Lu H, Tang S, Xue C et al. · International journal of molecular sciences · PMID 31109005
Study summary
Main finding
MOTS-c treatment improved cold tolerance and altered brown-fat thermogenic genes and white-fat browning. ERK inhibition disrupted some of these responses.
Cold-exposed mice and adipose thermogenesis measurements
How the study was set up
Experimental cold-exposure models examined MOTS-c-related responses in fat tissue, with ERK-pathway inhibition.
What the researchers measured
Cold tolerance, serum peptide levels, liver lipid handling, and brown- and white-fat thermogenic genes were measured.
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 reported mechanism concerns adaptation to cold in the experimental model. It is not a human weight-loss or cold-tolerance trial.
What this does not establish
Cold-stressed animal findings do not establish human fat loss, exercise performance, or benefit from administering MOTS-c.
Publication & source
Why this paper is included
The compound is a named subject of the publication title.
Publication indexing
Journal Article
Indexed subjects
Adaptation, Physiological · Adipose Tissue, Brown · Adipose Tissue, White · Animals · Cold-Shock Response · Disease Models, Animal · Gene Expression Regulation · Hypothermia · MAP Kinase Signaling System · Male · Mice · Peptides · Phosphorylation · Thermogenesis
Source checked
October 4, 2026. Years follow journal issues; online-first dates may differ.