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PubMed1980

An experimental study of thiamine metabolism in acute ethanol intoxication.

A dose of 3.9 g/kg b.wt of ethanol was administered to rabbits, and ethanol and thiamine concentrations, transketolase activity and thiamine pyrophosphate (TPP) effect in blood samples were determined. It was established that ethanol ingestion produced a rapid decrease in blood thiamine levels and transketolase activity in erythrocytes and an increase in TPP effect in erythrocytes. These values reverted to normal within 2 or 3 days after the ingestion of alcohol.

Alcoholic Intoxication↗
PubMed1987

Ethanol-induced alteration in thiamin status of young turkey poults.

The effect of ethanol on thiamin status was determined in the turkey poult, a new animal model for alcohol-induced cardiomyopathy in humans. The poults were given ethanol (4 to 5% v/v) in the drinking water for six weeks post-hatch. This treatment decreased body weights and increased significantly the relative weights of the hearts. Ethanol consumption increased significantly the blood concentrations of pyruvate and lactate, decreased the activity of erythrocyte transketolase (TK), and increased the stimulation of TK activity of thiamin pyrophosphate (TPP) in lyzed blood cells (TPP effect). These findings indicate that ethanol treatment has an adverse effect on the thiamin status of the turkey poult.

Animals↗
PubMed1995

Improved left ventricular function after thiamine supplementation in patients with congestive heart failure receiving long-term furosemide therapy.

PURPOSE: We have previously found thiamine (vitamin B1) deficiency in patients with congestive heart failure (CHF) who had received long-term furosemide therapy. In the present study, we assessed the effect of thiamine repletion on thiamine status, functional capacity, and left ventricular ejection fraction (LVEF) in patients with moderate to severe CHF who had received furosemide in doses of 80 mg/d or more for at least 3 months. PATIENTS AND METHODS: Thirty patients were randomized to 1 week of double-blind inpatient therapy with either i.v. thiamine 200 mg/d or placebo (n = 15 each). All previous drugs were continued. Following discharge, all 30 patients received oral thiamine 200 mg/d as outpatients for 6 weeks. Thiamine status was determined by the erythrocyte thiamine-pyrophosphate effect (TPPE). LVEF was determined by echocardiography. RESULTS: TPPE, diuresis, and LVEF were unchanged with i.v. placebo. After i.v. thiamine, TPPE decreased (11.7% +/- 6.5% to 5.4% +/- 3.2%; P < 0.01). LVEF increased (0.28 +/- 0.11 to 0.32 +/- 0.09; P < 0.05), as did diuresis (1,731 +/- 800 mL/d to 2,389 +/- 752 mL/d; P < 0.02), and sodium excretion (84 +/- 52 mEq/d to 116 +/- 83 mEq/d, P < 0.05). In the 27 patients completing the full 7-week intervention, LVEF rose by 22% (0.27 +/- 0.10 to 0.33 +/- 0.11, P < 0.01). CONCLUSIONS: Thiamine repletion can improve left ventricular function and biochemical evidence of thiamine deficiency in some patients with moderate-to-severe CHF who are receiving longterm furosemide therapy.

Aged↗
PubMed1991

Thiamine responsive anemia: report of a new case associated with a thiamine pyrophosphokinase deficiency.

We report a new case of thiamine responsive anemia in a three years old boy with the characteristic association of anemia, diabetes mellitus and deafness. Thiamine therapy corrected anemia as described. A thiamine pyrophosphokinase deficiency (TPK) was found which was not influenced by treatment. However normal levels of thiamine pyrophosphate (TPP) were obtained without correction of all symptoms particularly dyserythropoïesis. Thus, etiology of the syndrome is not only a thiamine pyrophosphokinase deficiency as previously suggested.

Abnormalities, Multiple↗
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↗
PubMed1996

Biochemical evidence of thiamine depletion during the Cuban neuropathy epidemic, 1992-1993.

During an epidemic outbreak of neuropathy in Cuba during 1992-1993, blood and urine samples were collected from 107 persons with confirmed neuropathy, from 106 control subjects without clinical abnormality who were broadly matched with the affected persons by age and domicile, and from 537 unmatched subjects, also free from clinical abnormality. The unmatched subjects lived in two locations in Cuba; at each location they were drawn from two age ranges: 11-15-y-old secondary school students and 16-64-y-old adults. Measurements of urinary thiamine and blood transketolase and its activation with thiamine pyrophosphate were made. For the neuropathy subjects, these measurements were repeated after 3 wk of rehabilitation. All groups showed biochemical evidence of thiamine depletion affecting 30-70% of their members, which is a high prevalence. Severity of biochemical depletion was, however, no greater in the neuropathy subjects than in the control subjects (P > 0.05). However, it was greater in Pinar del Rio, where the incidence of disease was higher, than in the city of Havana, where less disease was seen. Although the majority of the affected subjects responded biochemically to a daily oral multivitamin supplement containing thiamine (P < 0.001), in some cases normal biochemical status was not achieved even after 3 wk of intensive treatment. In the affected group, thiamine status was inversely correlated with the amount of alcohol consumed (P = 0.007). Thiamine status at the outset was correlated with clinical outcome after treatment. Although neither thiamine depletion nor alcohol abuse were likely to have been the sole cause of the neuropathy epidemic, they may have been contributory factors. Thiamine supplementation or food fortification may therefore be necessary in Cuba.

Adolescent↗
PubMed1992

Role of thiamine status in sulphur induced polioencephalomalacia in sheep.

The effects of excess dietary sulphur were studied in sheep supplemented and unsupplemented with thiamine. The diets contained either 0.19 per cent sulphur (LS) or 0.63 per cent sulphur (HS) in combinations with 14 mg kg-1 thiamine (LB1) or 243 mg kg-1 thiamine (HB1). A total of 56 two-month-old lambs were used. Groups consisting of nine, nine, 22 and 16 lambs were fed LS-LB1, LS-HB1, HS-LB1 and HS-HB1 diets, respectively for 14 weeks. Out of 22 lambs fed the HS-LB1 diet, seven lambs developed neurological signs between the third and eighth week of the trial. Two of these lambs died, three that were in extremis were euthanased, and two recovered completely. All clinically affected animals had extensive malacic lesions in the cerebral cortex, midbrain and brainstem. None of the lambs from the LS groups or HS-HB1 group developed clinical signs. Several clinically normal lambs from the HS-LB1 group had necrotic lesions in their brains at gross and microscopic examination. Supplementation with dietary thiamine prevented development of clinical signs, but did not totally prevent development of microscopic brain lesions. Brain thiamine concentration, transketolase activity and thiamine pyrophosphate (TPP) effect were not different (P greater than 0.05) among groups. There was a strong effect (P less than 0.0001) of dietary thiamine supplementation on blood thiamine concentration and TPP effect. Blood thiamine concentration was higher whereas TPP effect was lower in the thiamine supplemented sheep. Blood and tissue thiamine concentrations in sheep exposed to high dietary sulphur did not indicate either systemic or local thiamine deficiency per se. Increased TPP effect in sheep fed the HS-LB1 diet indicated mild to moderate metabolic thiamine deficiency. Thiamine inadequacy may be an effect of an increased requirement for thiamine in animals exposed to excess dietary sulphur.

Animals↗
PubMed1985

Effect of some monoamine oxidase inhibitors on the thiamin status of rabbits.

The monamine oxidase (MAO) inhibitors harmaline, tranylcypromine, deprenyl, clorgyline and iproniazid were injected intraperitoneally for five days to rabbits at doses that produced significant MAO inhibition. The first three inhibitors raised the concentrations of pyruvate and lactate in blood, decreased the activity of erythrocyte transketolase (TK) and increased the thiamin pyrophosphate (TPP) effect. The drugs also produced anorexia and loss of body weight. The changes were suggestive of an adverse effect on the thiamin status. Clorgyline and iproniazid, however, raised the blood concentrations of pyruvate and lactate but did not affect significantly erythrocyte TK activity or TPP effect. Treatment of rabbits for 14 days with the thiamin antagonists pyrithiamine (20 micrograms kg-1) or oxythiamine (0.8 mg kg-1) produced a significant drop in TK activity and increase in the lactate and pyruvate concentrations as well as an increase in TPP effect. Pyrithiamine (5, 10 or 20 micrograms kg-1, 14 days) lowered significantly the activity of MAO in the liver and brain of rabbits. Treatment with the other antagonist, oxythiamine, at doses of 0.2 or 0.4 mg kg-1 for 14 days had no significant effect on MAO activity. At a dose of 0.8 mg kg-1 a significant drop in MAO activity occurred. A pair-feeding trial indicated that the biochemical changes produced in animals treated with MAO inhibitors were attributable to the drugs per se, and not to the ensuing anorexia. Thiamin (100 micrograms kg-1, subcutaneously) when given concomitantly with pyrithiamine, oxythiamine, harmaline, deprenyl and tranylcypromine was effective in preventing the development of thiamin deficiency.

Animals↗
PubMed2000

Prevalence of thiamin deficiency in anorexia nervosa.

OBJECTIVE: Deficiency of thiamin (vitamin B1) causes a range of neuropsychiatric symptoms that resemble those reported in patients with anorexia nervosa (AN) but the prevalence of thiamin deficiency in AN has not been reliably established. This study was designed to investigate the prevalence of thiamin deficiency in AN. METHOD: Thirty-seven patients attending a specialist eating disorders unit and meeting all or some of the DSM-IV criteria for AN were compared with 50 blood donor controls. All subjects underwent measurement of erythrocyte transketolase activation following the addition of thiamin pyrophosphate, the standard biochemical test for thiamin deficiency. Deficiency was defined as a result more than 2 SD above the mean of the control population. RESULTS: Fourteen patients (38%) had results in the deficient range; 7 (19%) met the most stringent published criterion for deficiency. Deficiency was not related to duration of eating restraint, frequency of vomiting, or alcohol consumption. DISCUSSION: Thiamin deficiency may account for some of the neuropsychiatric symptoms of AN and routine screening or supplementation may be indicated.

Adolescent↗
PubMed2005

Data mining of the transcriptome of Plasmodium falciparum: the pentose phosphate pathway and ancillary processes.

The general paradigm that emerges from the analysis of the transcriptome of the malaria parasite Plasmodium falciparum is that the expression clusters of genes that code for enzymes engaged in the same cellular function is coordinated. Here the consistency of this perception is examined by analysing specific pathways that metabolically-linked. The pentose phosphate pathway (PPP) is a fundamental element of cell biochemistry since it is the major pathway for the recycling of NADP+ to NADPH and for the production of ribose-5-phosphate that is needed for the synthesis of nucleotides. The function of PPP depends on the synthesis of NADP+ and thiamine pyrophosphate, a co-enzyme of the PPP enzyme transketolase. In this essay, the transcription of gene coding for enzymes involved in the PPP, thiamine and NAD(P)+ syntheses are analysed. The genes coding for two essential enzymes in these pathways, transaldolase and NAD+ kinase could not be found in the genome of P. falciparum. It is found that the transcription of the genes of each pathway is not always coordinated and there is usually a gene whose transcription sets the latest time for the full deployment of the pathway's activity. The activity of PPP seems to involve only the oxidative arm of PPP that is geared for maximal NADP+ reduction and ribose-5-phosphate production during the early stages of parasite development. The synthesis of thiamine diphosphate is predicted to occur much later than the expression of transketolase. Later in the parasite cycle, the non-oxidative arm of PPP that can use fructose-6-phosphate and glyceraldehyde-3-phosphate supplied by glycolysis, becomes fully deployed allowing to maximize the production of ribose-5-phosphate. These discrepancies require direct biochemical investigations to test the activities of the various enzymes in the developing parasite. Notably, several transcripts of PPP enzyme-coding genes display biphasic pattern of transcription unlike most transcripts that peak only once during the parasite cycle. The physiological meaning of this pattern requires further investigation.

Animals↗
PubMed1981

Erythrocyte transketolase activity in alcoholic liver disease.

Erythrocyte transketolase activity and its stimulation in vitro by the addition of thiamine pyrophosphate (TPP effect) was measured in 64 normally nourished alcoholics with well-compensated liver disease and in 20 control subjects. Biochemical evidence of thiamine deficiency as judged by low transketolase activity was found in 19 alcoholics (29.7%). In 5 of these 19 patients the TPP effect was abnormally high, indicating depleted thiamine stores. IN the other 13 patients the TPP effect was either normal or low, suggesting a deficiency or an inability to use the transketolase apoenzyme, probably as a result o long-standing thiamine deficiency or the presence of liver disease. a further eight patients (12.5%) had normal transketolase activity but a low TPP effect, perhaps reflecting failure of hte coenzyme TPP to recombine with the transketolase apoenzyme in the presence of normal thiamine stores. There was no relationship between transketolase activity and the daily alcohol consumption, the duration of alcoholism, or the histological severity of the liver disease. Thiamine should be given routinely to alcoholics even if their diet appears adequate and their liver disease is minimal or well compensated.

Aged↗
PubMedDate not supplied

What the practicing nurse should know about thiamine.

Thiamine (vitamin B1) is an essential nutritional component that acts as a coenzyme in the oxidative decarboxylation of alpha-keto acids. It also serves as the connection between the glycolytic cycle and the high energy-producing Krebs (or citric acid) cycle. Unlike other B vitamins, it activates the guanylate cyclase/cyclic guanosine monophosphate (GMP) system but not the adenylate cyclase system. The active coenzyme, thiamine pyrophosphate (TPP) is an antiberiberi substance. Thiamine itself is a pharmacologic antagonist of acetylcholine, which may explain the nerve lesions caused by thiamine deficiency. Liver, pork, yeast, and rice-polishings are rich in thiamine; however, several antithiamine factors are also found in common foods. For example, a thermal labile factor in the viscera of fresh water fish and tea leaves antagonizes thiamine.

Fluid Therapy↗
PubMed1989

Acute pernicious beriberi in a patient receiving parenteral nutrition. A case report.

Parenteral nutrition is being used increasingly in the treatment of the critically ill patient but it causes complications and metabolic derangement. A patient receiving parenteral nutrition in whom protracted vomiting from intestinal obstruction led to the development of acute cardiovascular beriberi (Shoshin) with severe metabolic acidosis--probably lactic--is described. The acidosis was refractory to bicarbonate infusion and inotropic support but the administration of intravenous thiamine 100 mg resulted in a dramatic recovery. Biochemical confirmation of thiamine deficiency was obtained by the measurement of an elevated thiamine pyrophosphate level (24.4%). The patient received thiamine 2.4 mg weekly, a dose that proved insufficient. Thiamine deficiency should be considered when patients receiving parenteral nutrition develop metabolic acidosis with a wide anion gap, even if vitamin supplementation appears adequate.

Acidosis↗
PubMed1984

Improved determination of transketolase activity in erythrocytes.

We describe a new and better method for determining transketolase (EC 2.2.1.1) activity in human erythrocytes. Heating the hemolysate (55 degrees C, 5 min) inactivates transaldolase (EC 2.2.1.2), the enzyme that catalyzes the formation of fructose 6-phosphate and erythrose 4-phosphate from sedoheptulose 7-phosphate and glyceraldehyde 3-phosphate. The net effect is that the quantity of sedoheptulose 7-phosphate formed more precisely represents the transketolase activity, which is unaffected under these conditions. Use of ribosephosphate isomerase (EC 5.3.1.6) and ribulose-phosphate 3-epimerase (EC 5.1.3.1) to establish an equilibrium among the pentoses allowed us to confirm the stoichiometry of the transketolase reaction. We also discuss the effect of thiamin pyrophosphate, which is used to reflect thiamin deficiency.

Adult↗
PubMedDate not supplied

[Effect of thiamine and its derivatives on acetylcholinesterase activity of the blood and brain of albino mice].

Thiamine, thiaminepyrophosphate and 4-methyl-5-beta-oxyethylthiazole are studied for their effect on the acetylcholinesterase activity in the brain, blood plasma and cells. The activity of acetylcholinesterase in blood cells is shown to be inhibited most of all by thiamine and thiazole. Acetylcholinesterase of the brain has been efficiently inhibited only by thiamine pyrophosphate.

Acetylcholinesterase↗
PubMed2001

Thiamin auxotrophy in yeast through altered cofactor dependence of the enzyme acetohydroxyacid synthase.

The THI1 gene of Saccharomyces cerevisiae has been identified and found to be allelic with the previously characterized gene ILV2 that encodes acetohydroxyacid synthase (AHAS). This enzyme catalyses the first step in the parallel biosyntheses of the branched-chain amino acids isoleucine and valine, using thiamin pyrophosphate (TPP) as a cofactor. The ilv2-thi1 allele encodes a functional AHAS enzyme with an altered dependence for the cofactor TPP resulting in the thiamin auxotrophic phenotype. Nucleotide sequence analysis and site-directed mutagenesis revealed that the thi1 mutation is a single base substitution which causes the conserved amino acid substitution D176E in the AHAS protein. This study therefore implicates aspartate 176 as another amino acid residue important either for the efficient binding of TPP by AHAS or for the functional stability of the holoenzyme.

Acetolactate Synthase↗
PubMed2005

The electrochemical investigation of the catalytic power of pyruvate decarboxylase and its coenzyme.

The change in the energy barriers for the heterogeneous reduction of pyruvate decarboxylase (PDC) relative to its coenzyme, thiamin pyrophosphate (ThPP), was determined experimentally using square wave voltammetry (SWV) to be 5.3 kcal/mol. These results are in agreement with those of reaction rate acceleration provided by thiamin-dependent decarboxylases relative to their coenzyme as determined kinetically based on the pK(a) suppression by the enzyme environment.

Catalysis↗