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Reprogramming the mitochondrial–circadian energy code with incretins
Changing the body's daily energy cycle through incretin hormones
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Abstract
Mitochondrial dysfunction, circadian disruption, and senescent cell accumulation are associated with impaired metabolic flexibility, a common feature of obesity and aging.
- Obesity is framed as a nutrient-driven expression of disrupted mitochondrial and circadian energy regulation.
- Aging is viewed as a time-driven expression of similar disruptions.
- Impaired substrate switching and flattened energy rhythms are shared consequences of these disruptions.
- Restoring mitochondrial-circadian code integrity may enhance metabolic flexibility, potentially guiding therapeutic approaches.
- GLP-1 and dual GLP-1/GIP agonists could improve mitochondrial efficiency and support circadian alignment.
- Node-specific and combination strategies may help reprogram energy coordination and delay age-related metabolic decline.
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