Study Reveals How Mitochondrial Damage in Muscle Fuels Diabetes Progression
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A new study has revealed critical insights into how impaired mitochondrial dynamics and quality control mechanisms in skeletal muscle influence insulin sensitivity in patients with Type 2 Diabetes. The findings are published in the Journal of Cachexia, Sarcopenia and Muscle.
The research team 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 Type 2 Diabetes.
This adaptation may help maintain mitochondrial function despite impaired mitophagy.
In other words, the study shows that people with Type 2 Diabetes have fewer healthy mitochondria, the parts of the cell that produce energy, because a certain protein - dynamin-related protein 1, or DRP1 - is working too much.
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