Study record

The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance

Lee C, Zeng J, Drew BG et al. · Cell Metab · 2015

AnimalMOTS-c administeredEvidence tier CAlso: Cell study (in vitro)

What this study reported

Identified a short open reading frame in the mitochondrial 12S rRNA encoding a 16-amino-acid peptide, MOTS-c. In cells, MOTS-c was reported to inhibit the folate cycle and tethered de novo purine biosynthesis, leading to AMPK activation, with skeletal muscle as the apparent primary target. In mice, MOTS-c treatment was associated with less age-dependent and high-fat-diet-induced insulin resistance and less diet-induced obesity.

Limitations

Sample sizes, sex balance and administration details are not given in the abstract; findings come from mouse models and cell lines only.

Study record

Annotated fields for this study
Study modelAnimal study (in vivo)
Substance studiedMOTS-c administeredSynthetic MOTS-c was given to cells, animals or people.
Speciesmouse
System studiedAged mice and high-fat-diet-fed mice; cultured cell lines (HEK293, HeLa per MeSH)
PopulationNot reported
DesignDiscovery study with controlled animal experiments and cell culture experiments
Sample size as reportedNot reported
Control groupuntreated aged and high-fat-diet mice (comparison implied; details not reported in abstract)
Route (data field only)Not reported
Endpoints measuredinsulin sensitivity; diet-induced weight gain; folate cycle and de novo purine biosynthesis; AMPK activation
Pathways measuredFolate cycle / purines / AICAR · AMPK signalling · Insulin & glucose handling
Research areasMetabolic · Skeletal muscle · Aging · Mitochondrial biology
Evidence tierC — Animal in vivo
Publication typesJournal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't

Appraisal

Each dimension is recorded separately and never combined into a single score. A study can be well controlled and still tell you little about people.

Relevance to MOTS-c
Direct
Model applicability
Mammalian
Sample size
Not reported
Controls
Appropriate
Outcome validity
Surrogate
Support for its own conclusion
Moderate

Provenance

  • Bibliographic fields retrieved from PubMed E-utilities efetch (title, journal, date, authors, DOI) on 2026-11-11.
  • Annotated from the published abstract.
  • Editorial review: approved (2026-11-11).
  • Classification follows the site methodology; the record describes the study, not what MOTS-c does in people.