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Reprogramming the mitochondrial-circadian energy code with incretins.

Enzo Nisoli1, Maurizio Ragni1, Chiara Ruocco1

  • 1Center for Study and Research on Obesity, Department of Medical Biotechnology and Translational Medicine, University of Milan, Milan 20129, Italy.

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Summary
This summary is machine-generated.

Obesity and aging impair metabolic flexibility by disrupting the mitochondrial-circadian energy code. Restoring this code through therapies like GLP-1 agonists may improve metabolic health and delay aging.

Keywords:
GLP-1 receptor agonistsGLP-1/GIP dual agonistscircadian rhythmsmetabolic flexibilitymitochondrial dysfunctionsenescence

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Area of Science:

  • Metabolic health
  • Aging research
  • Mitochondrial biology
  • Circadian rhythm research

Background:

  • Mitochondrial dysfunction, circadian disruption, and cellular senescence are key factors in metabolic inflexibility.
  • Obesity and aging share a common phenotype of impaired substrate switching and flattened energy rhythms due to a disrupted mitochondrial-circadian energy code.
  • Metabolic flexibility is a critical indicator of metabolic health and a potential therapeutic target.

Purpose of the Study:

  • To propose a unified framework for understanding obesity and aging as expressions of a disrupted mitochondrial-circadian energy code.
  • To highlight metabolic flexibility as a clinical index for therapeutic interventions.
  • To explore the potential of pharmacological and combination strategies to restore energy coordination and delay age-related metabolic decline.

Main Methods:

  • Conceptual framework integrating mitochondrial function, circadian rhythms, and cellular senescence.
  • Review of existing literature on obesity, aging, and metabolic flexibility.
  • Discussion of potential therapeutic targets including GLP-1 agonists and combination strategies (senolytics, mitophagy, chrono-entrainment).

Main Results:

  • Obesity and aging are characterized by impaired metabolic flexibility, stemming from a disrupted mitochondrial-circadian energy code.
  • GLP-1 and dual GLP-1/GIP agonists show potential to improve mitochondrial efficiency, circadian alignment, and reduce pro-senescent signaling.
  • Multi-pronged therapeutic strategies targeting specific nodes (e.g., senolytics, mitophagy) could reprogram energy coordination.

Conclusions:

  • Restoring the integrity of the mitochondrial-circadian energy code, evidenced by improved metabolic flexibility, should be a central goal in treating obesity and aging.
  • Pharmacological agents and combination therapies hold promise for enhancing metabolic health and mitigating age-related metabolic dysfunction.
  • Targeted interventions can reprogram systemic energy coordination, leading to more durable therapeutic responses and delayed aging.