Type 2 diabetes mellitus often leads to muscle atrophy driven by diminished differentiation capacity in myoblasts. Myogenesis is complex, and while many involved pathways have been described, there may still be yet undiscovered therapeutic targets. With this goal in mind, a recent study combined experiments in diabetic mice and cultured myoblasts to identify key proteins in diabetes-induced atrophy. The gene for the relatively undescribed solute carrier Slc2a6, also known as glut6, was up-regulated during myogenic differentiation and down-regulated during diabetes-induced myopathy. Silencing Slc2a6 with RNAi in cell culture impaired differentiation and myotube formation. Transcriptomics and metabolomics revealed that Slc2a6 silencing disproportionally impacted the glycolysis pathway . Further experiments and analysis determined that Slc2a6 regulates myogenic differentiation in cultured myoblasts and that this regulation was partly through the glycolysis pathway. Slc2a6 targeted one of the differentially expressed genes, LDHB, and affected lactic acid accumulation. Overall, this study expanded the current understanding of myogenic differentiation, particularly in the context of diabetes-induced atrophy and suggests that the Slc2a6-LDHB axis could be a potential therapeutic target for this kind of atrophy.