Regulation of reactive oxygen species in L6 myoblasts by glucose transporter 1 (693.5)

Abstract

Elevated reactive oxygen species (ROS) levels are associated with metabolic abnormalities such as insulin resistance. Glucose transporter 1 (GLUT1) transports glucose and dehydroascorbic acid, both of which play roles in antioxidant defense. We hypothesized that conditions that would increase GLUT1 activity would result in decreased ROS levels and conditions that would decrease GLUT1 activity would increase ROS levels. . L6 myoblasts loaded with H2‐DCFDA, a fluorescent ROS probe, were treated under various conditions to alter GLUT1 activity, and fluorescence readings were taken under basal conditions or after increases in ROS were induced by exposure to pyrogallol or antimycin A. GLUT1 inhibitors, fasentin and phloretin, increased induced ROS levels. Ataxia telangiectasia mutated inhibitors and activators, previously shown to inhibit and augment GLUT1 activity, increased and decreased basal and induced ROS levels, respectively. GLUT1‐S490A, previously shown to decrease GLUT1 activity, enhanced basal and induced ROS levels. GLUT1‐S490D, previously shown to increase GLUT1‐mediated transport, lowered basal ROS levels. Thus, the data suggest that GLUT1 plays a role in regulation of ROS levels. Grant Funding Source: Supported by: William Townsend Porter Predoctoral Fellowship from the American Physiological Society