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Pagina 1 a partire dal 56 risultati
Fructose-1,6-diphosphate inhibits seizure acquisition in fast hippocampal kindling.
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Inhibition of glycolytic metabolism may provide a new therapy for refractory epilepsy. Fructose-1,6-diphosphate (FDP), which inhibits glycolysis and diverts glucose into the pentose phosphate pathway, has strong inhibitory action on seizures induced by chemical convulsants. Here, we investigated the
[Protective effects of fructose-1,6-diphosphate on brain damage caused by febrile seizures in rats].
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OBJECTIVE
Febrile seizure (FS) is a pediatric emergency. The reiterative attacks of FS may result in brain damage to various extents. Fructose-1,6-diphosphate, serving as a cellular energy substance, has been applied to clinical practice for many years and has shown its importance in adjuvant
Fructose-1,6-bisphosphate has anticonvulsant activity in models of acute seizures in adult rats.
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A variety of observations suggest that decreasing glycolysis and increasing levels of reduced glutathione, generated by metabolism of glucose through the pentose phosphate pathway, would have an anticonvulsant effect. Because fructose-1,6-bisphosphate (F1,6BP) shifts the metabolism of glucose from
Incidence of seizures that follow rehydration of hypernatremic rabbits with intravenous glucose or fructose solutions.
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Hypernatremic dehydration was induced in rabbits during a 3- to 5-day period resulting in mean plasma sodium concentrations of 187 meq/liter. The animals were then rehydrated during a 4-h period by intravenous administration of a 2.5% glucose or fructose solution. The water content of four regions
[Protective effect of fructose-1,6-diphosphate against ultrastructural damage in the hippocampus of rats with repeated febrile seizures].
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OBJECTIVE
Fructose-1, 6-diphosphate (FDP), serving as a cellular energy substance, has shown its roles in the treatment of hypoxic-ischemic encephalopathy and myocardial damage. The present study aimed at exploring the potentiality of the protective effect of FDP against ultrastructural damage of
Repeated febrile convulsions impair hippocampal neurons and cause synaptic damage in immature rats: neuroprotective effect of fructose-1,6-diphosphate.
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Fructose-1,6-diphosphate is a metabolic intermediate that promotes cell metabolism. We hypothesize that fructose-1,6-diphosphate can protect against neuronal damage induced by febrile convulsions. Hot-water bathing was used to establish a repetitive febrile convulsion model in rats aged 21 days,
Fructose-1,6-bisphosphatase deficiency presented with complex febrile convulsion.
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Fructose-1,6-bisphosphatase (FBPase) deficiency is a rare inborn error of metabolism affecting gluconeogenesis caused by FBP1 gene mutations. It could be more fatal to infants and children when glycogen reserves are insufficient. A 4-year-old girl was admitted with complex febrile convulsion.
Peripheral glucose metabolism is altered by epileptic seizures.
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The aim of the present study was to investigate the status of jejunal absorption and peripheral metabolism of glucose in Wistar Audiogenic Rats (WAR), a genetic model of epilepsy, after seizures induced by intensive sound exposure. The jejunal loop of rats was isolated and infused (0.5 mL min(-1))
Glycogen content and fructose-1, 6-biphosphatase activity in methionine sulfoximine epileptogenic mouse brain and liver after protein synthesis inhibition.
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Mice given intraperitoneal injections of methionine sulfoximine (MSO) (100 mg/kg body weight) showed tonic-clonic seizures 7 to 8 h later. The protein synthesis inhibitors actinomycin D and cycloheximide, when combined with MSO delayed the onset of seizures. Methionine completely abolished the
Possible mechanisms for the anticonvulsant activity of fructose-1,6-diphosphate.
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Fructose-1,6-diphosphate (FDP), an intracellular metabolite of glucose, has anticonvulsant activity in several models of acute seizures in laboratory animals. The anticonvulsant effect of FDP is most likely due to a direct effect since intraperitoneal and oral administration results in significant
Oral administration of fructose-1,6-diphosphate has anticonvulsant activity.
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Recently it has been shown that fructose-1,6-diphosphate (FDP) has dose-dependent anticonvulsant activity in rat models of acute generalized motor seizures induced with chemical convulsants. The present study asked whether FDP also has activity in an epileptic brain after oral administration and
[Genetic diagnosis of fructose-1, 6-bisphosphatase deficiency: a case report].
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OBJECTIVE
To report the first case of fructose-1,6-bisphosphatase (FBPase) deficiency diagnosed by genetic sequencing in China, and to improve the cognition of this rare disease.
METHODS
The clinical and laboratory characteristics of FBPase deficiency were reviewed, and the findings of direct
Use of topiramate in childhood generalized seizure disorders.
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Topiramate is a sulfamate derivative of the naturally occurring monosaccharide D-fructose. It was initially approved in the United States as adjunctive therapy for partial seizures in 1997. However, there is increasing evidence that it is effective in the treatment of generalized seizures and
Seizures and stupor during intravenous mannose therapy in a patient with CDG syndrome type 1b (MPI-CDG).
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MPI-CDG (formally called CDG 1b), caused by phosphomannose isomerase (MPI) deficiency, leads to hypoglycaemia, protein losing enteropathy, hepatopathy, and thrombotic events, whereas neurologic development remains unaffected. Dietary supplementation of mannose can reverse clinical symptoms by
Status epilepticus due to fructose-1,6-bisphosphatase deficiency caused by FBP1 gene mutation
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Introduction: Fructose-1,6-bisphosphatase (FBPase) deficiency is a rare inherited disorder in gluconeogenesis, characterized by hypoglycemia, ketonuria, metabolic acidosis and convulsions.
Case
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