MOTS-c
MOTS-c is a mitochondrial-derived peptide encoded within the mitochondrial 12S rRNA region. Research links it to cellular stress responses, metabolism, exercise biology, AMPK-related signaling, and aging, with a mix of mechanistic, animal, and human observational evidence.
What kind of evidence exists?
MOTS-c has genuine human physiology data, but most intervention claims still come from animal or cellular systems.
Endogenous MOTS-c is not the same question as administering MOTS-c.
Finding that circulating MOTS-c changes during exercise or metabolic challenges demonstrates physiology. It does not by itself establish safety, efficacy, or an appropriate intervention with externally supplied peptide.
Selected studies.
Selected sources are grouped by study type so model limitations remain visible.
Acute endurance exercise stimulates circulating levels of mitochondrial-derived peptides in humans
In randomized exercise conditions, circulating mitochondrial-derived peptides were measured before and after resistance or endurance exercise. MOTS-c showed a trend to increase after endurance exercise; the study examined endogenous physiology, not peptide treatment.
Lipids and insulin regulate mitochondrial-derived peptide (MOTS-c) in PCOS and healthy subjects
Metabolic-clamp experiments showed lipid- and insulin-associated changes in circulating MOTS-c in controls and subjects with PCOS.
The Effect of Chronic Endurance Exercise on Serum Levels of MOTS-c and Humanin in Professional Athletes
Serum MOTS-c and humanin were compared across non-athletes and professional endurance athletes, adding human observational context for chronic exercise exposure.
MOTS-c: A novel mitochondrial-derived peptide regulating muscle and fat metabolism
This review summarizes early evidence connecting MOTS-c with skeletal muscle, glucose metabolism, fat biology, exercise, and aging.
Mitochondria-derived peptide MOTS-c: effects and mechanisms related to stress, metabolism and aging
The review details stress-responsive nuclear translocation and the folate-AICAR-AMPK pathway while surveying metabolic, inflammatory, exercise, and aging-related research.
Primary sources.
Direct PubMed links are used wherever possible.