Open AccessInterleukin-13 drives metabolic conditioning of muscle to endurance exercise
Author(s) -
Nelson H. Knudsen,
Kristopher J. Stanya,
Alexander L. Hyde,
Mayer M. Chalom,
Ryan Alexander,
Yae-Huei Liou,
Kyle A. Starost,
Matthew R. Gangl,
David Jacobi,
Sihao Liu,
Danesh H. Sopariwala,
Diogo FonsecaPereira,
Jun Li,
Frank B. Hu,
Wendy S. Garrett,
Vihang A. Narkar,
Eric A. Ortlund,
Jonathan H. Kim,
Chad M. Paton,
Jamie A. Cooper,
ChihHao Lee
Publication year - 2020
Publication title -
science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 12.556
H-Index - 1186
eISSN - 1095-9203
pISSN - 0036-8075
DOI - 10.1126/science.aat3987
Subject(s) - mediator , mitochondrial biogenesis , cytokine , inflammation , endurance training , endocrinology , biology , receptor , immunology , medicine , physical exercise , microbiology and biotechnology , mitochondrion
IL-13 hits the gym Interleukin-13 (IL-13) is a cytokine secreted by T cells, innate lymphoid cells (ILC2s), and granulocytes. It acts as a central mediator in allergy and antihelminth defense with various effects. Knudsenet al. report a distinct role for IL-13 in exercise and metabolism (see the Perspective by Correia and Ruas). Mice subjected to endurance training showed increases in circulating IL-13, which correlated with ILC2 expansion in the muscles. By contrast, exercise-induced increases in muscle fatty acid utilization and mitochondrial biogenesis were erased when mice lacked IL-13. Activation of signaling pathways downstream of the muscle IL-13 receptor was key to this effect. Intramuscular injection of adenoviral IL-13 could recapitulate exercise-induced metabolic reprogramming. This signaling pathway may have evolved to combat the metabolic stresses of parasite infection.Science , this issue p.eaat3987 ; see also p.470
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