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Mitochondrial‑encoded 16‑mer peptide involved in metabolic regulation. Preclinical studies suggest improved insulin sensitivity, AMPK activation, and exercise‑like adaptations, with possible roles in healthy aging. Early human data are limited; translational relevance and dosing are still being defined.
Description
MOTS‑c (mitochondrial open reading frame of the 12S rRNA‑c) is a 16‑amino‑acid, mitochondrial‑derived peptide encoded within the 12S rRNA region of mitochondrial DNA. The peptide sequence is Met‑Arg‑Trp‑Gln‑Glu‑Met‑Gly‑Tyr‑Ile‑Phe‑Tyr‑Pro‑Arg‑Lys‑Leu‑Arg (MRWQEMGYIFYPRKLR). MOTS‑c functions as a metabolic regulator: it promotes insulin sensitivity and glucose uptake, activates AMPK signaling, and under metabolic stress can translocate to the nucleus to regulate gene expression.
Chemical Structure / Identifiers
| Property | Detail |
| Sequence | H‑Met‑Arg‑Trp‑Gln‑Glu‑Met‑Gly‑Tyr‑Ile‑Phe‑Tyr‑Pro‑Arg‑Lys‑Leu‑Arg‑OH (MRWQEMGYIFYPRKLR) |
| Molecular Formula | C101H152N28O22S2 (PubChem) |
| Molecular Weight | ≈ 2174.6 g/mol (PubChem/MedChemExpress) |
| CAS Number | 1627580‑64‑6 |
| PubChem CID | 146675088 (also listed as 155885767 in alternate entry) |
| Primary Pathways | AMPK activation; AICAR biosynthesis; retrograde mito‑nuclear signaling |
Primary Research Focus
• Metabolic homeostasis: improves insulin sensitivity and glucose handling; reduces diet‑induced obesity in mouse models.
• Skeletal muscle metabolism: enhances glucose uptake and exercise‑like adaptations; targets skeletal muscle as a key effector tissue.
• Stress response and gene regulation: translocates to the nucleus during metabolic stress to modulate nuclear genes linked to antioxidant and metabolic programs.
• Aging and chronic disease research: explored for roles in healthy aging, cardiometabolic disease, and inflammatory/fibrotic conditions.
Safety / Limitations
• Predominantly preclinical evidence (cell and animal studies); limited human data available.
• Not approved as a therapeutic; Research Use Only. Long‑term safety, dosing, and pharmacokinetics in humans remain under investigation.
• Reported mechanisms and benefits may be context‑dependent (nutritional status, stress, tissue type).
Key Publications / References
Cell Metabolism (2015): The mitochondrial‑derived peptide MOTS‑c promotes metabolic homeostasis and reduces obesity and insulin resistance. PubMed: https://pubmed.ncbi.nlm.nih.gov/25738459/ Cell Metab full text: https://www.cell.com/cell-metabolism/fulltext/S1550-4131%2815%2900061-3
Cell Metabolism (2018): The mitochondrial‑encoded peptide MOTS‑c translocates to the nucleus to regulate nuclear gene expression in response to metabolic stress. https://www.cell.com/cell-metabolism/fulltext/S1550-4131%2818%2930390-5
Frontiers in Endocrinology (2023) review: MOTS‑c as a promising mitochondrial‑derived peptide for metabolic regulation and aging. PubMed: https://pubmed.ncbi.nlm.nih.gov/36761202/ Full text: https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2023.1120533/full
BMC Translational Medicine (2023) review: MOTS‑c effects and mechanisms in energy metabolism, stress homeostasis, and aging. https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-023-03885-2
UniProtKB entry (human MOTS‑c; MT‑RNR1‑encoded): https://www.uniprot.org/uniprotkb/A0A0C5B5G6/entry
PubChem Compound Summary (MOTS‑c): https://pubchem.ncbi.nlm.nih.gov/compound/146675088 Alternate entry: https://pubchem.ncbi.nlm.nih.gov/compound/155885767
Reviews
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