Sestrins are evolutionarily conserved mediators of exercise benefits
Myungjin Kim,
Alyson Sujkowski,
Sim Namkoong,
Bondong Gu,
Tyler Cobb,
Boyoung Kim,
Allison H. Kowalsky,
Chun-Seok Cho,
Ian Semple,
Seung-Hyun Ro,
Carol Davis,
Susan V. Brooks,
Michael Karin,
Robert J. Wessells () and
Jun Hee Lee ()
Additional contact information
Myungjin Kim: University of Michigan
Alyson Sujkowski: Wayne State University School of Medicine
Sim Namkoong: University of Michigan
Bondong Gu: University of Michigan
Tyler Cobb: Wayne State University School of Medicine
Boyoung Kim: University of Michigan
Allison H. Kowalsky: University of Michigan
Chun-Seok Cho: University of Michigan
Ian Semple: University of Michigan
Seung-Hyun Ro: University of Michigan
Carol Davis: University of Michigan
Susan V. Brooks: University of Michigan
Michael Karin: University of California San Diego
Robert J. Wessells: Wayne State University School of Medicine
Jun Hee Lee: University of Michigan
Nature Communications, 2020, vol. 11, issue 1, 1-14
Abstract:
Abstract Exercise is among the most effective interventions for age-associated mobility decline and metabolic dysregulation. Although long-term endurance exercise promotes insulin sensitivity and expands respiratory capacity, genetic components and pathways mediating the metabolic benefits of exercise have remained elusive. Here, we show that Sestrins, a family of evolutionarily conserved exercise-inducible proteins, are critical mediators of exercise benefits. In both fly and mouse models, genetic ablation of Sestrins prevents organisms from acquiring metabolic benefits of exercise and improving their endurance through training. Conversely, Sestrin upregulation mimics both molecular and physiological effects of exercise, suggesting that it could be a major effector of exercise metabolism. Among the various targets modulated by Sestrin in response to exercise, AKT and PGC1α are critical for the Sestrin effects in extending endurance. These results indicate that Sestrin is a key integrating factor that drives the benefits of chronic exercise to metabolism and physical endurance.
Date: 2020
References: Add references at CitEc
Citations:
Downloads: (external link)
https://www.nature.com/articles/s41467-019-13442-5 Abstract (text/html)
Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.
Export reference: BibTeX
RIS (EndNote, ProCite, RefMan)
HTML/Text
Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-019-13442-5
Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/
DOI: 10.1038/s41467-019-13442-5
Access Statistics for this article
Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie
More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().