Mitochondria-derived peptide MOTS-c restores mitochondrial respiration in type 2 diabetic heart

What this study reported

Measured cardiac mitochondrial bioenergetics in a rat model of diet- and streptozotocin-induced type 2 diabetes and reported that untreated diabetic rats had hyperglycaemia, poor glucose control, left ventricular hypertrophy and decreased oxygen flux at oxidative phosphorylation, with unchanged ROS, ATP production and hydrolysis rates. Reported that diabetic rats given MOTS-c had lower fasting glucose, improved glucose homeostasis and a lesser degree of cardiac hypertrophy, and that their cardiac mitochondria showed increased OXPHOS respiration, increased ROS levels and a decreased ATP hydrolysis rate under anoxic conditions.

Limitations

Group sizes, sex and randomisation are not reported in the abstract; a single chemically induced diabetes model; endpoints are tissue-homogenate surrogates rather than in vivo cardiac function, and the reported increase in ROS is not reconciled with the stated benefit.