||Although mitochondrial dysfunction has been linked to many human diseases, mitochondrial interacting proteins and protein quality controls are just beginning to be understood. The objective of our study was to characterize the function of the VMS1 protein in mammals. We determined the role of Vms1 on mitochondrial respiration by measuring oxygen consumption, ATP concentration, and glucose tolerance in mice. We aimed to determine the Vms1 mechanism of action by immunoprecipitation of interacting proteins. Whether Vms1 knockout in mice resulted in increased ROS production was determined by aconitase assay. We found that Vms1 is involved with mitochondrial oxygen consumption (P = 0.027), ATP production (P = 0.041), and glucose metabolism (P = 0.018). The Vms1-VCP/p97 interaction is also conserved from yeast to mammals. Although Vms1 interacts with VCP/p97, Vms1 knockout did not result in the accumulation of ubiqitinated proteins. Furthermore, loss of Vms1 in mice liver did not impair aconitase activity. We have also discovered a link between Vms1 and ER protein glycosylation. Continued research on the VMS1 protein may help us identify its role in the cell, and possibly determine the proteins connection to the many mitochondrial and ER associated human diseases.