glutamate dehydrogenase/seizures

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Effect of vigabatrin on glutamate dehydrogenase in the hippocampus of seizure prone gerbils.

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Vigabatrin (VGB, gamma-vinyl-gamma-aminobutyric acid (GABA)), an irreversible inhibitor of GABA transaminase, increases regional inhibitory effects by elevating GABA concentration and reducing glutamate synthesis. In the present study, changes in glutamate dehydrogenase (GDH) activity and its

Modulation of brain glutamate dehydrogenase as a tool for controlling seizures.

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Glutamate (Glu) is a major excitatory neurotransmitter involved in epilepsy. Glu is synthesized by glutamate dehydrogenase (GDH, E.C. 1.4.1.3) and dysfunction of the enzymatic activity of GDH is associated with brain pathologies. The main goal of this work is to establish the role of GDH in the

[Metabolic investigations of epileptic seizures: the role of aminotransferases and glutamate dehydrogenase in convulsions].

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Clinical and Molecular Spectrum of Glutamate Dehydrogenase Gene Defects in 26 Chinese Congenital Hyperinsulinemia Patients.

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UNASSIGNED To characterize the genotype and phenotype of Chinese patients with congenital hyperinsulinism (CHI) caused by activating mutations in GLUD1, the gene that encodes mitochondrial enzyme glutamate dehydrogenase (GDH). UNASSIGNED The clinical data of glutamate dehydrogenase hyperinsulinism

Hyperinsulinism associated with GLUD1 mutation: allosteric regulation and functional characterization of p.G446V glutamate dehydrogenase.

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Gain-of-function mutations in the GLUD1 gene, encoding for glutamate dehydrogenase (GDH), result in the hyperinsulinism/hyperammonemia HI/HA syndrome. HI/HA patients present with harmful hypoglycemia secondary to protein-induced HI and elevated plasma ammonia levels. These symptoms may

Changes in the activity of glutamate related enzymes in cerebral cortex, during insulin-induced seizures.

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The activity of glutamate related enzymes and the concentration of glutamine, glutamate and gamma-amino n-butyric acid (GABA) were investigated in the cerebral cortex of rats, in different stages of insulin-induced hypoglycemia. Hypoglycemia was produced by intraperitoneal injection of insulin

Regulation of glutamate metabolism and insulin secretion by glutamate dehydrogenase in hypoglycemic children.

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In addition to its extracellular roles as a neurotransmitter/sensory molecule, glutamate serves important intracellular signaling functions via its metabolism through glutamate dehydrogenase (GDH). GDH is a mitochondrial matrix enzyme that catalyzes the oxidative deamination of glutamate to

A Japanese case of congenital hyperinsulinism with hyperammonemia due to a mutation in glutamate dehydrogenase (GLUD1) gene.

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We describe a Japanese case of neonatal hyperinsulinism due to a de novo mutation (Gly446Asp) in glutamate dehydrogenase gene (GLUD1). A boy suffered from hypoglycemic coma with relative hyperinsulinemia on day 1 after birth, and received subtotal pancreatectomy. Examination of the resected pancreas

Seizures and diagnostic difficulties in hyperinsulinism-hyperammonemia syndrome.

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Hyperinsulinism/hyperammonemia (HI/HA) syndrome is a rare disorder presented with recurrent hypoglycemia and elevated serum ammonia, which may lead to development delays, permanent neurologic damages, if it remains underdiagnosed. It is caused by activating mutations in the GLUD1 gene which encodes

Novel missense mutations in the glutamate dehydrogenase gene in the congenital hyperinsulinism-hyperammonemia syndrome.

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OBJECTIVE The objectives of this study were to clarify the involvement of the glutamate dehydrogenase gene in congenital hyperinsulinemia-hyperammonemia syndrome (CHHS) and the relationships between the mutation of the gene and clinical severity. METHODS Five unrelated Japanese patients (3 girls and

[Cytophotometric study of changes in glutamate dehydrogenase and GABA transaminase in the cerebral cortex during corazole kindling].

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It has been demonstrated in (CBA X C57BL/6) F1 mice that daily corazole injections (30 mg/kg) lead to the development of pharmacological kindling that manifests in a progressive increase of seizure susceptibility, seizure occurrence in response to the subthreshold convulsant dose and in demonstrable

Deregulation of glutamate dehydrogenase in human neurologic disorders.

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Mammalian glutamate dehydrogenase is an allosterically regulated enzyme that is central to glutamate metabolism. It contributes to important cellular processes, including Krebs cycle anaplerotic mechanisms, energy production, and ammonia homeostasis. In addition to this housekeeping hGDH1, humans

A novel mutation in the glutamate dehydrogenase (GLUD1) of a patient with congenital hyperinsulinism-hyperammonemia (HI/HA).

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Hyperinsulinism-hyperammonemia (HI/HA) syndrome, often characterized by recurrent symptomatic hypoglycemia and persistent hyperammonemia, is the second most frequent cause of the congenital hyperinsulinism (CHI). Here, we reported a patient with normal birth weight, repeated seizures, untreatable

Central nervous system hyperexcitability associated with glutamate dehydrogenase gain of function mutations.

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OBJECTIVE To describe seizure phenotypes associated with the hyperinsulinism/hyperammonemia syndrome (HI/HA), which is caused by gain of function mutations in the enzyme glutamate dehydrogenase (GDH). METHODS A retrospective review of records of 14 patients with HI/HA. RESULTS Nine patients had

A severe case of hyperinsulinism due to hemizygous activating mutation of glutamate dehydrogenase.

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Activating mutations in the GLUD1 gene, which encodes glutamate dehydrogenase (GDH), result in the hyperinsulinism-hyperammonemia syndrome. GDH is an allosterically regulated enzyme responsible for amino acid-mediated insulin secretion via the oxidative deamination of glutamate to 2-oxoglutarate,

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