| Autor: |
Mehl KA; Division of Applied Physiology, Dept. of Exercise Science, University of South Carolina, Columbia, SC 29208, USA., Davis JM, Berger FG, Carson JA |
| Jazyk: |
angličtina |
| Zdroj: |
Journal of applied physiology (Bethesda, Md. : 1985) [J Appl Physiol (1985)] 2005 Dec; Vol. 99 (6), pp. 2379-87. |
| DOI: |
10.1152/japplphysiol.00778.2005 |
| Abstrakt: |
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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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