Metabolic adaptation of murine skeletal muscle to nicotinamide nucleotide transhydrogenase and to hypoxia

Summary

This thesis explores how a mitochondrial protein called NNT affects muscle function, especially when oxygen levels drop (hypoxia). NNT helps produce NADPH, which protects from oxidative damage. NNT is dysfunction in C57BL/6J, the widely used mouse model for biomedical research.
The research showed that in normal mice, short-term low oxygen (6 hours) triggers muscle breakdown and slows growth. But in mice with dysfunctional NNT, this response was weaker. These mice also had lower lipid utilization and higher stress hormone under normal conditions, suggesting NNT is key for muscle adaptation.
The work highlights how NNT dysfunction might make muscles more vulnerable to stress during development. Future studies could focus on older or female mice to see if age or sex changes these effects. Overall, this helps scientists better understand muscle metabolism and choose mouse models for human disease research.