Mitochondrial-encoded MOTS-c prevents pancreatic islet destruction in autoimmune diabetes.
Kong BS, Min SH, Lee C et al. · Cell reports · PMID 34320351
A published correction is linked in the original PubMed record.
Study summary
Main finding
The study reported islet protection in mice, lower endogenous MOTS-c in people with type 1 diabetes, and altered T-cell activation in experimental assays.
NOD mice, human type 1 diabetes observations, and T-cell assays
How the study was set up
Autoimmune-diabetes mouse models and transferred mouse T cells were studied alongside human serum and isolated human T-cell analyses.
What the researchers measured
Blood glucose, islet immune-cell infiltration, diabetes incidence, T-cell metabolism, and activation-related signaling were measured.
How to read this evidence
This paper combines observations in people with laboratory or animal experiments. Measuring a naturally occurring peptide in people is different from testing peptide administration.
Results in context
Human samples contributed biomarker and cell findings, while disease-prevention experiments were in mice. The paper does not test MOTS-c administration as a diabetes treatment in patients.
What this does not establish
People were not treated with MOTS-c in a clinical trial. Observations and ex vivo assays do not establish a diabetes therapy.
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
Indexed subjects
Animals · Female · Humans · Male · Adoptive Transfer · CD4-Positive T-Lymphocytes · Cell Differentiation · Diabetes Mellitus, Type 1 · Glycolysis · HEK293 Cells · Islets of Langerhans · Jurkat Cells · Mechanistic Target of Rapamycin Complex 1 · Mice, Inbred NOD · Mice, SCID · Mitochondria · Mitochondrial Proteins · Models, Molecular · Protein Binding · Regulatory-Associated Protein of mTOR · Signal Transduction · Spleen · Mice · Peptides
Source checked
October 4, 2026. Years follow journal issues; online-first dates may differ.