論文

査読有り 国際誌
2019年

Aging- and obesity-related peri-muscular adipose tissue accelerates muscle atrophy.

PloS one
  • Shunshun Zhu
  • ,
  • Zhe Tian
  • ,
  • Daisuke Torigoe
  • ,
  • Jiabin Zhao
  • ,
  • Peiyu Xie
  • ,
  • Taichi Sugizaki
  • ,
  • Michio Sato
  • ,
  • Haruki Horiguchi
  • ,
  • Kazutoyo Terada
  • ,
  • Tsuyoshi Kadomatsu
  • ,
  • Keishi Miyata
  • ,
  • Yuichi Oike

14
8
開始ページ
e0221366
終了ページ
記述言語
英語
掲載種別
DOI
10.1371/journal.pone.0221366

Sarcopenia due to loss of skeletal muscle mass and strength leads to physical inactivity and decreased quality of life. The number of individuals with sarcopenia is rapidly increasing as the number of older people increases worldwide, making this condition a medical and social problem. Some patients with sarcopenia exhibit accumulation of peri-muscular adipose tissue (PMAT) as ectopic fat deposition surrounding atrophied muscle. However, an association of PMAT with muscle atrophy has not been demonstrated. Here, we show that PMAT is associated with muscle atrophy in aged mice and that atrophy severity increases in parallel with cumulative doses of PMAT. We observed severe muscle atrophy in two different obese model mice harboring significant PMAT relative to respective control non-obese mice. We also report that denervation-induced muscle atrophy was accelerated in non-obese young mice transplanted around skeletal muscle with obese adipose tissue relative to controls transplanted with non-obese adipose tissue. Notably, transplantation of obese adipose tissue into peri-muscular regions increased nuclear translocation of FoxO transcription factors and upregulated expression FoxO targets associated with proteolysis (Atrogin1 and MuRF1) and cellular senescence (p19 and p21) in muscle. Conversely, in obese mice, PMAT removal attenuated denervation-induced muscle atrophy and suppressed upregulation of genes related to proteolysis and cellular senescence in muscle. We conclude that PMAT accumulation accelerates age- and obesity-induced muscle atrophy by increasing proteolysis and cellular senescence in muscle.

リンク情報
DOI
https://doi.org/10.1371/journal.pone.0221366
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/31442231
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6707561
ID情報
  • DOI : 10.1371/journal.pone.0221366
  • PubMed ID : 31442231
  • PubMed Central 記事ID : PMC6707561

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