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Research & insights

MOTS-c in the 2015 Cell Metabolism Paper: Cells, Mice and the Human Evidence Gap

By NHD Technical TeamPublished
Mitochondrial cell microscopy and preclinical research equipment
Article-specific editorial image.

The paper that introduced MOTS-c combined cell experiments with mouse metabolic models. It is an important discovery record, but the intervention findings were preclinical.

What the record shows

  • MOTS-c was described as a 16-amino-acid peptide encoded within mitochondrial 12S rRNA.
  • The authors linked cellular effects to folate/purine metabolism and AMPK activation.
  • Diet-induced obesity and insulin-resistance findings came from mice, not a controlled human treatment study.
Scientist reviewing mitochondrial membrane imaging and energy-metabolism data
Original editorial illustration of the research context. It is not a study figure, patient image, supplied-product photograph or representation of trial material.

Study record

The cell work used gene-expression and metabolomic analyses to connect MOTS-c with one-carbon metabolism, purine synthesis and AMPK signaling. These mechanistic results are conditional on the cells and exposure used.

DiscoveryMitochondrial short open reading frame in 12S rRNA
Peptide length16 amino acids
Experimental systemsCultured cells and mouse metabolic models
Human efficacy endpointNone

Results in context

In mice, the paper reported protection against age-dependent and high-fat-diet-associated insulin resistance and diet-induced obesity. Those are model-specific observations, not human outcome data.

Later human studies measuring endogenous circulating MOTS-c or exercise-related expression are observational or physiological evidence; they do not establish that administering synthetic MOTS-c produces benefit.

What this study cannot answer

Species, exposure route and experimental metabolic conditions limit translation.

The paper does not establish a clinical dose, long-term safety or catalog-lot equivalence.

Sources & editorial method

The editorial workflow starts with linked peer-reviewed papers, trial registries or regulatory records; extracts the population or model, endpoints, numerical results and limitations; and separates the studied intervention from catalog material. AI-assisted drafting was used to structure the first version. Claims, figures, evidence labels and limitations were checked against the linked records in the site editorial workflow. This is not independent peer review.

3 linked records are listed in the references below. Read the editorial and AI-assistance policy.

How to interpret this article

Source-checked on 2026-08-28. Null findings and study limitations are retained. This is not independent peer review, medical advice, a customer case, or validation of a catalog lot.

Research-use boundary: Catalog materials discussed on this website are for laboratory research, development and manufacturing use only, not for human or veterinary use. This content is not medical advice and does not provide administration instructions.

Primary records and authoritative sources

  1. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasisLee C, et al. Cell Metabolism. 2015. PMID 25738453.
  2. Review of mitochondrial-derived peptides in energy metabolismEvidence-context review; PMID 32776825.
  3. Certain Bulk Drug Substances That May Present Significant Safety RisksU.S. FDA. Current compounding safety-information page.
Research pathways

Continue with structured records

Move from this editorial analysis to the product identity, filtered evidence and controlled terminology behind it.

Editorial source check: NHD evidence editorial workflow · 2026-08-28