Seminar
Time: 10:30am, May 18, 2026
Venue: Lecture Hall, Shanghai Brain Center
Speaker: Prof. Vedrana Montana
International Translational Neuroscience Research Institute, Zhejiang Chinese Medical University, Hangzhou, China
Host：Dr. Goran Angelovski
Abstract:
Astrocytes, subtype of glial cells, are essential for maintaining physiological homeostasis in the brain. Their functions are fueled by D-glucose, systemically delivered to the brain by the blood, and L-lactate, locally generated or systemically delivered. The effect of these fuels (alone or as a hybrid) on astrocytes, be that healthy or cancerous glioblastoma cells, reflects upon the function of the entire brain. Dr. Montana will discuss the impact of the type of metabolic fuel or a lack thereof on normal rat astrocytes and human glioblastoma cells, cancerous astrocytes expressing the wild type isocitrate dehydrogenase. Effects of metabolic fuels was assessed by transcriptomics, proteomics and functional assays, in particular that of gliotransmisison. Our data reveal that normal rat astrocytes deprived of both fuels display reduced exocytotic glutamate release. Presence of D-glucose, either taken-up from the extracellular space or mobilized from the intracellular glycogen storage, sustained glutamate release, while the availability of lactate (as sole of hybrid fuel) significantly reduced the release of glutamate from astrocytes. Further changes in presence of lactate were evidenced in an altered expression of cytoskeletal proteins (10), proteins of secretory organelle/vesicle traffic (2) and recycling at the plasma membrane (2). Thus, metabolic microenvironment can affect gliotrasmission and, consequently, the operation of the tripartite synapse. Changes in human glioblastoma cells caused by differential fueling, while numerous at transcriptomics level, were comparatively limited at proteomics levels, indicating a high degree of post-translational regulation. Briefly and selectively, the presence of lactate mostly affected expression of proteins involved in lipid metabolism (17), and signaling (12), migration (8) and invasion (5) pathways.
In conclusion, our data suggest that the metabolic microenvironment has profound, but differential effects on healthy vs cancerous astrocytes.