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Mots-C

Mitochondrial open reading frame of the 12S rRNA-c, MT-RNR1, Mitochondrial-derived peptide MOTS-c

Quick Stats
Studies 137
Trials 5
Score 3
2015 pubmed 52 citations

A mitochondrially encoded hormone ameliorates obesity and insulin resistance.

Zarse. Kim K; Ristow. Michael M

Key Findings

  • MOTS‑c boosts production of AICAR, an AMP analog
  • Increased AICAR activates AMPK, a key metabolic regulator
  • Animal models showed reduced obesity and better insulin sensitivity after MOTS‑c treatment

Practical Outcomes

  • For now, MOTS‑c is a promising research target rather than a ready‑to‑use supplement. Biohackers should watch for upcoming human trials and dosing studies before trying it, and consider focusing on established AMPK‑activating strategies (like exercise, fasting, or AICAR‑mimetic compounds) in the meantime.

Summary

MOTS‑c is a tiny protein made by mitochondria that helps the body make more AICAR, a natural compound that turns on the AMPK pathway, which is known to improve metabolism. In animal studies it reduced obesity and insulin resistance, hinting it could help prevent type‑2 diabetes and slow aging, but human data and dosing guidelines are still missing.

Abstract

MOTS-c, a mitochondrially encoded open reading frame-derived peptide recently discovered by Lee et al. 2015 (this issue of Cell Metabolism) promotes biosynthesis of an endogenous AMP analog, AICAR. As AICAR activates AMPK, the discovery of MOTS-c offers an unexpected therapeutic option to be exploited toward the prevention of type 2 diabetes and delaying of the aging processes.

Study Information

Provider

pubmed

Year

2015

Date

2015-03-03T00:00:00.000Z

DOI

10.1016/j.cmet.2015.02.013

Citations

52

References

8