Muscle atrophy attenuation by N-terminal peptide for PIF receptor
Author Information
Author(s): Mirza K A, Wyke S M, Tisdale M J
Primary Institution: Nutritional Biomedicine, School of Life and Health Sciences, Aston University, Birmingham, UK
Hypothesis
Can peptides derived from the N-terminal amino acids of the PIF receptor neutralize the action of proteolysis-inducing factor (PIF) in muscle atrophy?
Conclusion
The peptides may be too hydrophilic to be used as therapeutic agents, but confirm the importance of the receptor in the action of PIF on muscle protein degradation.
Supporting Evidence
- The D- and L-forms of the peptide attenuated PIF-induced protein degradation in vitro.
- In vivo studies showed a tendency to increase lean body mass with the D-peptide.
- The study reports a new method for the preparation of PIF from the MAC16 tumor.
Takeaway
This study looked at how certain peptides can help prevent muscle loss in cancer patients. They found that while the peptides worked in the lab, they didn't help much in real mice.
Methodology
The study involved in vitro tests on murine myotubes and in vivo tests on mice with the MAC16 tumor, using D- and L-forms of a 20mer peptide derived from the PIF receptor.
Limitations
The peptides were ineffective in significantly reducing weight loss in vivo, possibly due to their hydrophilic nature leading to rapid excretion.
Participant Demographics
Male NMRI mice bearing the cachexia-inducing MAC16 tumor.
Statistical Information
P-Value
0.09
Statistical Significance
p=0.09
Digital Object Identifier (DOI)
Want to read the original?
Access the complete publication on the publisher's website