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DOI | 10.1126/science.aat3987 |
Interleukin-13 drives metabolic conditioning of muscle to endurance exercise | |
Knudsen N.H.; Stanya K.J.; Hyde A.L.; Chalom M.M.; Alexander R.K.; Liou Y.-H.; Starost K.A.; Gangl M.R.; Jacobi D.; Liu S.; Sopariwala D.H.; Fonseca-Pereira D.; Li J.; Hu F.B.; Garrett W.S.; Narkar V.A.; Ortlund E.A.; Kim J.H.; Paton C.M.; Cooper J.A.; Lee C.-H. | |
发表日期 | 2020 |
ISSN | 0036-8075 |
卷号 | 368期号:6490 |
英文摘要 | 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-13Ra1 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. © 2020 American Association for the Advancement of Science. All rights reserved. |
关键词 | glucoseinterleukin 13interleukin 13 receptor alpha1interleukin 6STAT3 proteinfatty acidglycogeninterleukin 13interleukin 13 receptor alpha1STAT3 proteinStat3 protein, mousefatty acidmetabolismmuscleoxidationphysiological responseproteinrespirationaerobic exerciseanimal cellanimal experimentanimal tissueArticleC2C12 cell linecohort analysiscontrolled studyendurance trainingenergy metabolismex vivo studyexercise intensityfemalegastrocnemius muscleglucose tolerancehumanin vitro studymalemitochondrial biogenesismitochondrial dynamicsmitochondrial respirationmousemuscle metabolismmuscle mitochondrionnonhumanobesitypriority journalprotein blood levelprotein expressionrunningsedentary lifestylesignal transductiontreadmill exerciseadaptationanimalbloodC57BL mousecell lineendurancegeneticsglucose blood levelimmunologyknockout mousemetabolismmyoblastoxidation reduction reactionskeletal muscleMusAdaptation, PhysiologicalAnimalsBlood GlucoseCell LineFatty AcidsFemaleGlycogenHumansInterleukin-13Interleukin-13 Receptor alpha1 SubunitMaleMiceMice, Inbred C57BLMice, KnockoutMitochondria, MuscleMuscle, SkeletalMyoblastsOxidation-ReductionPhysical Conditioning, AnimalPhysical EnduranceRunningSTAT3 Transcription Factor |
语种 | 英语 |
来源机构 | Science |
文献类型 | 期刊论文 |
条目标识符 | http://gcip.llas.ac.cn/handle/2XKMVOVA/133532 |
推荐引用方式 GB/T 7714 | Knudsen N.H.,Stanya K.J.,Hyde A.L.,et al. Interleukin-13 drives metabolic conditioning of muscle to endurance exercise[J]. Science,2020,368(6490). |
APA | Knudsen N.H..,Stanya K.J..,Hyde A.L..,Chalom M.M..,Alexander R.K..,...&Lee C.-H..(2020).Interleukin-13 drives metabolic conditioning of muscle to endurance exercise.,368(6490). |
MLA | Knudsen N.H.,et al."Interleukin-13 drives metabolic conditioning of muscle to endurance exercise".368.6490(2020). |
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