UC San Diego

Metabolic syndrome (MetSyn) is a term used to describe risk factors associated with the increased risk of chronic diseases including cardiovascular disease, type 2 diabetes (T2DM), and certain forms of cancer. Exercise and caloric restriction have been shown to ameliorate features of the MetSyn, in part by improving insulin sensitivity and overall metabolic function. Improved metabolism and insulin action is thought to occur in response to enhanced mitochondrial functional capacity, number, and mtDNA integrity. Surprisingly, despite the recent boom of mitochondrial dynamics and metabolic research, little is still known about exercise-induced alterations to mitochondrial dynamics. In this study I sought to characterize changes in expression and signaling of proteins involved in mitochondrial dynamics in response to acute exercise. Wild type C57Bl6/J female mice (n=24) were exercised on a treadmill with various durations. Quadriceps muscles were collected and flash frozen for subsequent analysis by PCR and immunoblotting. Acute single bout exercise led to increased Fis1 gene expression and protein levels. Mff protein levels on the mitochondria were increased with prolonged exercise. A novel and interesting finding was the increase of Drp1Ser616 phosphorylation in the 90-minute exercise group. This work provides novel and essential information on the exact mechanisms of mitochondrial fission. Now, more research on the recruiter proteins of the mitochondrial membranes will be able to build upon the discoveries of this thesis