Study summary · research use only
Mitochondrial-encoded peptide MOTS-c prevents pancreatic islet cell senescence to delay diabetes
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study examined the mitochondrial-encoded peptide MOTS-c in pancreatic β-cell senescence, using aged C57BL/6 mice, S961-treated C57BL/6 mice, nonobese diabetic mice, and human blood samples. MOTS-c levels decreased with aging and senescence in mouse pancreatic islet cells, and treating aged mouse islets with MOTS-c was associated with reduced islet senescence via changes in nuclear gene expression and metabolites involved in β-cell senescence. MOTS-c treatment was also associated with improved pancreatic islet senescence and glucose intolerance in S961-treated and nonobese diabetic mice. In humans, circulating MOTS-c levels were reported to be lower in people with type 2 diabetes than in healthy controls; the authors suggest MOTS-c may regulate pancreatic islet cell senescence relevant to diabetes progression.
Abstract
Mitochondria are crucial for cell survival and function, partly through peptides encoded by the mitochondrial genome. Although mitochondrial dysfunction is a hallmark of age-related diseases and senescence, the role of mitochondrial-genome-encoded peptides in pancreatic β-cell senescence during type 1 and type 2 diabetes pathogenesis is largely unexplored. Here we show that MOTS-c levels decrease with aging and senescence in pancreatic islet cells. Treating aged C57BL/6 mouse pancreatic islets with MOTS-c reduced pancreatic islet senescence by modulating nuclear gene expression and metabolites involved in β-cell senescence. MOTS-c treatment improved pancreatic islet senescence and glucose intolerance in S961-treated C57BL/6 and in nonobese diabetic mice. In humans, circulating MOTS-c levels are lower in type 2 diabetes patients compared with healthy controls. Our findings suggest that mitochondrial-encoded MOTS-c regulate pancreatic islet cell senescence and that MOTS-c could act as a senotherapeutic agent to prevent pancreatic islet cell senescence and diabetes progression.
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