MOTS-c (Mitochondrial Open Reading Frame of the 12S rRNA-c) is a mitochondria-derived peptide encoded within the mitochondrial genome. Discovered in 2015 by Dr. Changhan David Lee at USC, it represents a paradigm shift in understanding mitochondrial-nuclear communication. MOTS-c is the first mitochondrial-encoded peptide shown to regulate nuclear gene expression, positioning it at the frontier of longevity and metabolic research.

MOTS-c activates AMPK (5' AMP-activated protein kinase), a master metabolic regulator. It translocates to the nucleus under metabolic stress where it regulates adaptive nuclear gene expression via an AMPK-dependent mechanism. Research shows it enhances glucose uptake, increases fatty acid oxidation, and improves mitochondrial function. It has been described as an 'exercise mimetic' due to its ability to activate many of the same metabolic pathways as physical exercise.

• Prevented age-dependent and diet-induced insulin resistance in mouse models (Lee et al., 2015)
• Improved exercise capacity and physical performance in aged mice
• Endogenous MOTS-c levels correlate with metabolic health and decline with age in human studies
• Regulated skeletal muscle metabolism through AMPK activation
• Demonstrated protective effects against metabolic stress in cellular models

1. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis
   Cell Metab, 2015
2. MOTS-c is an exercise-induced mitochondrial-encoded regulator
   Cell Metab, 2020
3. Mitochondrial-derived peptides in aging and age-related diseases
   Ageing Res Rev, 2021

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