Effects of astrocytic absence of glucose transporter 1 (GLUT1) on the cortical astrocytic translatome

Brain activities rely on a steady supply of blood glucose, which is shuttled into the brain by glucose transporters and used to fuel metabolic pathways and energy demands in all neural cells. Astrocytes express glucose transporter 1 (GLUT1), which is considered the key glucose uptake route for glycolytic astrocytes to ensure their metabolic support functions to neurons and other glial cells in vivo. GLUT1 deficiency causes severe developmental impairments, however, the role of GLUT1 in astroglial glucose metabolism and brain function is poorly understood. Here we examine the effect of astrocytic GLUT1 deletion on the active translatome of astrocytes in the the mouse cortex. GLUT1 knockout animals were compared to control animals under naïve conditions. To assess the astrocytic translatome we employed aTranslating Ribosome Affinity Purification (TRAP) approach.