The mitochondria-targeted peptide SS-31 prevented pancreatic islet cell apoptosis, preserved insulin secretion, and improved diabetes outcomes in animal models — protecting the insulin-producing cells that diabetes destroys.
Key findingSS-31 (mitochondria-targeted peptide) prevented mitochondrial depolarization and apoptosis in pancreatic islet cells, preserved glucose-stimulated ins
What the researchers found
SS-31 (mitochondria-targeted peptide) prevented mitochondrial depolarization and apoptosis in pancreatic islet cells, preserved glucose-stimulated insulin secretion, and improved glycemic control in diabetic animals — protecting the beta-cells that diabetes progressively destroys.
Why it matters
Relevant for opioid-peptides, diabetes, neuroprotection.
How the study worked
animal-study study.
What this study cannot tell us
See abstract.
How to read the evidence
moderate evidence.
When this study was published
Published in 2007.
The bigger picture
Advances peptide research.
Questions still open
- Further research needed.
- Clinical translation to evaluate.
Common questions
What was studied?
What was found?
Read the original research
Mitochondrial targeting with antioxidant peptide SS-31 prevents mitochondrial depolarization, reduces islet cell apoptosis, increases islet cell yield, and improves posttransplantation function.
Journal of the American Society of Nephrology : JASN, 18(1), 213-22
Citation
Thomas, Dolca A; Stauffer, Craig; Zhao, Kesheng; Yang, Hua; Sharma, Vijay K; Szeto, Hazel H; Suthanthiran, Manikkam. (2007). Mitochondrial targeting with antioxidant peptide SS-31 prevents mitochondrial depolarization, reduces islet cell apoptosis, increases islet cell yield, and improves posttransplantation function.. Journal of the American Society of Nephrology : JASN, 18(1), 213-22.