- The prevalence of obesity is increasing worldwide, causing a subsequent increase in insulin resistance (IR), metabolic disorders, and cardiovascular diseases. Although these conditions significantly impact both the individual and society, their etiologies have not been discovered, inhibiting potential prevention and treatment. Alterations to mitochondrial metabolism are implicated in the development of IR and progression to Type 2 Diabetes (T2D), raising the need for an investigation of mitochondrial metabolism in skeletal muscle. Understanding metabolism on an individual substrate basis within a model system enables identification of each nutrient’s contribution to respiration and potential mitochondrial dysfunction. As such, the purpose of this investigation was to characterize mitochondrial metabolism and determine mitochondrial respiratory control in L6 rat myoblasts. High-resolution respirometry and three Substrate-Uncoupler-Inhibitor-Titration (SUIT) protocols were used to examine respiration. Mitochondrial capacity was not limited by the electron transfer system, although the presence of multiple substrates potentially flooded the Q-junction, resulting in lower respiratory control and indicating the presence of a potential limiting factor. In sum, L6 myoblasts exhibit no overt defects in mitochondrial metabolism, but may have a propensity for substrate overload, thereby limiting respiration.
Key Words: Mitochondria, L6 myoblasts, oxidative phosphorylation, electron transfer