PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “THIAMINE DEFICIENCY”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources
PubMed1982

Cholinergic therapy of abnormal open-field behavior in thiamin-deficient rats.

Although thiamin deficiency is associated with impaired acetylcholine metabolism, the functional significance of the cholinergic lesion is controversial. Therefore, we tested the effect of cholinergic drugs on abnormal open-field behaviors in rats that were treated with a thiamin-deficient diet and thiamin antagonist. After only 1 day of treatment, staring increased significantly in rats given pyrithiamin, a centrally acting thiamine antagonist, but not in rats given oxythiamin, which acts only peripherally. Sniffing, resting and grooming were not altered by either treatment. The acetylcholinesterase inhibitor physostigmine was as effective as thiamin in decreasing staring in pyrithiamin-treated rats, but its peripherally acting analogue neostigmine had no effect. The central muscarinic blocker, atropine, blocked the effect of physostigmine. Methatropine, which acts only peripherally, did not. Arecoline, a direct muscarinic agonist, was as effective as physostigmine in decreasing staring. Nicotine had no effect, and the nicotinic ganglionic blocker mecamylamine did not block the effect of physostigmine. Increased staring behavior in pyrithiamin-treated rats appears to reflect an early central cholinergic muscarinic deficit.

Animals↗
PubMed1993

Neuronal changes in the cerebral cortex of the rat following alcohol treatment and thiamin deficiency.

The contribution of thiamin deficiency to the pathology of alcohol-related brain damage is still unclear. This study used a model of prolonged alcohol abuse in which animals were subjected to a brief period of mild thiamin deficiency. The episode of thiamin deficiency was early (after 4 weeks), in the middle (after 15 weeks) or late (after 26 weeks) in their 28 week alcohol treatment period. A control group of animals fed no alcohol and maintained on a thiamin-replete diet was used for comparison. The brains were removed and sectioned in the coronal plane at 50 microns intervals. Successive serial sections were stained with cresyl violet for Niss1 substance and immunohistochemically with antibodies to the calcium-binding proteins parvalbumin and calbindin. These calcium-binding proteins identify the majority of GABA-containing neurons in the cerebral cortex. The number of cells in the Fr1 region of the cerebral cortex was quantitated. A significant loss of Niss1-stained neurons was identified from the early group, while a loss of parvalbumin-immunoreactive neurons was seen in the early and middle groups. No loss of neurons was identified from the late group. In addition, no loss of calbindin-immunoreactive neurons was seen. This study represents the first report of cortical neuronal loss in an animal model of alcohol abuse and thiamin deficiency. Moreover, the results imply that thiamin deficiency is integrally involved in the pathogenesis of alcohol-related cortical neuronal loss.

Alcoholism↗
PubMed1985

Alterations in muscarinic cholinergic receptor densities induced by thiamine deficiency: autoradiographic detection of changes in high- and low-affinity agonist binding.

Animals fed a diet deficient in thiamine or treated with a drug preventing the utilization of thiamine (thiamine antagonist) exhibited alterations in ligand binding to muscarinic receptors in several brain regions. Using quantitative techniques of receptor autoradiography, an increase in muscarinic receptor binding was demonstrated in such regions as the corpus callosum, lamina VI of the parietal cortex, caudate-putamen, ventral nucleus of the thalamus, stratum lacunosum moleculare and stratum oriens of the hippocampus, and the hilus of the area dentata. As a result of thiamine deficiency, this increase in muscarinic receptor populations was primarily due to an increase in the binding of the low-affinity agonist site. In the same experiment, a decrease in muscarinic receptor binding was found in the ventromedial region of the hypothalamus. Thiamine deficiency thus causes an up-regulation of muscarinic receptor binding in several regions of rat brain while causing a down-regulation of these same receptors in other brain areas.

Animals↗
PubMed2001

In vivo and in vitro proton NMR spectroscopic studies of thiamine-deficient rat brains.

Thiamine deficiency (TD) in rats produces lesions similar to those found in humans with Wernicke's encephalopathy, an organic mental disorder associated with alcoholism. Male Sprague-Dawley rats (n = 24) were deprived of thiamine in a regimen of thiamine-deficient chow and daily intraperitoneal injections of the thiamine antagonist pyrithiamine hydrobromide for 12 days (0.5 mg/kg). In rats with TD, significant changes were observed in the choline peak (reduction and dose-dependent recovery after thiamine replenishment), which was confirmed by the extraction study. Changes were mainly due to the reduction in glycerophosphorylcholine (GPC), suggesting that a reduction in GPC may be relevant to the primary biochemical lesion in TD. These data are compatible with the hypothesis that a decrease in choline compounds is the cause of the biochemical abnormalities that precede neuroanatomic damage characteristic of Wernicke's encephalopathy.

Animals↗
PubMed1995

In vivo localized proton NMR spectroscopy of thiamine-deficient rat brain.

Thiamine deficiency (TD) in rats produces lesions similar to those found in humans suffering from Wernicke's encephalopathy, an organic mental disorder associated with alcoholism. Male Sprague-Dawley rats (n = 29) were deprived of thiamine via a regimen of thiamine-deficient chow and daily intraperitoneal injections of the thiamine antagonist pyrithiamine hydrobromide. Spectra were obtained by using the STEAM sequence. No significant change occurred in the ratio of Cr/NAA, while the ratio of Cho/NAA declined significantly (60 +/- 11%) on Day 14. Eleven rats received intraperitoneal injections of thiamine hydrochloride at the end of 12 days, and dose-dependent recovery in Cho/NAA was observed.

Alcohol Amnestic Disorder↗
PubMed1996

Nitric oxide synthase activities are selectively decreased in vulnerable brain regions in thiamine deficiency.

Pyrithiamine-induced thiamine deficiency in the rat exhibits many neuropathological and biochemical similarities to Wernicke's Encephalopathy in human. Activities of constitutive nitric oxide synthase (NOS) were measured in vulnerable (thalamus and cerebellum) and non-vulnerable (hippocampus and striatum) brain regions of pyrithiamine-induced thiamine-deficient rats. NOS activities were significantly decreased in the thalamus (by 26%, P < 0.05) of presymptomatic thiamine-deficient rats compared to pair-fed controls. Following onset of symptoms, in addition to thalamus (-38%, P < 0.01), cerebellum (-50%, P < 0.01) also manifested significantly decreased activities of NOS. Hippocampal and striatal activities of NOS were unchanged at both presymptomatic and symptomatic stages of thiamine deficiency. Selectively decreased activities of neuronal NOS in the thalamus and the cerebellum extends the previous observations of region-selective metabolic changes and, ultimately, neuronal cell loss observed in thiamine deficiency.

Animals↗
PubMed2005

Functional vulnerability of developing central nervous system to maternal thiamine deficiencies in the rat.

Thiamine deficiency (B1 vitamin) was induced during three periods of rat central nervous system (CNS) ontogenesis. Females were fed a thiamine deficient diet such that developing offspring were exposed either to pre-, peri-, or postnatal thiamine deficiency. To control the effects of undernourishment generated by different thiamine deficiencies, every treatment group had its own pair-fed control pup from a non drug-treated but undernourished dam. Seven different developmental abilities (exploratory activity, emotional reaction, hind paws lifting reflex, wire grasping times, crawling and leap execution latencies, and nociception) were recorded in the offspring from the 10th to the 45th postnatal day. The vulnerability of developing brain to the specific lack of B1 vitamin increases from prenatal (28%) to perinatal (43%) and postnatal periods (57%).

Animals↗
PubMed2001

Chorea induced by thiamine deficiency in hemodialysis patients.

Thiamine deficiency is mainly encountered in alcoholics or food faddists, but it may complicate chronic dialysis because of low intake and accelerated loss of thiamine in dialysis patients. We report here 2 hemodialysis (HD) patients who developed chorea induced by thiamine deficiency. We propose that thiamine deficiency, with a consequent dysfunction of the basal ganglia, may induce chorea in HD patients.

Aged↗
PubMed1993

Reappraisal of regional thiamine content in the central nervous system of the normal and thiamine-deficient mice.

The regional distribution of thiamine and its phosphate esters was measured in the central nervous system (CNS) of normal and thiamine-deficient mice. Twelve small areas were punched out from frozen sections and they were individually analyzed by high performance liquid chromatography (HPLC). Regional difference was noted in both the content and ratio of thiamine and its phosphate esters in the normal CNS. In pyrithiamine-induced thiamine deficiency, thiamine pyrophosphate (TPP) content in all the areas was reduced to less than 13% of the control values on day 10, when the neurological signs developed. Although there were considerable regional variations in the reduction rate of thiamine and its phosphate esters, no correlation was established between the severity of tissue damage and the magnitude of thiamine reduction in individual areas. These results indicate that a derangement in TPP-dependent processes, either alone or in combination with other factors, plays a more critical role in the neuronal damage under thiamine deficiency than depletion of thiamine compounds per se.

Animals↗
PubMed2004

Increased brain endothelial nitric oxide synthase expression in thiamine deficiency: relationship to selective vulnerability.

Thiamine deficiency results in selective neuronal cell death in thalamic structures. Previous studies provide evidence for a role implicating nitric oxide (NO) in the pathogenesis of cell death due to thiamine deficiency. In order to ascertain the origin of increased NO in the thiamine deficient brain, expression of endothelial nitric oxide synthase isoform (eNOS), was measured in the medial thalamus and in the inferior colliculus and compared to the frontal cortex (a spared region) of rats in which thiamine deficiency was induced through a feeding protocol of thiamine-deficient diet concomitant with daily administration of pyrithiamine, a central thiamine antagonist. eNOS mRNA and protein expression were significantly increased as a function of the severity of neurological impairment and the degree of neuronal cell loss in the medial thalamus and in the inferior colliculus. These findings suggest that the vascular endothelium is a major site of NO production in the brain in thiamine deficiency and that eNOS-derived NO could account for the selective damage to the thalamic structures that are observed in this particular disorder.

Animals↗
PubMed1975

Glucose uptake in the brainstem of thiamine-deficient rats.

Acute dietary deficiency of thiamine was produced in immature female rats. Uptake of glucose by brainstem nuclei was determined by autoradiographic examination of tissue concentrations of 14-C-3-O-methyl-d-glucose following a test dose, and compared with levels in normal and isocaloric control animals. The experiment showed that glucose uptake was depressed in the lesions of thiamine deficiency as compared with the controls, that the depression occurred with the occurrence of morphologic evidence of tissue edema, and that the depression was temporally independent of the breakdown of the blood-brain barrier to protein which is found in the late, necrotic lesions.

Animals↗
PubMed1976

Cycloleucine uptake in the brainstem of thiamine-deficient rats.

Immature female rats were subjected to acute dietary deficiency of thiamine. An autoradiographic method was used in the semi-quantitative determination of concentration of 1-aminocyclopentane-1-carboxylic acid-carboxylic-14C (cycloleucine) in brainstem regions after intravenous administration of tracer quantities. The time course of tissue concentrations was followed and compared with that of normal and isocaloric control animals. Our data indicate that thiamine deficiency of sufficient magnitude to induce brainstem lesions has an effect on the transport of cycloleucine. The initial 2 min values in the nuclear areas are appreciably reduced whereas the 6 min values are significantly elevated as compared with controls; no change was demonstrated in the white matter of the inferior cerebellar peduncle. The effect on transport appears to be more on the mechanism of efflux than of influx in terms of blood brain barrier function.

Amino Acids↗
PubMed1977

Thiamine pyrophosphokinase activity in liver, heart and brain crude extracts of control and thiamine deficient rats.

The activity of thiamine pyrophosphokinase has been measured in liver, heart muscle and brain of normal and thiamine deficient rats. The activity measurement has been performed by use of thiamine-35S as substrate and separation of the reaction products by high voltage electrophoresis. KM has been determined as 7.1.10(-6) mol/l. The activity of thiamine pyrophosphokinase is reduced in liver and heart muscle of thiamine deficient rats significantly, whereas no decrease of the enzyme activity has been found in the brain. The content of thiamine pyrophosphate has been measured in the liver of normal and thiamine deficient rats. Injection of thiamine to deficient rats normalized the content of thiamine pyrophosphate in the liver within 6 hours. Our data suggest that thiamine pyrophosphokinase is an adaptive enzyme, the activity of which depends on the thiamine content of the cells.

Animals↗
PubMed1991

Enzyme-cytochemical study of small ganglion cells in experimental thiamine deficiency: concerning the pain mechanism.

In an effort to clarify the mechanism of pain accompanying thiamine deficiency, thiamine monophosphatase (TMPase) activity was demonstrated, by means of electron microscopic cytochemistry, in small ganglion cells in pyrithiamine-treated thiamine-deficient rats. TMPase activity was seen to be present in the reticular part of the Golgi complex and vesicle-like bodies around the trans side of the Golgi complex. By the 10th day after the initial pyrithiamine treatment, a significant increase in the number of TMPase-positive vesicle-like body was observed. These results indicate that thiamine deficiency causes a disturbance in the transportation and/or production of TMPase, which is an integral part of the synaptic transmission of the nociception impulses.

Animals↗
PubMed1980

Thiamin deficiency in the lamb: changes in thiamin phosphate esters in the brain.

Concentration of thiamin (unphosphorylated), thiamin monophosphate (TMP), thiamin diphosphate (TDP), and thiamin triphosphate (TTP) were measured in three regions of the brain of seven pairs of lambs. The lambs were maintained on a thiamin-free synthetic diet for 2, 3, or 4 weeks. Controls were pair-fed and supplemented with thiamin. The three brain regions were: (1) dorso-lateral aspect of the cortex [common site for lesions of polioencephalomalacia (PEM)]; (2) pyriform lobe of the cortex (no PEM lesions are found here); (3) white matter of the internal capsule (no PEM lesions found here). The concentration of TTP ina ll three sections of brain was maintained at control values for up to 4 weeks on the thiamin-deficient diet. TDP concentration decreased to 22% of control values in both regions of grey matter after 4 weeks on the diet. Unphosphorylated thiamin and TMP decreased to a smaller extent than TDP.

Animals↗
PubMed1994

Thiamine deficiency in hospitalized elderly patients.

Necropsy studies suggest that thiamine deficiency is underdiagnosed in life, in part because the classical clinical presentations are uncommon. Anecdotal reports suggest that thiamine deficiency may contribute to the development of delirium, heart failure and peripheral neuropathy in elderly patients, but little systematic research has been reported. We examined thiamine levels in 36 consecutive non-demented, community-dwelling patients admitted to an acute geriatric unit. Marginal thiamine deficiency [thiamine pyrophosphate effect (TPPE) 15-24%] was present in 11 (31%) and definite thiamine deficiency (TPPE > 25%) in 6 (17%) patients. Delirium occurred in 6/19 (32%) patients with normal thiamine status and 13/17 (76%) thiamine-deficient patients (p < 0.025, chi 2 test). One or more other possible causes for delirium were present in all cases. One patient had ocular signs and a dramatic clinical response to vitamin B complex therapy. Absent ankle jerks were noted in 2/19 (10%) patients with normal thiamine status and 7/17 (41%) patients with thiamine deficiency (p = 0.06). There was no difference in anthropometric indices or in the prevalence of other nutrient deficiencies between the two groups. Thiamine deficiency is common in elderly patients admitted to hospital and may contribute to the development of delirium.

Aged↗