The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance.
Level 5 - mechanism / opinion, no new human data
Preclinical in vitro and mouse model research without human clinical data.
PubMed 25738459 · doi:10.1016/j.cmet.2015.02.009
What was done
Researchers identified a short open reading frame within mitochondrial 12S rRNA encoding a 16-amino-acid peptide termed MOTS-c. They investigated its target tissue, cellular mechanism involving the folate cycle, de novo purine biosynthesis, and AMPK activation, and tested systemic MOTS-c treatment in mice with diet-induced obesity as well as age-dependent and high-fat-diet-induced insulin resistance.
What was found
The abstract reports no numerical values. It reports that MOTS-c primarily targets skeletal muscle, inhibits the folate cycle and de novo purine biosynthesis to activate AMPK, and that treatment in mice prevented diet-induced obesity as well as age-dependent and high-fat-diet-induced insulin resistance.
Why it matters
This study identifies a functional signaling peptide encoded in the mitochondrial genome that directly influences systemic metabolic regulation and insulin sensitivity.
Limits
The study is restricted entirely to cellular and mouse models, with no human in vivo data. The abstract provides no specific sample sizes, dosage details, effect magnitudes, or statistical confidence intervals.
Cited by
- supports MOTS-c peptide activates AMP-activated protein kinase (AMPK) to regulate energy metabolism.