MOTS-C
10mgVolume Pricing
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About MOTS-C
MOTS-c (Mitochondrial Open Reading Frame of the 12S rRNA Type-c) is a 16-amino acid mitochondrial-derived peptide that acts as a metabolic regulator and exercise mimetic. Research demonstrates its role in activating AMPK, enhancing insulin sensitivity, improving glucose metabolism, and supporting skeletal muscle homeostasis. Endogenous MOTS-c levels decline with age, making it a subject of significant interest in longevity and metabolic research.
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Published Study Findings on MOTS-C
Detailed Research & Citations
In-depth findings from peer-reviewed preclinical and clinical studies
MOTS-c (Mitochondrial Open Reading Frame of the 12S rRNA Type-c) is a 16-amino acid mitochondrial-derived peptide (MDP) encoded within the mitochondrial 12S rRNA gene, identified as an endogenous metabolic regulator and exercise mimetic with significant roles in energy homeostasis and aging.
AMPK Activation & Glucose Metabolism
MOTS-c activates the AMP-activated protein kinase (AMPK) pathway in skeletal muscle, enhancing glucose uptake, metabolic flexibility, and insulin sensitivity. In mouse models, MOTS-c treatment prevented diet-induced obesity and improved glucose homeostasis.
Cell Metabolism (2015)Obesity & Insulin Resistance Prevention
Administration of MOTS-c to mice on a high-fat diet significantly reduced weight gain and improved insulin resistance. The peptide targeted skeletal muscle metabolism, promoting fatty acid oxidation and reducing lipid accumulation.
Cell Metabolism (2015)Exercise-Induced Metabolic Regulator
MOTS-c levels increase in skeletal muscle and plasma during exercise. Exogenous MOTS-c administration in aged mice improved physical capacity, enhanced exercise endurance, and activated exercise-sensitive signaling intermediates including AMPK, SIRT1, and PGC-1α.
Nature Communications (2021)Skeletal Muscle Homeostasis
MOTS-c regulates skeletal muscle metabolism by promoting mitochondrial biogenesis and improving fuel utilization. In aged mice, MOTS-c treatment restored muscle function and physical performance to levels comparable to younger animals.
Nature Communications (2021)Age-Related Decline Reversal
Endogenous MOTS-c levels in skeletal muscle and circulation decline significantly with age. Replenishment of MOTS-c in aged mice reversed age-dependent physical decline and restored insulin sensitivity, suggesting a role in mitigating age-related metabolic dysfunction.
Nature Communications (2021)Mitochondrial Function in Cellular Senescence
MOTS-c modulates mitochondrial function during cellular senescence, influencing mitochondrial membrane potential and bioenergetics. This mitochondrial-to-nuclear signaling (retrograde signaling) positions MOTS-c as a key mediator in the biology of aging.
Aging (2018)Inflammatory Pathway Modulation
MOTS-c exerts anti-inflammatory effects through AMPK-dependent inhibition of inflammatory signaling cascades including MAP kinase/c-Fos pathways. Preclinical models of sepsis and acute lung injury showed reduced inflammatory markers with MOTS-c treatment.
Frontiers in Physiology (2022)Mitochondrial-Nuclear Communication
Under metabolic stress, MOTS-c translocates from the cytoplasm to the nucleus where it regulates adaptive gene expression, including genes involved in antioxidant defense and metabolic adaptation — a novel retrograde signaling mechanism.
Frontiers in Physiology (2022)View All 4 Sources
- The Mitochondrial-Derived Peptide MOTS-c Promotes Metabolic Homeostasis and Reduces Obesity and Insulin Resistance
- MOTS-c is an Exercise-Induced Mitochondrial-Encoded Regulator of Age-Dependent Physical Decline and Muscle Homeostasis
- Mitochondrial Peptides Modulate Mitochondrial Function During Cellular Senescence
- MOTS-c: A Novel Mitochondrial-Derived Peptide — From Discovery to Clinical Applications
All findings above are sourced from peer-reviewed journals for educational reference. This product is for research purposes only — not for human consumption. Preclinical results may not translate to human outcomes.
Chemical Identity
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