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The Effect of Treadmill Exercise on the Regulation of Protein Synthesis during IL‐6 Induced Cancer Cachexia
Author(s) -
Puppa Melissa,
White James,
Sato Shu,
Carson James
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1149.2
Subject(s) - cachexia , skeletal muscle , pi3k/akt/mtor pathway , endocrinology , medicine , phosphorylation , protein kinase b , treadmill , myofibril , signal transduction , chemistry , cancer , biochemistry
Cachexia is associated with the loss of skeletal muscle mass and a reduction in myofibrillar protein synthesis related to the suppression of the IGF‐1/mTOR signaling pathway. The purpose of this study was to determine if treadmill exercise training could offset IL‐6 over‐expression induced suppression of IGF‐1/mTOR signaling pathway. ApcMin/+ mice, an IL‐6 dependent model of colon caner cachexia, were trained on a treadmill 6d/wk 1h/d at 18m/min starting at 6wk of age. Between 12–14wks of age mice were electroporated with either an IL‐6 overexpression (IL6+) or control (CON) vector. Muscle IGF‐1 mRNA was reduced 50% by IL6+, while exercise increased muscle IGF‐1 mRNA 1.3 fold regardless of IL‐6 overexpression. Phosphorylation of mTOR(S2448), p70(T389), and 4EBP‐1(S65) were decreased 50% by IL6+. Exercise was able to attenuate the decrease in mTOR, p‐70, and 4EBP‐1 phosphorylation independent of changes in p‐AKT. These data show that treadmill exercise training can prevent IL‐6 induced skeletal muscle loss by attenuating the suppression of IGF‐1/mTOR signaling in skeletal muscle. Funded by RO1CA121249‐01