In brief
Mitochondria carry their own small genome, and one short reading frame in it, humanin, was already known to encode a signalling peptide. This paper reports a second: a 16-residue peptide encoded within the mitochondrial 12S ribosomal RNA gene, named MOTS-c. Its main target organ appears to be skeletal muscle, where it inhibits the folate cycle and the purine synthesis tethered to it, which activates the energy sensor AMPK. In mice, MOTS-c treatment prevented the insulin resistance that develops with age and with a high-fat diet, and prevented diet-induced obesity. The authors suggest that mitochondria may regulate whole-body metabolism through peptides encoded in their own DNA.
Study design
Discovery paper: identification of a mitochondrial open reading frame, cell signalling work, and treatment of mice on normal and high-fat diets.
What it does not show
A first description in mice and cells. The metabolic results are in animals, and human evidence for MOTS-c is limited to subsequent small studies not cited here.
Results in rodents or other animals often do not reproduce in people. Species, route, dose and the injury or disease model all shape the outcome, and an effect in a rat is a reason for further study, not a conclusion.
Where this paper is cited
- MOTS-c — MOTS-c, encoded in mitochondrial DNA, acted on skeletal muscle via AMPK and prevented diet-induced obesity and insulin resistance in mice.
Further reading
- Research library: every paper cited on this site, by compound and by study type.
- Cognitive and longevity peptide comparison
- How to read a certificate of analysis
- Lyophilised peptide storage and stability
How this page was made: the citation was retrieved from PubMed by PMID and checked against the title on the product page; the summary was written from the paper's abstract and reports only what the abstract reports. Read the paper itself before relying on any figure here.