The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance.
Lee C, Zeng J, Drew BG et al. · Cell metabolism · PMID 25738459
Study summary
Main finding
The study identified MOTS-c and linked its cellular activity to AMPK signaling. Treated mice showed changes in insulin sensitivity and diet-related metabolic outcomes.
The researchers identified MOTS-c and investigated its activity in cell experiments and mouse models of diet- and age-related metabolic changes.
What the researchers measured
Cellular metabolic pathways, AMPK signaling, insulin sensitivity, and diet-related metabolic outcomes in mice. AMPK is a protein involved in regulating cellular energy use.
How to read this evidence
Researchers studied cells, isolated tissue, or animals. These experiments can help explain a mechanism, but do not establish benefits or safety in people. Human cells grown in a laboratory also belong in this category.
Results in context
The paper connects a possible cellular mechanism with metabolic observations in mice. It does not test administered MOTS-c as a treatment in people; the origin of the peptide in mitochondria does not change that evidence boundary.
What this does not establish
Mouse treatment outcomes and cellular mechanisms do not demonstrate therapeutic benefit from MOTS-c administration in humans.
Publication & source
Why this paper is included
The compound is a named subject of the publication title.
Publication indexing
Journal Article · Research Support, N.I.H., Extramural · Research Support, Non-U.S. Gov't