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MOTS-c Peptide: Insights Into Metabolic and Mitochondrial Research

by | Aug 20, 2025 | MOTS-C, Research and Studies, ResearchOnly | 0 comments

MOTS-c: Mitochondrial-Derived Peptide Signals in Metabolic Research

Research-focused overview of MOTS-c biology and preclinical findings. For laboratory use only.

Research Use Only: The content below summarizes non-clinical findings and is not intended for human or veterinary use.

What is MOTS-c?

MOTS-c is a 16-amino-acid mitochondrial-derived peptide encoded within the 12S rRNA region. Under metabolic stress, it can translocate to the nucleus and influence nuclear gene expression—linking mitochondrial status to cellular stress responses and energy homeostasis. Scholarly reviews highlight putative roles across glucose handling, inflammation, aging biology, and stress adaptation in experimental systems.

Preclinical Highlights

Metabolic Homeostasis
In mice, MOTS-c prevented diet-induced obesity and insulin resistance, with signals through AMPK/glucose-transport pathways (preclinical).
PubMed ·
PMC
Exercise-Like Signaling
Described as an “exercise-mimetic” in experimental models with effects on insulin sensitivity and lipid metabolism.
PubMed
Stress & Aging Context
Reviews summarize nuclear retrograde signaling, potential anti-inflammatory effects, and age-linked changes in circulating levels (research context).
PubMed ·
PMC
Human Observations (Exploratory)
Small studies report exercise-associated, transient increases of MOTS-c in muscle/blood; clinical applications remain unestablished.
PMC

Mechanistic Snapshot (Experimental)

Axis Model Reported Effect
AMPK & Glucose Uptake Mouse & in-vitro ↑ AMPK signaling; ↑ GLUT4; improved insulin sensitivity (preclinical).
PubMed
Nuclear Translocation Cell stress models Stress-induced shift to nucleus influencing gene-expression programs.
PubMed
Exercise-Linked Signals Human/ex-vivo Exercise associated with transient increases in MOTS-c in muscle/blood (exploratory).
PMC


View MOTS-c 10 mg

Research Notes

  • Most data are preclinical (mice/cell). Clinical applications are not established.
  • Signals frequently converge on AMPK pathways and stress-response programs.
  • Reported human observations (e.g., exercise-linked changes) are exploratory and variable.
  • Interpretation depends on dose, route, timing, and model design in each study.

Sources

  1. Zheng Y, et al. MOTS-c: mitochondrial-derived peptide in aging-related disease research (review). Front Pharmacol. 2023.
    PubMed ·
    PMC
  2. Lee C, et al. MOTS-c promotes metabolic homeostasis and reduces obesity/insulin resistance in mice. Cell Metab. 2015.
    PubMed ·
    PMC
  3. Wan W, et al. MOTS-c, stress-response, metabolism, and aging—overview (review). J Transl Med. 2023.
    PMC

Disclaimer: For laboratory research use only. Not intended for human or veterinary consumption, medical, or diagnostic use.

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