptor alpha) mRNA, and hepcidin mRNA levels.
Main Results:
- CsA treatment significantly reduced plasma IL-6 levels post-exercise.
- The rise in IL-6 responsive genes in the liver was blunted in CsA-treated rats.
- Hepcidin mRNA levels increased post-exercise, but significantly less in CsA-treated rats.
Conclusions:
- Plasma IL-6 is involved in the exercise-induced increase of hepcidin gene expression.
- These findings suggest a molecular mechanism linking exercise, IL-6, and hepcidin regulation.
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