ArticleNeurochemical research2013
The antiepileptic effect of the glycolytic inhibitor 2-deoxy-D-glucose is mediated by upregulation of K(ATP) channel subunits Kir6.1 and Kir6.2.
Article in Neurochemical research, 2013. 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, 40 citations in OpenAlex.
- Metabolic and redox modulation by 2-deoxy-D-glucose and sodium selenite protects against pentylenetetrazole-kindled seizures, neuroinflammation and cognitive dysfunction.Metabolic brain disease · 2026Article
- Harnessing metabolic control for synaptic stability: REST/NRSF links glycolytic inhibition to excitatory neurotransmission.The Journal of physiology · 2025Article
- Effects of Ketogenic Diet on Increased Ethanol Consumption Induced by Social Stress in Female Mice.Nutrients · 2024Article
- Glycolysis inhibition partially resets epilepsy-induced alterations in the dorsal hippocampus-basolateral amygdala circuit involved in anxiety-like behavior.Scientific reports · 2023Article
- 2DG and glycolysis as therapeutic targets for status epilepticus.Epilepsy & behavior : E&B · 2023Review
- 2-Deoxy-D-Glucose: A Novel Pharmacological Agent for Killing Hypoxic Tumor Cells, Oxygen Dependence-Lowering in Covid-19, and Other Pharmacological Activities.Advances in pharmacological and pharmaceutical sciences · 2023Review
- Article
- AntiZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022Article
- The expression of ATP-sensitive potassium channels in human umbilical arteries with severe pre-eclampsia.Scientific reports · 2021Article
- Role of Modulation of Hippocampal Glucose Following Pilocarpine-Induced Status Epilepticus.Molecular neurobiology · 2021Article
- The Pharmacology of ATP-Sensitive KHandbook of experimental pharmacology · 2021Article
- Glycolytic inhibitor 2-deoxyglucose prevents cortical hyperexcitability after traumatic brain injury.JCI insight · 2019Article
- Ketogenic and anaplerotic dietary modifications ameliorate seizure activity in Drosophila models of mitochondrial encephalomyopathy and glycolytic enzymopathy.Molecular genetics and metabolism · 2019Article
- 2-Deoxy-D-Glucose Exhibits Anti-seizure Effects by Mediating the Netrin-G1-KATP Signaling Pathway in Epilepsy.Neurochemical research · 2019Article
- 2-Deoxyglucose and Beta-Hydroxybutyrate: Metabolic Agents for Seizure Control.Frontiers in cellular neuroscience · 2019Review
- Glycolytic inhibition: A novel approach toward controlling neuronal excitability and seizures.Epilepsia open · 2018Article
- Dysregulated Glucose Metabolism as a Therapeutic Target to Reduce Post-traumatic Epilepsy.Frontiers in cellular neuroscience · 2018Review
- Nonclinical Safety Evaluation of 2-Deoxy-D-Glucose Following Twice-Daily Oral Administration for 28 Days in Beagle Dogs.International journal of toxicologyArticle
- The ATP-sensitive K channel is seizure protective and required for effective dietary therapy in a model of mitochondrial encephalomyopathy.Journal of neurogeneticsArticle
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic modulation of neuronal excitability is becoming increasingly important as an antiepileptic therapy. It was reported that the glycolytic inhibitor 2-deoxy-D-glucose (2-DG) and the activation of the ATP-sensitive potassium ion channel (K(ATP) channel) had an antiepileptic effect in models of epilepsy. To explore whether 2-DG exerts an antiepileptic effect through upregulation of the K(ATP) channel subunits Kir6.1 and Kir6.2, the expression of these subunits in hippocampus of five groups of mice with pilocarpine-induced status epilepticus (SE) was evaluated. A seizure group with pilocarpine-kindling convulsions (EP) was compared to similar groups treated with high, medium, and low 2-DG concentrations (100-500 mg/kg) and a normal control group (Con). Kir6.1 and Kir6.2 mRNAs and proteins were analyzed at 4 h, 1 days (acute period), 7 days (latent period), 30, and 60 days (chronic period) following SE. In the seizure group (compared to the Con group), hippocampal expression of Kir6.1 and Kir6.2 increased dramatically at 1, 7, and 30 days, and was further increased after treatment with medium and high dose 2-DG (all P < 0.05). Our results suggest that 2-DG may exert an antiepileptic effect through up-regulation of mRNAs and protein levels of Kir6.1 and Kir6.2, which may therefore be used as molecular targets in the treatment of epilepsy with 2-DG.
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