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Publication
Sestrins are evolutionarily conserved mediators of exercise benefits.
Authors Kim M, Sujkowski A, Namkoong S, Gu B, Cobb T, Kim B, Kowalsky AH, Cho CS, Semple
I, Ro SH, Davis C, Brooks SV, Karin M, Wessells RJ, Lee JH
Submitted By Submitted Externally on 3/31/2020
Status Published
Journal Nature communications
Year 2020
Date Published 1/1/2020
Volume : Pages 11 : 190
PubMed Reference 31929512
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 PGC1a 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.





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