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Deletion of skeletal muscle Akt1/2 causes osteosarcopenia and reduces lifespan in mice
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Deletion of skeletal muscle Akt1/2 causes osteosarcopenia and reduces lifespan in mice
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Journal Article
Deletion of skeletal muscle Akt1/2 causes osteosarcopenia and reduces lifespan in mice
2022
Overview
Aging is considered to be accelerated by insulin signaling in lower organisms, but it remained unclear whether this could hold true for mammals. Here we show that mice with skeletal muscle-specific double knockout of
Akt1
/
2
, key downstream molecules of insulin signaling, serve as a model of premature sarcopenia with insulin resistance. The knockout mice exhibit a progressive reduction in skeletal muscle mass, impairment of motor function and systemic insulin sensitivity. They also show osteopenia, and reduced lifespan largely due to death from debilitation on normal chow and death from tumor on high-fat diet. These phenotypes are almost reversed by additional knocking out of
Foxo1
/
4
, but only partially by additional knocking out of
Tsc2
to activate the mTOR pathway. Overall, our data suggest that, unlike in lower organisms, suppression of Akt activity in skeletal muscle of mammals associated with insulin resistance and aging could accelerate osteosarcopenia and consequently reduce lifespan.
Sasako et al. show that disruption of the insulin/IGF-1 signaling by suppressing Akt activity in mouse skeletal muscle can accelerate osteosarcopenia and shortens lifespan, which is reversed by inactivation of FoxOs rather than activation of mTOR, suggesting FoxOs as therapeutic targets.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 49/91
/ 64/60
/ 692/4017
/ Aging
/ Animals
/ Humanities and Social Sciences
/ Insulin
/ Insulin Resistance - genetics
/ Insulin-like growth factor I
/ Mammals
/ Mice
/ Muscle, Skeletal - metabolism
/ Muscles
/ Proto-Oncogene Proteins c-akt - metabolism
/ Science
/ TOR Serine-Threonine Kinases - metabolism
/ Tuberous Sclerosis Complex 2
/ Tumors
