Interleukin-13 drives metabolic conditioning of muscle to endurance exercise.

Autor: Knudsen NH; Department of Molecular Metabolism, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA., Stanya KJ; Department of Molecular Metabolism, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA., Hyde AL; Department of Molecular Metabolism, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA., Chalom MM; Department of Molecular Metabolism, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA., Alexander RK; Department of Molecular Metabolism, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA., Liou YH; Department of Molecular Metabolism, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA., Starost KA; Department of Molecular Metabolism, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA., Gangl MR; Department of Molecular Metabolism, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA., Jacobi D; Department of Molecular Metabolism, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA., Liu S; Department of Molecular Metabolism, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA., Sopariwala DH; Metabolic and Degenerative Diseases, Institute of Molecular Medicine, University of Texas McGovern Medical School, Houston, TX 77030, USA., Fonseca-Pereira D; Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA., Li J; Department of Nutrition and Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA., Hu FB; Department of Nutrition and Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA.; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA., Garrett WS; Department of Molecular Metabolism, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA.; Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA., Narkar VA; Metabolic and Degenerative Diseases, Institute of Molecular Medicine, University of Texas McGovern Medical School, Houston, TX 77030, USA., Ortlund EA; Emory University School of Medicine, Atlanta, GA 30322, USA., Kim JH; Emory University School of Medicine, Atlanta, GA 30322, USA.; Emory Clinical Cardiovascular Research Institute, Atlanta, GA 30322, USA., Paton CM; Department of Foods and Nutrition, University of Georgia, Athens, GA 30602, USA., Cooper JA; Department of Foods and Nutrition, University of Georgia, Athens, GA 30602, USA., Lee CH; Department of Molecular Metabolism, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA. clee@hsph.harvard.edu.
Jazyk: angličtina
Zdroj: Science (New York, N.Y.) [Science] 2020 May 01; Vol. 368 (6490). Date of Electronic Publication: 2020 Apr 30.
DOI: 10.1126/science.aat3987
Abstrakt: Repeated bouts of exercise condition muscle mitochondria to meet increased energy demand-an adaptive response associated with improved metabolic fitness. We found that the type 2 cytokine interleukin-13 (IL-13) is induced in exercising muscle, where it orchestrates metabolic reprogramming that preserves glycogen in favor of fatty acid oxidation and mitochondrial respiration. Exercise training-mediated mitochondrial biogenesis, running endurance, and beneficial glycemic effects were lost in Il13 -/- mice. By contrast, enhanced muscle IL-13 signaling was sufficient to increase running distance, glucose tolerance, and mitochondrial activity similar to the effects of exercise training. In muscle, IL-13 acts through both its receptor IL-13Rα1 and the transcription factor Stat3. The genetic ablation of either of these downstream effectors reduced running capacity in mice. Thus, coordinated immunological and physiological responses mediate exercise-elicited metabolic adaptations that maximize muscle fuel economy.
(Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.)
Databáze: MEDLINE
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