Topic: SLC2A1

Microglia activation is a metabolically demanding process that implies the transition to a pro- or anti-inflammatory phenotype. During inflammation, microglia undergo metabolic reprogramming to meet their energy needs. Thus, the pro-inflammatory phenotype derives its energy mainly from aerobic glycolysis, whereas the anti-inflammatory phenotype depends on oxidative phosphorylation. The modulation of metabolic pathways in activated microglia could change their phenotype. Exogenously administered agmatine pretreatment (Agm, 100 µM) modulates the Lps-activated BV-2 microglial cell line towards an

Using a mouse model of Glucose Transporter 1 (Glut1) haploinsufficiency which faithfully replicates the core characteristics of De Vivo disease, a human Glut1 Deficiency Syndrome (Glut1DS), we found an early and pronounced decrease in brain glucose, lactate, and glycogen levels. To elucidate the cellular and molecular mechanisms underlying Glut1DS, we conducted an RNA-sequencing analysis on the somatosensory and motor cerebral cortex of a mouse model for Glut1DS.Our analysis revealed 195 up-regulated and 71 down-regulated genes in Glut1-deficient mice compared to wild type controls. Gene set a