MOTS-c
MOTS-c (Mitochondrial ORF of the Twelve-S rRNA-c) is a 16-amino-acid peptide encoded by mitochondrial DNA (mtDNA). In preclinical literature it has been investigated as a mitochondrial-derived signaling molecule ("mitokine") associated with cellular energy regulation, metabolic homeostasis, and stress adaptation. Since its description in 2015, MOTS-c has been reported to engage AMP-activated protein kinase (AMPK) pathways and to participate in mitonuclear communication under nutrient or energetic stress in cell and animal models.
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The information provided is for educational and informational purposes only and should not be interpreted as medical advice. All products described herein are intended strictly for laboratory and research use. They are not approved for human or veterinary administration, and should only be handled by qualified professionals in controlled research environments. Any clinical research must be conducted under the supervision and approval of an Institutional Review Board (IRB), and all preclinical studies must adhere to Institutional Animal Care and Use Committee (IACUC) guidelines in accordance with the Animal Welfare Act (AWA). Users are encouraged to conduct their own due diligence, referencing trusted scientific sources and verifying all information independently before making any purchasing or experimental decisions.
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MOTS-c
Overview
MOTS-c (Mitochondrial ORF of the Twelve-S rRNA-c) is a 16-amino-acid peptide encoded by mitochondrial DNA (mtDNA). In preclinical literature it has been investigated as a mitochondrial-derived signaling molecule (“mitokine”) associated with cellular energy regulation, metabolic homeostasis, and stress adaptation. Since its description in 2015, MOTS-c has been reported to engage AMP-activated protein kinase (AMPK) pathways and to participate in mitonuclear communication under nutrient or energetic stress in cell and animal models.
Mechanistic Insights
1. AMPK Engagement
- MOTS-c activates AMPK signaling in cell and rodent systems, increasing glucose uptake and mitochondrial respiration while down-modulating lipogenesis and inflammatory cues.
2. Glucose Transport Programs
- Skeletal-muscle and hepatic models reported enhanced GLUT4 translocation and improved insulin-signaling fidelity following MOTS-c exposure.
3. Nuclear Translocation Under Stress
- Under metabolic stress, MOTS-c translocates to the nucleus and regulates gene programs linked to metabolism and stress defense, consistent with mitonuclear signaling (Kim 2018).
4. Mitochondrial Biogenesis and Fatty-Acid Oxidation
- AMPK–PGC-1α pathway activation was associated with increased markers of mitochondrial biogenesis and β-oxidation, with reduced lipogenic signaling in preclinical models.
5. Inflammation and Stress Pathways
- Suppression of JNK/NF-κB activity was observed in cell and animal studies, aligning with lower pro-inflammatory signaling and improved oxidative-stress markers.
6. Hormetic Adaptation (Mitohormesis)
- As a mitokine, MOTS-c has been proposed to contribute to hormetic responses, enhancing cellular resilience to metabolic and oxidative stressors in controlled paradigms.
Key Research Findings / Observations
1. Metabolic Regulation & Insulin Sensitivity
- Rodent models of diet-induced obesity/insulin resistance demonstrated improved insulin signaling and glucose clearance with MOTS-c; up-regulated GLUT4 and attenuation of JNK/NF-κB–linked insulin resistance (Lee 2015; Lu 2022).
2. Fatty-Acid Oxidation & Mass Gain in HFD Models
- Increased β-oxidation markers and energy expenditure; decreased hepatic lipid accumulation and adipogenic signaling; high-fat-fed mice exhibited resistance to mass gain with more favorable lipid readouts (Du 2021).
3. Exercise-Related and Muscle Homeostasis
- “Exercise-mimetic” transcriptional signatures reported, improved mitochondrial efficiency, and reduced fatigue indices in murine models (Reynolds 2020).
4. Aging-Associated Metrics
- Endogenous MOTS-c declines with age; supplementation in aged mice associated with improved physical capacity and survival-related metrics (Reynolds 2020; Cobb 2016).
5. Neuroprotective Readouts (Preclinical)
- Murine aging models showed mitigation of neuroinflammation and preservation of neuronal mitochondrial function; Alzheimer’s-like pathology markers were reduced (Lu 2023).
6. Cardiovascular/Endothelial Indices
- Improved cardiac mitochondrial efficiency and maintenance of endothelial function under metabolic stress conditions (Yin & Lee 2023).
7. Cellular Stress Resistance Programs
- Up-regulated autophagy and antioxidant pathways (e.g., NRF2, FOXO3a) with improved adaptation to fasting, thermal, and nutrient stressors in experimental systems.
Research References
- Lee C. et al. (2015). Cell Metab 21:443–454.
- Reynolds J.C. et al. (2020). Nat Commun 11:1–11.
- Kim K.H. et al. (2018). Cell Metab 28:516–524.
- Lu H. et al. (2022). Metabolism 129:155135.
- Cobb L.J. et al. (2016). Aging (Albany NY) 8:796–809.
- Du C. et al. (2021). Metab Brain Dis 36:1919–1930.
- Lu H. et al. (2023). Front Aging Neurosci 15:1123987.
- Yin X., Lee C. (2023). Front Physiol 14:1186629.
Product Specifications
C₁₉₀H₂₉₄N₅₂O₅₄S
2178.3 g/mol
1643124-36-6
Mitochondrial-Derived Peptide MOTS-c; Mitochondrial ORF of the 12S rRNA-c
Lyophilized powder
Keep refrigerated upon reconstitution
Soluble in sterile water and 0.9% NaCl solution
Research-use only. All information summarizes preclinical and in-vitro studies and is not intended for diagnostic, therapeutic, or personal use.
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