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PubMed2001

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 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.

Animals↗

PubMed1983

Metabolic and histological reversibility of thiamine deficiency.

The rapid improvement in the clinical manifestations of thiamine deficiency with thiamine supplementation is well known. To study this process in more detail, we rendered rats thiamine deficient either by dietary deprivation alone (DD) or, in addition, by daily pyrithiamine administration (DD + PT). We observed the cerebral metabolic and histological responses of these rats after 1 or 7 days of thiamine supplementation both prior to and at the onset of clinical sequelae. The cerebral metabolic response to thiamine deficiency and replenishment was determined with the [14C]deoxyglucose technique for measurement of local cerebral glucose utilization (LCGU). Our results indicate that thiamine replenishment reverses the LCGU changes resulting from thiamine deprivation of short duration. However, prolonged thiamine deprivation may result in LCGU changes that are not completely reversible by thiamine replenishment, before the appearance of the clinical or histological consequences of thiamine deficiency.

Animals↗

PubMed1987

Muricidal suppression by chlorpheniramine and changes in brain levels following dietary-induced thiamine deficiency in rats.

The effects of thiamine deficiency on pharmacological and pharmacokinetic activities of chlorpheniramine were investigated in rats. Chlorpheniramine (5-10 mg/kg) showed a dose-dependent suppressive effect on muricide induced by thiamine deficiency. The ED50 value for muricidal suppression at 1 hr was approximately 7.1 mg/kg (95% confidence limits, 5.4-9.3 mg/kg) after oral administration. Using a high-performance liquid chromatographic (HPLC) method, chlorpheniramine was detectable at 10 min in the blood and brain of rats. The present pharmacokinetic data suggest that chlorpheniramine can easily pass through the blood-brain barrier (B.B.B.) and enter the brain. It is stored therein and is later slowly released and excreted. In thiamine deficient rats, chlorpheniramine entered the brain in much higher concentrations than in normal and pair-fed rats, and significantly higher levels were maintained for a period of 1.5 hr. These results suggest that thiamine deficiency affects pharmacological and pharmacokinetic activities in rats, and support the view that there is a malfunction of the B.B.B. in thiamine deficient rats. These factors should be taken into consideration in clinical usage and dosage.

Aggression↗

PubMed1999

Thiamine deficiency and malaria in adults from southeast Asia.

BACKGROUND: Thiamine deficiency (beriberi) is common in some parts of southeast Asia. Acute thiamine deficiency can mimic many complications of malaria, such as encephalopathy and lactic acidosis. We examined the incidence of thiamine deficiency in adults admitted to hospital with malaria in Thailand. METHODS: For this prospective study, we recruited consecutive patients with malaria or other febrile illness who presented to Paholpolpayuhasena Hospital, Kanchanaburi, Thailand, between May and July, 1992. We used the activation coefficient (alpha) for transketolase activity in erythrocytes to measure thiamine deficiency (defined as alpha>1.31) in patients with severe and uncomplicated malaria and in controls (patients' relatives and healthy volunteers). To exclude the possibility of interference in the assays, transketolase activity was also measured in erythrocytes used to culture parasites. FINDINGS: 12 (52%) of 23 patients with severe malaria and ten (19%) of 54 patients with uncomplicated malaria had alpha values above the normal range (p<0.0001 and p=0.0014, respectively, compared with controls), which indicated severe thiamine deficiency. Thiamine deficiency was more severe in patients with cerebral malaria than in those with uncomplicated malaria and the controls (p=0.008). INTERPRETATION: In adults admitted to hospital in Thailand, thiamine deficiency commonly complicates acute falciparum malaria, particularly in severe infections, and could contribute to dysfunction of the central nervous system.

Acidosis, Lactic↗

PubMed1991

In thiamine deficiency, activation of erythrocyte transketolase by thiamine in vivo exceeds activation by cofactor in vitro.

In 60 thiamine deficient patients, the mean erythrocyte transketolase activity after activation by thiamine diphosphate cofactor in vitro, representing the apparent sum of holoenzyme and apoenzyme activities, was 0.609 (SD 0.166) U/g Hb before thiamine therapy and rose to 0.772 (SD 0.152) U/g Hb immediately after the administration of thiamine to the patients. The difference between these values, 0.163 (SD 0.130) U/g, is the mean activity of transketolase protein which can be activated by thiamine in vivo but not by thiamine diphosphate in vitro. This difference correlated with low initial erythrocyte transketolase activity in these patients, but not with their alcohol intake, liver function or diagnoses.

Alcoholism↗

PubMed1987

Decrease of high affinity ouabain binding in rat cerebellum and hypothalamus by thiamin deficiency.

The effect of dietary thiamin deficiency on high affinity [3H]ouabain binding was examined in different regions of rat brain. The binding activity in the cerebellum and hypothalamus was significantly lower in the thiamin-deficient group than in the pair-fed control and freely fed control groups. The decrease was due to a change in Bmax but not in Kd. The results suggest a possible involvement of (Na+,K+)-ATPase in neurological manifestations of thiamin deficiency.

Adenosine Triphosphatases↗

PubMed2002

Thiamine deficiency in hepatitis C virus and alcohol-related liver diseases.

Thiamine deficiency is a common feature in chronic alcoholic patients, and its pathophysiology remains poorly understood. Until now, thiamine deficiency has been considered to be mainly the result of alcoholism irrespective of the underlying liver disease. The aims of the study were to compare the prevalence of thiamine deficiency in alcohol- and hepatitis C virus-(HCV-) related cirrhosis and in patients with chronic hepatitis C without cirrhosis. Forty patients with alcoholic cirrhosis (group A), 48 patients with HCV-related cirrhosis (group B), and 59 patients with chronic hepatitis C without cirrhosis (group C) were included prospectively. Thiamine status was evaluated by concomitant determination of erythrocyte transketolase activity, thiamine diphosphate (TDP) effect, and direct measurement of erythrocyte thiamine and its phosphate esters by HPLC. Thiamine was mainly present in erythrocytes in its diphosphorylated form. Prevalence of thiamine deficiency and levels of TDP in thiamine-deficient patients were similar in patients of group A (alcoholic cirrhosis) and of group B (viral C cirrhosis). None of the patients with chronic hepatitis (group C) was deficient. Thiamine deficiency was not correlated with the severity of the liver disease or disease activity. No impairment of thiamine phosphorylation was found in the three groups. conclusion, alcoholic or HCV-related cirrhotics have the same range of thiamine deficiency, while no patient without cirrhosis has thiamine deficiency, and impaired phosphorylation does not account for the deficiency observed in cirrhotics. We suggest that thiamine should be given to patients with cirrhosis irrespective of its cause.

Chromatography, High Pressure Liquid↗

PubMed1988

Regional changes in brain histamine levels following dietary-induced thiamine deficiency in rats.

Histamine levels in thiamine deficient rats were significantly lower in the hippocampus, amygdala, olfactory bulb, thalamus and pons-medulla oblongata than those of normal and pair-fed groups. In the case of the hypothalamus, thiamine deficiency produced a significant increase in histamine levels. These changes observed in the thiamine deficient group were reversed to the normal levels by supplying the normal diet. These data present a new finding that thiamine deficiency affects the central histaminergic neuron system as well as other monoaminergic systems.

Animals↗

PubMed1978

Lipogenesis in the brain of thiamine-deficient rat pups.

(1) The effect of thiamine deficiency during pregnancy and lactation on lipogenesis in the brain of rat pups was determined. (2) Acetate incorporation to brain lipids in thiamine-deficient rats in vivo was no less than in pair fed control rats, apart from slightly reduced fatty acid synthesis in the cerebrum. (3) Glucose incorporation to brain lipids in vivo was considerably reduced in thiamine-deficient pups. (4) The inducible NADP dependent malic enzyme activity was increased in thiamine-deficient pup brains. (5) The synthesis of acetyl-CoA appears to be the rate limiting step in lipogenesis in thiamine-deficient pup brains.

Acetates↗

PubMed1979

Effect of 5-hydroxytryptophan on muricide response induced by thiamine deficiency.

Male Wistar rats maintained on a thiamine deficient diet showed the mouse-killing response (muricide). On the 30th day of experimental feeding, the incidence of the muricide response was 78% in the thiamine deficient group. Intraperitoneal (i.p.) injection of 5-hydroxytryptophan (5-HTP) suppressed the muricide response in a dose-dependent manner. The suppressive effect of 5-HTP on the muricide response was potentiated by pretreatment with Ro4-4602. On the 20th day of experimental feeding, the incidence of the muricide response was 42.9% in the thiamine deficient group, 14.3% in the pair-fed group and 0% in the control group, respectively. The incidence increased to 92.5% in the thiamine deficient rats 24 hr after the i.p. injection of 100 mg/kg parachlorophenylalanine. The results of the present sutdy indicate that the injection of 5-HTP was effective in suppressing the muricide response induced by thiamine deficiency.

5-Hydroxytryptophan↗

PubMed1987

Thiamine deficiency in black male hostel-dwellers. The need for thiamine supplementation of sorghum beer.

Some indices of nutrition have been examined in hostel- and non-hostel-dwelling groups of industrially employed black males. Hostel-dwellers in the large metropolitan areas have to prepare their own food and many are accustomed to excessive alcohol intake, especially of sorghum beer. In the two groups studied, blood levels of vitamin B12, folate, pyridoxal and albumin were similar, but erythrocyte thiamine levels were significantly lower in the hostel-dwellers. Although the proportion of subjects with elevated levels of gamma-glutamyltransferase, an index of alcoholic liver disease, was similar in the two groups, thiamine-deficient hostel-dwellers had a greater proportion of elevated values suggesting that thiamine deficiency was related to both inadequate diet and excessive alcohol consumption. Fortification of sorghum beer with thiamine might prevent or reduce thiamine deficiency in this group. The cost would not materially affect the price of the beer.

Adult↗

PubMed1982

Effect of a single, large dose injection of pyrithiamin on the thiamin deficiency of the mouse.

The effect of pyrithiamin on thiamin deficient mice was studied clinically and pathologically. Thiamin deficiency was produced in the mice fed with a thiamin deficient diet by a single injection of pyrithiamin (10 mg/kg, s.c.) on day 0 to produce a mild illness and on day 14 to produce a severe disorder. Clinically, the mild illness showed only Wooley-White sign and histologically, it was characterized by edema in the thalamus, mammillary bodies, and pontine tegmentum. The severe illness showed convulsion and multiple hemorrhages in the same area. This pyrithiamin-induced thiamin deficient animal model can also be useful for research on thiamin deficient encephalopathy.

Animals↗

PubMed1978

[Enzyme-histochemical behaviour of the tanycyte ependyma in the III. ventricle of the rat with thiamin deficiency (author's transl)].

The influence of experimental thiamine deficiency in rats on enzyme-histochemical parameters was carried out in the diencephalon. The degree of thiamine deficiency was measured by the activity coefficient of transketolase in the red blood cells. The alpha-ETK of thiamine deficient animals was 1,45 +/- 0,36, of equal-fed animals 1,04 +/- 0.04 and of control animals 1,08 +/- 0,04. We got the following results: Lactatdehydrogenase, acid phosphatases and thiamine pyrophosphatase did not indicate any difference in enzyme activity between the groups of control, equal-fed and thiamine deficient rats. However, the enzyme activity of nonspecific lysosome-bound esterases in the tanycyte ependyma and in the investigated nuclear regions (nucleus supraopticus, ncl. paraventricularis, ncl. ventromedialis) of the thiamine deficient animals was significantly decreased in comparison to control and equal-fed animals. The possibility of a restriction of the hypophyseal-adrenal-cortex-system is discussed, since the results are similar to those obtained with bilaterally adrenalectomized rats.

Acid Phosphatase↗

PubMed1990

Effects of thiamine deficiency on hepatic cytochromes P450 and drug-metabolizing enzyme activities.

To elucidate the mechanisms by which thiamine deficiency affects hepatic microsomal monooxygenase activities, the effect of thiamine deficiency on two constitutive cytochrome P450 isozymes, P450IIE1 and P450IIC11, was investigated, using weanling male Sprague-Dawley rats. The clinical signs of thiamine deficiency were apparent after feeding a thiamine-deficient diet for 3 weeks. Thiamine deficiency caused an increase in P450IIE1, which was determined by N-nitrosodimethylamine demethylase assay and immunoquantitation of P450IIE1. This increase in the P450IIE1 level was mainly attributed to thiamine deficiency per se but not to dietary restriction. Ketone bodies were not elevated in thiamine-deficient rats, whereas ketone bodies were elevated and may have served as inducing factors in calorically restricted pair-fed animals. Injections of pyruvate or pyrithiamine in addition to thiamine deficiency did not potentiate the induction effect. On the other hand, thiamine deficiency did not affect the level of P450IIC11 during the 3 weeks of feeding the thiamine-deficient diet. In addition, thiamine deficiency increased cytosolic glutathione S-transferase activity but not steroid isomerase activity. The present study demonstrates the specificity of thiamine deficiency per se in the induction of P450IIE1 which does not involve an increase in the ketone body level.

Animals↗

PubMed1989

Acceleration of ethanol metabolism by past thiamine deficiency.

Six months after severe thiamine deficiency, when their body and liver weights had normalized, male Sprague-Dawley rats were exposed to constant ethanol vapor concentrations for 6 days in an inhalation chamber and blood ethanol concentrations (BECs) were determined. Previously induced thiamine deficiency was associated with about a 50% reduction of BECs and a significant increase in liver alcohol dehydrogenase (ADH) activity suggesting a persistent acceleration of ethanol metabolism. No significant changes were found in liver aldehyde dehydrogenase activity, plasma levels of thyroxine, testosterone, or estradiol, or brain or liver histology. Plasma growth hormone concentrations were about 60% lower in the experimental group than in controls, but this effect of previous thiamine deprivation did not correlate with changes in ADH activity. Therefore, it remains to be elucidated how thiamine deficiency-induced central nervous system alterations may contribute to the development of metabolic tolerance to ethanol.

Alcohol Dehydrogenase↗

PubMed2001

Thiamine deficiency in patients with B-chronic lymphocytic leukaemia: a pilot study.

Malignancy associated primary thiamine deficiency has been documented in several experimental tumours, sporadic clinical case reports, and in a number of patients with fast growing haematological malignancies. Thiamine status was assessed prospectively in 14 untreated B-chronic lymphocytic leukaemia (CLL) patients, and in 14 age matched control patients with non-malignant disease. Patients with any known cause of absolute, relative, or functional thiamine deficiency were excluded. High (>15%) thiamine pyrophosphate effect (TPPE), indicating thiamine deficiency, was found in five out of 14 CLL patients (35.7%) and in none of the controls (p=0.057). Mean (SD) TPPE in the thiamine deficient patients group was 21.6 (3.4)%. In all the patients, thiamine deficiency was subclinical. No correlates for the thiamine deficiency have been found save for an increment of more than 20% in the total leucocyte count over the preceding three months, which was found in all five thiamine deficient patients compared with only one of the nine non-thiamine deficient CLL patients. Thus, CLL patients may be prone to develop primary thiamine deficiency possibly promoted by the increased leucocytes span, which may increase thiamine consumption. Since even subclinical thiamine deficiency may be detrimental to the patient's clinical course, and in view of the theoretical danger of thiamine promoted tumour cell proliferation, further large scale studies are warranted to confirm this observation, and to elucidate the issue of thiamine supplementation to CLL patients.

Aged↗

PubMed1978

Thiamin deficiency effects on rat leukocyte pyruvate decarboxylation rates.

Thiamin status usually is assessed by urinary excretion of thiamin or by exogenous thiamin pyrophosphate (TPP) stimulation of erythrocyte transketolase activity. Because of the possible great utility of a biologically and chemically sensitive alternative method for thiamin status assessment, studies were made of rat leukocyte pyruvate decarboxylation activity in thiamin deficiency. Pyruvate decarboxylation rates were determined by assaying 14CO2 produced by leukocytes from 1-14C-pyruvic acid in vitro. Reaction conditions were 5 mumoles pyruvic acid, 2.2 X 10(4) DPM 1-14C-pyruvic acid, leukocytes from 5 ml whole blood, 50 mumoles NaH2PO4, 5 mumoles MgSO4, and 1 mumole MnSO4 at pH 7.4 in 1 ml reaction volume at 25 C. Four weeks of thiamin deficiency decreased leukocyte pyruvate decarboxylation rates and markedly increased the TPP effect on this reaction. Dual weekly assays in the same rats showed that 21 days of thiamin deficiency significantly increased the TPP effect on leukocyte pyruvate decarboxylation rates. In contrast, the TPP effect on erythrocyte transketolase activity was significantly increased after only 7 days of thiamin deficiency. Erythrocyte transketolase is more sensitive than leukocyte pyruvate decarboxylation rate to early thiamin deficiency in rats.

Animals↗

PubMed1991

Influence of thiamin supplementation on the health and general well-being of an elderly Irish population with marginal thiamin deficiency.

The effect of thiamin supplementation on the health and general well-being of 80 randomly selected healthy elderly Irish women, from a population with marginal thiamin deficiency, was studied. Key variables affecting thiamin status were controlled. Weekly dietary intakes, subjective feelings, and activity assessments were measured during a 4-week baseline and 6-week double blind treatment period. Clinical assessments were performed during the last week of each period. For treatment, subjects were randomly assigned to either thiamin (10 mg daily) or placebo groups. Compared to baseline and placebo supplemented values, thiamin-supplemented women experienced significantly increased appetite, energy intake, body weight and general well-being, and decreased fatigue. Thiamin supplementation also tended to reduce daytime sleep time, improve sleep patterns, and increase activity. These data suggest that evaluation of thiamin status is indicated when nonspecific conditions such as anorexia, weight loss, fatigue, depression, and sleep disorders are present in elderly persons.

Activities of Daily Living↗