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PubMed1979

Cardiovascular effects of exercise in hamsters with experimental thiamine deficiency.

The hemodynamic effects of daily treadmill exercise were evaluated in hamsters with experimental thiamine deficiency to test the hypothesis that increased energy consumption might be a contributory factor in the pathogenesis of beriberi heart disease. Daily exercise enhanced thiamine deficiency and was manifested by earlier development of symptoms of neuropathy compared to non-exercised animals. Hemodynamics of exercised thiamine deficient animals were characterized by significantly lower O2 consumption, lower cardiac output, and lower left ventricular minute work, compared to exercised, pair-fed control animals. Left ventricular end-diastolic pressure was slightly but not significantly higher in thiamine deficient animals. Left ventricular function, therefore, was depressed in this group. There was no evidence of hyperkinetic circulation, cardiomegaly or congestive heart failure. Neuropathy and depressed ventricular function, characteristic of pure thiamine deficiency, were observed in the absence of high cardiac output or high output failure, the pathogenesis of which may require other unknown factors.

Animals↗
PubMed1989

Effects of thiamine deficiency on brain metabolism: implications for the pathogenesis of the Wernicke-Korsakoff syndrome.

Chronic alcoholism results in thiamine deficiency as a consequence of inadequate dietary intake and of impaired absorption of the vitamin. In addition, there is evidence to suggest that alcohol reduces thiamine phosphorylation to thiamine pyrophosphate (TPP) in brain. TPP is a cofactor for the pyruvate dehydrogenase complex (PDHC), alpha-ketoglutarate dehydrogenase (alpha KGDH) and transketolase (TK), three enzymes involved in cerebral glucose and energy metabolism. Pyrithiamine-induced thiamine deficiency in the rat results in early, selective, reversible reductions of alpha KGDH in brain; PDHC activities are unaffected. Reductions of alpha KGDH are accompanied by decreased aspartate, glutamate and GABA and by concomitantly increased alanine in the brain of thiamine-deficient animals. It is suggested that decreased alpha KGDH, rather than decreased PDHC constitutes 'the biochemical lesion' in thiamine deficiency encephalopathy first enunciated by Peters in the 1930s. If sufficiently prolonged and severe, thiamine deficiency results in brain cell death. Possible mechanisms involved include compromised cerebral energy metabolism and focal accumulation of lactate, both of which could result from decreased activities of alpha KGDH. In addition, it is proposed that brain cell death in severe thiamine deficiency may result from excessive release of excitotoxic amino acids. Comparable mechanisms could be involved in the cell death and in the pathogenesis of the thiamine-unresponsive symptoms of the Wernicke-Korsakoff Syndrome in humans.

Alcohol Amnestic Disorder↗
PubMedDate not supplied

The effects of single and repeated episodes of thiamin deficiency on memory in alcohol-consuming rats.

The underlying pathogenesis of Korsakoff's syndrome, an amnesic disorder most commonly found in alcoholics, is not well understood. Chronic alcoholism is associated with thiamin deficiency and current thinking is that this may be the causal factor. In Experiment 1, rats were given a 20% (v/v) ethanol/water mix as their only source of fluid for 156 days. Three groups were made thiamin deficient through the combination of a thiamin-deficient diet and the centrally acting thiamin antagonist pyrithiamin hydrobromide, after 4, 15, and 26 weeks exposure to ethanol, respectively. The control group was given ad lib access to laboratory chow and water throughout this period. There were no differences between groups on either the working or reference versions of the Morris water tank paradigm. In Experiment 2, to test the hypothesis that a single bout of thiamin deficiency, with or without concurrent alcohol intake, is not sufficient to cause severe memory impairments, two groups of rats were subjected to three bouts of thiamin deficiency. One of these groups consumed an ethanol/water mix, the other tap water. A third group was made thiamin deficient on only one occasion. The control group was not made thiamin deficient and consumed lab chow and tap water throughout. Once again, there were no between-group differences in the data derived from testing in either the eight-arm radial maze or the Morris water tank task. These experiments indicate that the aetiology of Korsakoff's syndrome is more complex than previously thought.

Alcohol Drinking↗
PubMed2003

[Acute encephalopathy due to thiamine deficiency with hyperammonemia in a chronic hemodialysis patient: a case report].

Hemodialysis(HD) patients are at risk for thiamine deficiency because of low intake and accelerated loss of thiamine during HD. We report here an HD patient, an 82-year-old woman, who developed acute encephalopathy due to thiamine deficiency with hyperammonemia. She was admitted to Nishikawa Town Hospital due to pneumonia and was treated with ABPC/SBT for one week. While she was cured of pneumonia, she had a persistently poor appetite. On the twenty-fourth day after admission, HD with intradialytic parenteral nutrition(IDPN), which consisted of 10% glucose 500 ml, in order to correct her malnutrition, was started. She suddenly presented confusion, speech disturbance and ophthalmoplegia. HD with IDPN was stopped after two hours because of her symptoms. Laboratory studies disclosed plasma glucose of 186 mg/dl and serum ammonium of 155 micrograms/dl. Arterial blood gas analysis(inhaling 3 l/min O2) showed severe metabolic acidosis and respiratory acidosis (pH 7.138, pCO2 44.8 mmHg, pO2 108.9 mmHg, HCO3- 15.1 mmol/l). Her malnutrition, unexplained metabolic acidosis and neurological presentation raised the suspicion of acute encephalopathy due to thiamine deficiency. Fursultiamine 100 mg was administered intravenously. After two hours, metabolic acidosis disappeared (pH 7.437, pCO2 33.9 mmHg, pO2 161.0 mmHg, HCO3- 22.9 mmol/l), and she regained her clear consciousness and serum ammonium decreased at 16 micrograms/dl on the next morning. Serum lactate and thiamine level were shown later to be 57.5 mg/dl and 27 nmol/l, respectively. Her clinical course suggests that the glucose load including IDPN may have caused deterioration of the neurological disorder under the condition of thiamine deficiency. Furthermore, it is possible that a relationship exists between thiamine deficiency and hyperammonemia.

Acidosis, Lactic↗
PubMed1987

Oxalate metabolism in thiamine-deficient rats.

Male weanling rats were maintained on a thiamine-deficient diet for 4 weeks, and compared with ad libitum and pair-fed controls. Thiamine deficiency led to slow growth and finally a decrease in body weight. Liver and kidney weights of the deficient rats were low, but appropriate to the body weight. Thiamine deficiency also caused a significant decrease in erythrocyte transketolase levels. The decarboxylation of glyoxylate both via the glyoxylate oxidation cycle and alpha-ketoglutarate:glyoxylate (alpha-KG:GA) carboligase was significantly lower in the liver and kidney mitochondria, leading to accumulation of glyoxylate in the tissues and its excretion in the urine. Part of the accumulated glyoxylate is converted to oxalate, causing hyperoxaluria.

Aldehyde-Ketone Transferases↗
PubMed1985

Clinical and subclinical thiamine deficiency in clinical practice.

Six patients with gross thiamine deficiency found during normal psychiatric practice in England are described. Two surveys of newly admitted psychiatric patients are recounted. A major degree of biochemical deficiency, with or without minimal clinical manifestations, was found. Only three (1%) of 326 patients surveyed had gross clinical deficiency. It is thought that severe thiamine deficiency, though rare in the Western countries, has not been eradicated. Deficiency may cause psychiatric conditions like Wernicke's encephalopathy or may be a secondary feature in mental illness due to anorexia, in reduced food intake, and in poor nutrition. The importance of being aware of the possibility for correct diagnosis is emphasised.

Aged↗
PubMed1990

Altered contractile properties of rat cardiac muscle during experimental thiamine deficiency and food deprivation.

Alterations of cardiac contractility caused by thiamine deficiency were studied on three groups of 2 month old male Wistar rats: B1, fed a thiamine deficient diet, PF pair fed, which received an amount of thiamine free diet determined on the daily consumption of B1 animals, supplemented with appropriate thiamine supply, C ad libitum fed controls. The animals were studied after 35 days of dietary treatment. Force-velocity curves were determined in right ventricle papillary muscles. Shortening velocity was significantly lower in B1 and PF than in C muscles and in B1 than in PF muscles. The ability to develop tension was not altered. Myosin ATPase activity was assayed in preparations of myofibrils and in preparations of purified myosin. Both Ca-Mg activated myofibrillar ATPase activity and Ca-activated myosin ATPase activity were significantly reduced in B1 and PF compared to C myocardium. Furthermore Ca-activated ATPase activity was lower in B1 than in PF myocardium. Myosin isoenzyme distribution was determined by pyrophosphate gel electrophoresis of purified myosin preparations. When compared to C animals both B1 and PF animals showed a myosin electrophoretic pattern shifted towards the slow isoform V3; such a shift was more pronounced in B1 animals. Information concerning excitation-contraction coupling was obtained by determining the steady state and transient force-interval relation and by recording transmembrane action potential. B1 and PF myocardium exhibited, when compared to C, a less sensitivity to a reduction of the interval of stimulation, a faster mechanical restitution, a prolonged action potential duration. Such alterations were generally more pronounced in B1 than in PF myocardium. The results support the view that in the rat cardiac contractility is deeply affected by thiamine deficiency. The alterations of cardiac contractility seem to be caused by adaptive mechanisms rather than by cardiac failure and seem to be attributable for a big part to the reduction of food supply.

Action Potentials↗
PubMed1981

Sodium deprivation during thiamin deficiency in rats: hormonal, histological, and behavioral responses.

Adrenal function, determined by adrenocortical hormone measurement and histological studies, was examined in adult rats fed on of the following four diets for four weeks: thiamin-sufficient, sodium-adequate (+B/+Na) or inadequate (+B/-Na); and thiamin-deficient, sodium-adequate (-B/+NA) or inadequate (-B/-Na). Thiamin-deficiency significantly depressed plasma and urinary aldosterone responses to sodium deprivation; on the other hand, thiamin status had no consistent significant effect on aldosterone levels in sodium-adequate rats. Plasma corticosterone levels were significantly elevated by thiamin deficiency and yet unaffected by sodium deprivation. Histological examination of the adrenal glands in thiamin-deficient rats revealed a suboptimal zona glomerulosa response to sodium deprivation. Juxtaglomerular granulation in the kidneys indicated that renin secretion was adequate in thiamin-deficient rats. In another experiment, salt (NaCl) appetite development was confirmed in adult rats fed the -B/+Na diet. A direct role of aldosterone in producing salt appetite in thiamin-deficient rats seems unlikely since aldosterone levels were essentially unchanged in rats fed the -B/+Na diet. Instead, the elevated corticosterone levels in thiamin-deficient rats suggest a general stress mechanism for salt appetite development of which the reduced aldosterone response to sodium deprivation is a symptom.

Adrenal Glands↗
PubMed1999

Increased "peripheral-type" benzodiazepine receptor sites and mRNA in thalamus of thiamine-deficient rats.

"Peripheral-type" benzodiazepine receptors (PTBRs) are highly expressed on the outer mitochondrial membrane of several types of glial cells. In order to further elucidate the nature of the early glial cell changes in thiamine deficiency, PTBR sites and PTBR mRNA were measured in thalamus, a brain structure which is particularly vulnerable to thiamine deficiency, of thiamine-deficient rats at presymptomatic and symptomatic stages of deficiency. PTBR sites were measured using an in vitro binding technique and the selective radio ligand [3H]-PK11195. PTBR gene expression was measured by RT-PCR using oligonucleotide primers based upon the published sequence of the cloned rat PTBR. Microglial and astrocytic changes in thalamus due to thiamine deficiency were assessed using immunohistochemistry and antibodies to specific microglial (ED-1) and astrocytic (GFAP) proteins respectively. Significant increases of [3H]-PK11195 binding sites and concomitantly increased PTBR mRNA were observed in thalamus at the symptomatic stage of thiamine deficiency, coincident with severe neuronal cell loss and increased GFAP-immunolabelling (indicative of reactive gliosis). Positron Emission Tomography using 11C-PK11195 could provide a novel approach to the diagnosis and assessment of the extent of thalamic damage due to thiamine deficiency in humans with Wernicke's Encephalopathy.

Animals↗
PubMed1979

Biochemical and histological studies on thiamine-deficient and ethanol-fed rats.

Rats were separated into four groups and four different liquid diets were given to each group. Group 1: thiamine-sufficient diet with no ethanol, group 2: thiamine-sufficient diet with ethanol, group 3: thiamine-deficient diet with no ethanol, group 4: thiamine-deficient diet with ethanol. After four weeks, all rats were fasted for 24 hr and then ethanol was given orally to every rat. After one hour, every rat was sacrificed and biochemical and histological analyses were carried out. Transketolase activity in brain and liver decreased in groups 2, 3 and 4. There was significant decrease in transketolase activity in ethanol-fed groups (groups 2 and 4) as compared to control groups (groups 1 and 3). Ethanol concentrations in blood, liver and heart of rats in groups 2 and 4 were higher than in groups 1 and 3. When comparison was made between the thiamine-deficient groups and the corresponding thiamine-sufficient groups, ethanol concentrations in liver and heart were higher in the thiamine-deficient groups. Alcohol dehydrogenase activity in liver decreased significantly in groups 2 and 4. By histological analyses, fatty degeneration was observed in the livers of groups 2 and 4. The degeneration was more prominent in group 4 than group 2. These findings suggest that chronic ethanol administration may impair the ability to metabolize ethanol and the impairment may increase when rats are in the condition of thiamine deficiency.

Alcohol Oxidoreductases↗
PubMed1995

Loss of [3H]kainate and of NMDA-displaceable [3H]glutamate binding sites in brain in thiamine deficiency: results of a quantitative autoradiographic study.

Previous studies suggest that alterations of brain glutamate synthesis and release occur in experimental thiamine deficiency. In order to assess the integrity of post-synaptic glutamatergic receptors in thiamine deficiency, binding sites for [3H]glutamate (displaced by NMDA), [3H]-kainate, and [3H]quisqualate (AMPA sites) were evaluated using Quantitative Receptor Autoradiography in rat brain following 14 days of treatment with the central thiamine antagonist pyrithiamine. Compared to pair-fed controls, brains of symptomatic thiamine-deficient animals contained significantly fewer NMDA-displaceable binding sites in cerebral cortex, medial septum and hippocampus. It has been suggested that NMDA-receptor mediated glutamate excitotoxicity plays a role in the pathogenesis of neuronal loss in thiamine deficiency. If such is the case, the selective loss of NMDA binding sites in cerebral cortex and hippocampus offers a possible explanation for the relative nonvulnerability of these brain regions to pyrithiamine-induced thiamine deficiency. [3H]quisqualate (AMPA) binding sites were unchanged in all brain regions of pyrithiamine-treated rats whereas [3H]kainate sites were significantly reduced in density in medial and lateral thalamus. The decline in these binding sites may be due to neuronal loss in pyrithiamine-induced thiamine deficiency. Alterations of glutamatergic synaptic function involving both NMDA and kainate receptor subclasses could contribute to the pathogenesis of neurological dysfunction in Wernicke's Encephalopathy in humans.

Animals↗
PubMed1989

The increase of histamine levels in the amygdala caused by histidine administration and the suppression of muricide in thiamine deficient rats.

The effects of histidine treatment on histamine levels in brain regions and the muricidal suppression in thiamine deficient rats were examined. Intraperitoneal administration of L-histidine significantly increased the histamine levels in several regions of normal and thiamine deficient rats. A dose of 200 mg/kg of histidine suppressed muricide induced by thiamine deficiency. The histamine levels of those thiamine-deficient killer-rats, whose muricide was suppressed by histidine treatment, were significantly higher in the amygdala, striatum and hypothalamus than of those whose muricide was not suppressed. It is suggested that the activation of central histaminergic neuron systems, especially in the amygdala, may underlie the mechanism of muricidal suppression by histidine treatment in thiamine deficient rats.

Amygdala↗
PubMed1985

Intrauterine growth retardation induced by thiamine deficiency and pyrithiamine during pregnancy in the rat.

The role of nutritional factors in the development of prenatal and postnatal growth retardation is not well understood. We tested if thiamine deficiency may cause intrauterine growth retardation in rats. From the second day of gestation Sprague-Dawley rats were freely fed either a nutritionally complete or a thiamine-deficient diet. A similar group of rats was pair-fed with a complete or a thiamine-deficient diet and daily pyrithiamine injections (50 micrograms/100 gm of body weight) were given to precipitate thiamine deficiency during the short gestation of the rat. Maternal thiamine levels in blood and brain tissues, maternal erythrocyte transketolase activity with thiamine pyrophosphate effects, and fetal tissue thiamine levels were measured. The results indicate that feeding a thiamine-deficient diet in conjunction with pyrithiamine injections caused sufficient thiamine deficiency to induce intrauterine growth retardation in the progeny. We conclude that thiamine deficiency alone during in utero development in the rat may contribute to intrauterine growth retardation.

Animals↗
PubMed1983

Enhanced hepatotoxicity and inhibition of liver endoplasmic reticulum calcium pump by CCl4 in rats fed a thiamine deficient diet.

Male Sprague-Dawley rats were fed a thiamine deficient diet for three weeks, then treated with a range of CCl4 doses (0.01-1-ml/kg). Rats fed the deficient diet grew more slowly (body weight 65 percent of control) and had elevated liver glutathione (GSH) (220 percent of control). CCl4 hepatotoxicity, assessed by serum glutamicpyruvic transaminase (SGPT) activity and histological examination 24 hours after the hepatotoxin, was augmented in the group fed the thiamine deficient diet. Likewise, CCl4 inhibition of liver endoplasmic reticulum (ER) function (glucose-6-phosphatase (G6Pase) and calcium pump activities one hour after CCl4) was enhanced in rats fed the deficient diet. These results suggest that thiamine deficiency enhances CCl4 damage to membranes of the ER and enhances CCl4 hepatotoxicity.

Alanine Transaminase↗
PubMedDate not supplied

Brain lactate synthesis in thiamine deficiency: a re-evaluation using 1H-13C nuclear magnetic resonance spectroscopy.

Region-selective accumulation of brain lactate occurs in TD; however, the mechanisms responsible have not been elucidated fully. (1)H and (13)C nuclear magnetic resonance (NMR) spectroscopy were therefore used to investigate de novo lactate synthesis from [1-(13)C]glucose in vulnerable (medial thalamus) and nonvulnerable (frontal cortex) brain regions of rats made thiamine deficient by administration of the central thiamine antagonist pyrithiamine. De novo synthesis of lactate was increased in the medial thalamus to 148% and 226% of pair-fed control values at presymptomatic and symptomatic stages of thiamine deficiency, respectively, whereas no such changes were observed in the frontal cortex. Administration of a glucose load selectively worsened the changes in medial thalamus. Pyruvate recycling and peripherally derived lactate did not contribute significantly to the lactate increase within the thiamine-deficient brain. Increases in immunolabeling of the lactate dehydrogenase isoenzymes (LDH1 and LDH5) were observed in the medial thalamus of thiamine-deficient animals. Metabolic impairment due to thiamine deficiency thus results in increased glycolysis, increased LDH immunolabeling of neurons and astrocytes and increased de novo synthesis of lactate in brain regions vulnerable to thiamine deficiency. These results are consistent with the notion that focal lactate accumulation participates in the worsening of neurologic symptoms in thiamine-deficient patients.

Analysis of Variance↗
PubMed2003

Alcoholic neuropathy is clinicopathologically distinct from thiamine-deficiency neuropathy.

Characteristics of alcoholic neuropathy have been obscured by difficulty in isolating them from features of thiamine-deficiency neuropathy. We assessed 64 patients with alcoholic neuropathy including subgroups without (ALN) and with (ALN-TD) coexisting thiamine deficiency. Thirty-two patients with nonalcoholic thiamine-deficiency neuropathy (TDN) also were investigated for comparison. In ALN, clinical symptoms were sensory-dominant and slowly progressive, predominantly impairing superficial sensation (especially nociception) with pain or painful burning sensation. In TDN, most cases manifested a motor-dominant and acutely progressive pattern, with impairment of both superficial and deep sensation. Small-fiber-predominant axonal loss in sural nerve specimens was characteristic of ALN, especially with a short history of neuropathy; long history was associated with regenerating small fibers. Large-fiber-predominant axonal loss predominated in TDN. Subperineurial edema was more prominent in TDN, whereas segmental de/remyelination resulting from widening of consecutive nodes of Ranvier was more frequent in ALN. Myelin irregularity was greater in ALN. ALN-TD showed a variable mixture of these features in ALN and TDN. We concluded that pure-form of alcoholic neuropathy (ALN) was distinct from pure-form of thiamine-deficiency neuropathy (TDN), supporting the view that alcoholic neuropathy can be caused by direct toxic effect of ethanol or its metabolites. However, features of alcoholic neuropathy is influenced by concomitant thiamine-deficiency state, having so far caused the obscure clinicopathological entity of alcoholic neuropathy.

Adult↗
PubMed1978

[Free amino acid concentration in the tissues of rats with different forms of thiamine deficiency].

The levels of free amino acids in rat tissues under thiamine deficiency induced by antivitamin (oxithiamine) and under thiamine-deficient diet were studied. Changes in the amino acid pool at these two forms of vitamin B1 deficiency were revealed. The most typical change consists in extensive accumulation of alanine and glutamate with a simultaneous decrease in the amount of many other essential and non-essential amino acids. The disturbances in the amino acid pool under thiamine deficiency may be probably regarded as resulting from inhibition of alpha-keto acid dehydrogenase activities.

Amino Acids↗