
Cellular / Energy
MOTS-C
CโโโHโโโNโโOโโ
Key Research Findings
- First mitochondria-encoded peptide found to translocate to the nucleus in response to metabolic stress.
- Reduces obesity and insulin resistance in diet-induced obese mice without caloric restriction.
- Plasma MOTS-C levels decline with age and are correlated with metabolic health markers in human studies.
- Exercise increases circulating MOTS-C, suggesting it mediates some systemic benefits of physical activity.
Overview
MOTS-C is a mitochondria-derived peptide (MDP) encoded within the mitochondrial 12S rRNA gene. It is unique in that it is generated by the mitochondria themselves and translocated to the nucleus to act as a metabolic regulator, representing a novel category of inter-organelle signalling peptide.
Mechanism of Action
MOTS-C activates AMPK (AMP-activated protein kinase), a master energy-sensing enzyme that promotes glucose uptake, fatty acid oxidation, and mitochondrial biogenesis. Under metabolic stress it translocates to the nucleus and regulates gene expression involved in the folate cycle and one-carbon metabolism.
Research Effects
Metabolic Regulation
Moderate ResearchAMPK activation by MOTS-C promotes improved glucose homeostasis and lipid metabolism in multiple animal models.
Insulin Sensitivity
Moderate ResearchStudies in obese rodent models show significant improvement in insulin resistance following MOTS-C administration.
Muscle Function
Moderate ResearchResearch demonstrates enhanced endurance and preservation of muscle mass in aged and metabolically stressed animal models.
Anti-aging
Preliminary ResearchEarly data correlating MOTS-C with longevity phenotypes in human populations suggests anti-aging relevance, pending direct investigation.
Research Purposes Only โ All information on this page is provided for scientific research purposes only. This product is not intended for human consumption, diagnosis, treatment, or prevention of any disease.
Quick Facts
Research Status Key
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