The researchers found that inhibiting GSK-3ß led to less defects in the axonal transport process and less neuronal cell death, while inhibiting ERK1 led to more transport problems and more cell death.

Researchers at Pennington Biomedical Research Center have revealed critical insights into how impaired mitochondrial dynamics and quality control mechanisms in skeletal muscle influence insulin sensitivity in patients with Type 2 Diabetes, or T2D. The study, titled "Deubiquitinating Enzymes Regulate Skeletal Muscle Mitochondrial Quality Control and Insulin Sensitivity in Patients with Type 2 Diabetes," was recently published in the Journal of Cachexia, Sarcopenia and Muscle.​

The research team, led by Pennington Biomedical Executive Director Dr. John Kirwan, focused on the significance of deubiquitinating enzymes, or DUBs, in regulating mitochondrial dynamics within skeletal muscle. Findings suggest that mitochondrial fragmentation can bypass defects in mitophagy, the process by which cells remove damaged mitochondria, to sustain skeletal muscle quality control in patients with T2D. This adaptation may help maintain mitochondrial function despite impaired mitophagy.​