How Cancer Cachexia Affects Muscle Protein Turnover in Mice
Author Information
Author(s): White James P., Baynes John W., Welle Stephen L., Kostek Matthew C., Matesic Lydia E., Sato Shuichi, Carson James A.
Primary Institution: Department of Exercise Science, University of South Carolina
Hypothesis
Protein synthesis would be reduced only during late stages of cachexia, while ATP dependent protein degradation would be primarily responsible for the initiation of muscle loss.
Conclusion
IL-6 receptor antibody treatment blocked cachexia progression through the suppression of muscle protein degradation, but did not rescue the suppression of muscle protein synthesis.
Supporting Evidence
- Muscle wasting occurs due to an imbalance in protein synthesis and degradation.
- IL-6 receptor antibody treatment prevented body weight loss in mice.
- Protein degradation increased significantly during the progression of cachexia.
- AMPK activity increased as cachexia progressed.
- Muscle IGF-1 mRNA expression decreased during the initiation of cachexia.
Takeaway
When mice with cancer start losing weight, their muscles stop making proteins as well as they should, which makes them weaker. A special treatment can help stop this muscle loss.
Methodology
The study involved ApcMin/+ mice categorized by body weight loss, measuring muscle protein synthesis and degradation, and administering IL-6 receptor antibodies.
Potential Biases
Potential bias in the interpretation of results due to the specific strain of mice used.
Limitations
The study was conducted on a specific mouse model, which may not fully represent human cancer cachexia.
Participant Demographics
Male ApcMin/+ mice aged 14 to 20 weeks.
Statistical Information
P-Value
0.001
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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