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Fragile lifespan expansion by dietary mitohormesis in C. elegans
Diet-Triggered Mild Mitochondrial Stress May Slightly Extend Lifespan in C. elegans
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Abstract
High dietary glucose activates the mitochondrial unfolded protein response (UPRmt) to protect against lifespan reduction.
- Mitochondrial function is crucial for longevity, and imbalances in mitonuclear protein levels can trigger protective responses.
- Toxic compounds can activate the UPRmt, but sublethal doses may actually extend lifespan in simple organisms like C. elegans.
- Lifelong high glucose consumption decreases lifespan, while restricting glucose exposure to developmental stages can extend lifespan.
- The extension of lifespan from glucose exposure during development requires the activation of the UPRmt.
- Further mitochondrial stress in adult animals negates the lifespan extension benefits of prior UPRmt activation.
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