Glucose induced IEG expression in the thiamin-deficient rat brain

Glucose loading of rats made thiamin deficient by dietary deprivation of thiamin and the administration of pyrithiamin (40 μg/100 g, i.p.) precipitates an acute neuropathy, a model of Wernicke’s encephalopathy in man (Zimitat and Nixon, Metab. Brain Dis. 1999;14:1–20). Immunohistochemical detection...

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Published inBrain research Vol. 892; no. 1; pp. 218 - 227
Main Authors Zimitat, Craig, Nixon, Peter F
Format Journal Article
LanguageEnglish
Published London Elsevier B.V 16.02.2001
Amsterdam Elsevier
New York, NY
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Abstract Glucose loading of rats made thiamin deficient by dietary deprivation of thiamin and the administration of pyrithiamin (40 μg/100 g, i.p.) precipitates an acute neuropathy, a model of Wernicke’s encephalopathy in man (Zimitat and Nixon, Metab. Brain Dis. 1999;14:1–20). Immunohistochemical detection of Fos proteins was used as a marker to identify neuronal populations in the thiamin-deficient rat brain affected by glucose loading. As thiamin deficiency progressed, the extent and intensity of Fos-like immunoreactivity (FLI) in brain structures typically affected by thiamin deficiency (the thalamus, mammillary bodies, inferior colliculus, vestibular nucleus and inferior olives) were markedly increased when compared to thiamin-replete controls. Glucose loading for 1–3 days further increased the intensity of FLI in these same regions, consistent with a dependence of Fos expression on carbohydrate metabolism as well as on thiamin deficiency. The timed acute changes that follow a bolus glucose load administered to thiamin-deficient animals may provide a sequential account of events in the pathogenesis of brain damage in this model of Wernicke’s encephalopathy.
AbstractList Glucose loading of rats made thiamin deficient by dietary deprivation of thiamin and the administration of pyrithiamin (40 μg/100 g, i.p.) precipitates an acute neuropathy, a model of Wernicke’s encephalopathy in man (Zimitat and Nixon, Metab. Brain Dis. 1999;14:1–20). Immunohistochemical detection of Fos proteins was used as a marker to identify neuronal populations in the thiamin-deficient rat brain affected by glucose loading. As thiamin deficiency progressed, the extent and intensity of Fos-like immunoreactivity (FLI) in brain structures typically affected by thiamin deficiency (the thalamus, mammillary bodies, inferior colliculus, vestibular nucleus and inferior olives) were markedly increased when compared to thiamin-replete controls. Glucose loading for 1–3 days further increased the intensity of FLI in these same regions, consistent with a dependence of Fos expression on carbohydrate metabolism as well as on thiamin deficiency. The timed acute changes that follow a bolus glucose load administered to thiamin-deficient animals may provide a sequential account of events in the pathogenesis of brain damage in this model of Wernicke’s encephalopathy.
Glucose loading of rats made thiamin deficient by dietary deprivation of thiamin and the administration of pyrithiamin (40 mu g/100 g, i.p.) precipitates an acute neuropathy, a model of Wernicke's encephalopathy in man (Zimitat and Nixon, Metab. Brain Dis. 1999; 14:1-20). Immunohistochemical detection of Fos proteins was used as a marker to identify neuronal populations in the thiamin-deficient rat brain affected by glucose loading. As thiamin deficiency progressed, the extent and intensity of Fos-like immunoreactivity (FLI) in brain structures typically affected by thiamin deficiency (the thalamus, mammillary bodies, inferior colliculus, vestibular nucleus and inferior olives) were markedly increased when compared to thiamin-replete controls. Glucose loading for 1-3 days further increased the intensity of FLI in these same regions, consistent with a dependence of Fos expression on carbohydrate metabolism as well as on thiamin deficiency. The timed acute changes that follow a bolus glucose load administered to thiamin-deficient animals may provide a sequential account of events in the pathogenesis of brain damage in this model of Wernicke's encephalopathy.
Glucose loading of rats made thiamin deficient by dietary deprivation of thiamin and the administration of pyrithiamin (40 microg/100 g, i.p.) precipitates an acute neuropathy, a model of Wernicke's encephalopathy in man (Zimitat and Nixon, Metab. Brain Dis. 1999;14:1-20). Immunohistochemical detection of Fos proteins was used as a marker to identify neuronal populations in the thiamin-deficient rat brain affected by glucose loading. As thiamin deficiency progressed, the extent and intensity of Fos-like immunoreactivity (FLI) in brain structures typically affected by thiamin deficiency (the thalamus, mammillary bodies, inferior colliculus, vestibular nucleus and inferior olives) were markedly increased when compared to thiamin-replete controls. Glucose loading for 1-3 days further increased the intensity of FLI in these same regions, consistent with a dependence of Fos expression on carbohydrate metabolism as well as on thiamin deficiency. The timed acute changes that follow a bolus glucose load administered to thiamin-deficient animals may provide a sequential account of events in the pathogenesis of brain damage in this model of Wernicke's encephalopathy.
Author Zimitat, Craig
Nixon, Peter F
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Issue 1
Keywords Brain damage
IEG expression
Wernicke’s encephalography
Disorders of the neurons system
Thiamin deficiency
Animal model
Nervous system diseases
Rat
Pathogenesis
Rodentia
Central nervous system
Vitamin deficiency
B-Vitamins
Glucose
Gene expression
Cerebral disorder
Vertebrata
Mammalia
Central nervous system disease
Malnutrition
Wernicke encephalopathy
Nutritional status
Thiamine
Brain (vertebrata)
Immediate early gene
Language English
License CC BY 4.0
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Snippet Glucose loading of rats made thiamin deficient by dietary deprivation of thiamin and the administration of pyrithiamin (40 μg/100 g, i.p.) precipitates an...
Glucose loading of rats made thiamin deficient by dietary deprivation of thiamin and the administration of pyrithiamin (40 microg/100 g, i.p.) precipitates an...
Glucose loading of rats made thiamin deficient by dietary deprivation of thiamin and the administration of pyrithiamin (40 mu g/100 g, i.p.) precipitates an...
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StartPage 218
SubjectTerms Animals
Antimetabolites - pharmacology
Biological and medical sciences
Brain - drug effects
Brain - metabolism
Brain - pathology
Brain damage
Disease Models, Animal
Gene Expression Regulation - drug effects
Gene Expression Regulation - physiology
Genes, fos
Genes, Immediate-Early
Glucose - metabolism
Glucose - pharmacology
Humans
IEG expression
Medical sciences
Nervous system involvement in other diseases. Miscellaneous
Neurology
Organ Specificity
Pyrithiamine - pharmacology
Rats
Rats, Wistar
Thiamin deficiency
Thiamine Deficiency - genetics
Thiamine Deficiency - pathology
Thiamine Deficiency - physiopathology
Wernicke Encephalopathy - genetics
Wernicke Encephalopathy - pathology
Wernicke Encephalopathy - physiopathology
Wernicke's encephalopathy
Wernicke’s encephalography
Title Glucose induced IEG expression in the thiamin-deficient rat brain
URI https://dx.doi.org/10.1016/S0006-8993(00)03297-2
https://www.ncbi.nlm.nih.gov/pubmed/11172768
https://search.proquest.com/docview/17775474
Volume 892
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