Mitochondrial Peptide MOTS-c Directly Regulates Pancreatic Alpha and Beta Cell Functions
Background
The pancreas plays a critical role in glucose homeostasis through its islet cells: beta cells secrete insulin to lower blood glucose, while alpha cells secrete glucagon to raise it. Dysregulation of these cells is central to type 2 diabetes. While the mitochondrial-derived peptide MOTS-c is known to influence whole-body metabolism, its direct impact on the function of pancreatic alpha and beta cells has been poorly understood.
Results
Treatment with MOTS-c demonstrated significant regulatory effects on both pancreatic cell types. In beta cells, 100 nM MOTS-c notably increased glucose-stimulated insulin secretion (GSIS) by 35% compared to untreated controls (p<0.01), and this was supported by a 2.1-fold upregulation of insulin gene expression. Furthermore, MOTS-c at 1 µM enhanced beta cell viability by 15% after 48 hours of treatment (p<0.05).
Why It Matters
This study provides crucial in vitro evidence for the direct regulatory role of MOTS-c on pancreatic islet cells, suggesting its potential as a therapeutic agent for metabolic disorders. By simultaneously improving insulin secretion and suppressing glucagon, MOTS-c could offer a novel, dual-action approach to managing type 2 diabetes. These findings warrant further investigation in vivo, including animal models and eventually human clinical trials, to confirm efficacy and safety.