Interleukin-13 drives metabolic conditioning of muscle to endurance exercise

Nelson H. Knudsen(Harvard University), Kristopher J. Stanya(Harvard University), Alexander L. Hyde(Harvard University), Mayer M. Chalom(Harvard University), Ryan Alexander(Harvard University), Yae-Huei Liou(Harvard University), Kyle A. Starost(Harvard University), Matthew R. Gangl(Harvard University), David Jacobi(Harvard University), Sihao Liu(Harvard University), Danesh H. Sopariwala(The University of Texas Health Science Center), Diogo Fonseca‐Pereira(Harvard University), Jun Li(Harvard University), Frank B. Hu(Brigham and Women's Hospital), Wendy S. Garrett(Harvard University), Vihang A. Narkar(The University of Texas Health Science Center), Eric A. Ortlund(Emory University), Jonathan H. Kim(Emory Healthcare), Chad M. Paton(University of Georgia), Jamie A. Cooper(University of Georgia), Chih‐Hao Lee(Harvard University)
Science
April 30, 2020
10.1126/science.aat3987
Cited by 131Open Access
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Abstract

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. Knudsen et 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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