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Myofiber degeneration/regeneration is
induced in the cachectic ApcMin/+ mouse.
Mehl KA, Davis JM, Berger FG, Carson JA.
Division of Applied Physiology, Dept. of Exercise Science, University
of South Carolina, Columbia, SC 29208, USA.
Cachexia
is characterized as an inflammatory state induced by the cancer
environment, which is accompanied by the loss of muscle and fat mass.
Well-investigated mechanisms of cachexia include the suppression of
myofiber protein synthesis and the induction of the protein
degradation. However, it is not well characterized whether chronic
inflammation during cachexia induces myofiber degeneration, which
contributes to muscle mass loss and decreased functional capacity. The
purpose of this study was to determine whether Apc(Min/+) mice, which
demonstrate a chronic systemic inflammatory state due to an intestinal
tumor burden, undergo cachexia and whether the myofibers exhibit signs
of degeneration and/or regeneration. Six-month-old female Apc(Min/+)
body weight decreased 21% compared with C57BL/6 mice and was not the
result of blunted growth. Apc(Min/+) gastrocnemius muscle was reduced
45%, and soleus mean fiber cross-sectional area decreased 24% vs.
C57BL/6 mice. Soleus muscle morphology demonstrated pathology of
myofibers undergoing degeneration and/or regeneration. These data
demonstrate that the Apc(Min/+) mouse becomes cachectic by 6 mo of age
and that skeletal muscle degeneration and regeneration may be related
to the muscle loss.
PMID: 16288100 [PubMed - in process]
PubMed
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