Mitochondria-Derived Peptide MOTS-c Restores Mitochondrial Respiration in Type 2 Diabetic Heart

Plain-language summary

Using a high-fat diet and low-dose streptozotocin rat model of type 2 diabetes, this study found that exogenous MOTS-c treatment effectively delayed weight gain and showed promise in restoring mitochondrial respiratory function in diabetic cardiac tissue, where mitochondrial dysfunction is a key driver of reduced contractile performance. The results are consistent with prior reports that blood MOTS-c levels are lower in individuals with type 2 diabetes, gestational diabetes, and coronary endothelial dysfunction, supporting the peptide's role in metabolic homeostasis. These findings position MOTS-c as a promising investigational strategy for studying mitochondrial function in metabolic heart disease.