Healthy aging can be promoted by enhanced metabolic fitness and physical capacity. Mitochondria are chief metabolic organelles with strong implications in aging.
The progressive loss of metabolic homeostasis is a hallmark of aging, which impedes parenchymal function and ultimately diminishes physical capacity.
Mitochondria not only produce the bulk of cellular energy, but also coordinate adaptive cellular homeostasis.
MOTS-c (mitochondrial ORF of the 12S rRNA type-c) is an MDP that promotes metabolic homeostasis, in part, via AMPK, and by directly regulating adaptive nuclear gene expression following nuclear translocation. MOTS-c expression is age-dependent and detected in multiple tissues, including skeletal muscle, and in circulation, thus it has been dubbed a “mitochondrial hormone or “mitokine”.
It had been observed in aging mice that systemic MOTS-c treatment reversed diet-induced obesity and diet- and age-dependent insulin resistance.
This is designed to work to induce the productions of mtDNA-encoded MOTS-c. (its naturally induced with exercise) In experimental subjects it was observed that MOTS-c treatment significantly improves physical performance regulates skeletal muscle metabolism and gene expression, and finally enhances adaptation to metabolic stress in C2C12 cells in an HSF1-dependent manner.
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