| First Author | Knudsen NH | Year | 2020 |
| Journal | Science | Volume | 368 |
| Issue | 6490 | PubMed ID | 32355002 |
| Mgi Jnum | J:288122 | Mgi Id | MGI:6415660 |
| Doi | 10.1126/science.aat3987 | Citation | Knudsen NH, et al. (2020) Interleukin-13 drives metabolic conditioning of muscle to endurance exercise. Science 368(6490) |
| abstractText | 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-13Ralpha1 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. |
