ArticleNeurochemical research2019
Consequences of a Metabolic Glucose-Depletion on the Survival and the Metabolism of Cultured Rat Astrocytes.
Article in Neurochemical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 18 citations in OpenAlex.
- Consumption of Fructose by Cultured Primary Rat Astrocytes.Neurochemical research · 2026Article
- Lactate Dehydrogenase Inhibition Reverts the Fatty Acid-Induced Neurotoxic Phenotype of Astrocytes.Glia · 2026Article
- ATP Metabolism of Astrocytes: Consumption, Regeneration and Restoration.Neurochemical research · 2025Review
- Oxidative Stress Induces the Phosphorylation of NADNeurochemical research · 2025Article
- Consequences of a 2-Deoxyglucose Exposure on the ATP Content and the Cytosolic Glucose Metabolism of Cultured Primary Rat Astrocytes.Neurochemical research · 2024Article
- ATP Restoration by ATP-Deprived Cultured Primary Astrocytes.Neurochemical research · 2024Article
- Reversibility of Endoplasmic Reticulum Stress Markers During Long-Term Glucose Starvation in Astrocytes.Journal of molecular neuroscience : MN · 2024Article
- Exogenous Substrates Prevent the Decline in the Cellular ATP Content of Primary Rat Astrocytes During Glucose Deprivation.Neurochemical research · 2024Article
- Modulation of Pyruvate Export and Extracellular Pyruvate Concentration in Primary Astrocyte Cultures.Neurochemical research · 2024Article
- Modulation of Cellular Levels of Adenosine Phosphates and Creatine Phosphate in Cultured Primary Astrocytes.Neurochemical research · 2024Article
- Copper induces neuron-sparing, ferredoxin 1-independent astrocyte toxicity mediated by oxidative stress.Journal of neurochemistry · 2023Article
- G6PDi-1 is a Potent Inhibitor of G6PDH and of Pentose Phosphate pathway-dependent Metabolic Processes in Cultured Primary Astrocytes.Neurochemical research · 2023Article
- Endogenous Energy Stores Maintain a High ATP Concentration for Hours in Glucose-Depleted Cultured Primary Rat Astrocytes.Neurochemical research · 2023Article
- β-lapachone-mediated WST1 Reduction as Indicator for the Cytosolic Redox Metabolism of Cultured Primary Astrocytes.Neurochemical research · 2023Article
- Consumption and Metabolism of Extracellular Pyruvate by Cultured Rat Brain Astrocytes.Neurochemical research · 2023Article
- Early effects of LPS-induced neuroinflammation on the rat hippocampal glycolytic pathway.Journal of neuroinflammation · 2022Article
- Should We Void Lactate in the Pathophysiology of Delayed Onset Muscle Soreness? Not So Fast! Let's See a Neurocentric View!Metabolites · 2022Article
- The Menadione-Mediated WST1 Reduction by Cultured Astrocytes Depends on NQO1 Activity and Cytosolic Glucose Metabolism.Neurochemical research · 2021Article
- β-Lapachone Induces Acute Oxidative Stress in Rat Primary Astrocyte Cultures that is Terminated by the NQO1-Inhibitor Dicoumarol.Neurochemical research · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain astrocytes are considered to be highly glycolytic, but these cells also produce ATP via mitochondrial oxidative phosphorylation. To investigate how a metabolic depletion of glucose will affect the metabolism of astrocytes, we applied glucose at an initial concentration of 2 mM to cultured primary astrocytes and monitored the cell viability and various metabolic parameters during an incubation for up to 2 weeks. Already within 2 days of incubation the cells had completely consumed the applied glucose and lactate had accumulated in the medium to a concentration of around 3 mM. During the subsequent 10 days of incubation, the cell viability was not compromised while the extracellular lactate concentration declined to values of around 0.2 mM, before the cell viability was compromised. Application of known inhibitors of mitochondrial metabolism strongly accelerated glucose consumption and initial lactate production, while the lactate consumption was completely (antimycin A or 8-hydroxy efavirenz) and partially (efavirenz, metformin or tyrphostin 23) inhibited which caused rapid and delayed cell toxicity, respectively. The switch from glycolytic glucose metabolism to mitochondrial metabolism during the incubation was neither accompanied by alterations in the specific cytosolic lactate dehydrogenase activity or in the WST1 reduction capacity nor in the mitochondrial citrate synthase activity, but a cellular redistribution of mitochondria from a perinuclear to a more spread cytoplasmic localization was observed during the lactate consumption phase. These results demonstrate that cultured astrocytes survive a metabolism-induced glucose depletion very well by consuming lactate as fuel for mitochondrial ATP generation.
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