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At least 19 recordsLinked to original sources
PubMed1982

Intestinal thiamin transport in rats. Thiamin and thiamin phosphoester content in the tissue and serosal fluid of everted jejunal sacs.

Rat everted jejunal sacs were incubated at 37 degrees C for 15-60 min in Krebs-Henseleit buffer, pH 7.4, with or without (control experiments) 0.2 microM [thiazole-2-14C]-thiamin. The determination of thiamin and its phosphoesters in the sac wall and in serosal fluid was carried out by an electrophoretic micromethod. Irrespective of the presence of 14C-thiamin, the tissue content of endogenous thiamin pyro- and triphosphate decreased during the incubation, whilst that of thiamin-monophosphate remained relatively constant. The tissue content of free thiamin increased substantially only in control experiments. Endogenous free thiamin, together with a small amount of monophosphate, was found to enter the serosal fluid. The transfer of both compounds was greatly enhanced by the incubation with 14C-thiamin, when an efficient thiamin phosphorylation could be demonstrated. During incubation with 14C-thiamin, the concentration of 14C-thiamin-pyrophosphate and, to a lesser extent, that of free 14C-thiamin increased progressively in the tissue, while 14C- thiamin-monophosphate content remained almost unchanged. No 14C-thiamin-triphosphate was detected. There was a rapid increase in the tissue specific radioactivity of free thiamin and thiamin-monophosphate, which preceded the rise in the specific radioactivity of thiamin-pyrophosphate. The specific radioactivities of the former compounds in the serosal fluid reflected those observed in the intestinal tissue. These results are interpreted as evidence suggesting that the active transport of thiamin is efficient only when intracellular thiamin phosphorylation is operating.

Animals↗
PubMed1997

Dietary thiamin supply during lactation influences thiamin status in lactating rats and their offspring and the thiamin level in milk.

This study was conducted to examine the effect of dietary thiamin, ranging from deficient to excessive supplies, on thiamin status of lactating rats and their offspring, and the thiamin level in milk. Therefore, after parturition, rat dams were divided into eight groups of 10 each, and were fed diets with 0, 2, 4, 6, 7, 40, 350 and 3500 mg/kg thiamin over a total of 13 days during lactation. Milk for determining the thiamin concentration was obtained from day 6 and 13 of lactation. At day 14 of lactation rat dams and their offspring were used to ascertain the thiamin status including transketolase activity of blood, liver and brain, and thiamin concentration in body. Thiamin supplies ranging from deficient to excessive dietary concentrations influenced both the thiamin levels of the lactating dams and their offspring within 13 days. Lactating rat dams fed a thiamin-free diet and their offspring were classified as thiamin-deficient on the basis of growth retardation and a lower activity of transketolase in blood, liver and brain. Within these variables transketolase in blood has been shown to be most sensitive, and reached a plateau feeding 6 mg/kg thiamin. The concentration of thiamin in milk ranged between 0.1 and 19 mg/kg. The findings also show that dietary thiamin had the strongest effect on thiamin in milk obtained from day 6 and 13 of lactation, and a deficient or suboptimal supply with thiamin was therefore not compensated for an intensified transfer of reserved body thiamin into milk. Also thiamin levels in tissues and carcass, which did not show any clear-cut saturation characteristic, increased with increasing dietary thiamin, and this dose-dependence was more marked in blood and liver than in carcass.

Animals↗
PubMed1972

Biosynthetic pathway of thiamine pyrophosphate: a special reference to the thiamine monophosphate-requiring mutant and the thiamine pyrophosphate-requiring mutant of Escherichia coli.

Two types of mutants of Escherichia coli were isolated, one of which (mutant 70-23-107) responded to thiamine pyrophosphate, and the other (mutant 70-23-102) to thiamine monophosphate and thiamine pyrophosphate. They were produced by further mutation of a thiamine auxotroph of E. coli 70-23 with N-methyl-N'-nitro-N-nitrosoguanidine. The parent organism required thiamine because phosphohydroxymethylpyrimidine kinase activity was lacking in this organism, and hydroxymethylpyrimidine pyrophosphate was not permeable through the cell membrane of E. coli. Thiamine, thiamine monophosphate, and thiamine pyrophosphate were all equally active for the parent, whereas mutants 70-23-102 and 70-23-107 lost their ability to grow on thiamine. Both mutants differed only in the growth response to thiamine monophosphate: the former could grow on thiamine monophosphate, whereas the latter could not. Experimental results with the newly isolated mutants indicate that in E. coli the free form of thiamine is not involved in de novo synthesis of thiamine pyrophosphate, but thiamine monophosphate, an exclusive product formed by the reaction between hydroxymethylpyrimidine pyrophosphate and hydroxyethylthiazole monophosphate, is directly phosphorylated to form thiamine pyrophosphate. Exogenous thiamine, on the other hand, is converted to thiamine pyrophosphate via the intermediate formation of thiamine monophosphate.

Cell-Free System↗
PubMed1980

Thiamine and cholinergic transmission in the electric organ of Torpedo. I. Cellular localization and functional changes of thiamine and thiamine phosphate esters.

The electric organ of Torpedo marmorata was found to contain as much as 120 +/- 24 nmol of thiamine per g of fresh tissue. The vitamin was distributed as nonesterified thiamine (32%), thiamine monophosphate (22%), thiamine diphosphate (8%), and an important proportion of thiamine triphosphate (38%). A high level of thiamine triphosphate was found in synaptosomes isolated from the electric organ. In contrast, the synaptic vesicles did not show any enrichment in thiamine, whereas they contained a marked peak of acetylcholine (ACh) and ATP. Thus thiamine seems to be very abundant in cholinergic nerve terminals; its localization is apparently extravesicular, either in the axoplasm or in association with plasma membrane. When calcium was reduced and magnesium increased in the external medium, the efficiency of transmission was diminished, owing to inhibition of ACh release; in a parallel manner the degree of thiamine phosphorylation was found to increase--this condition is known to modify the repartition of ACh between vesicular and extravesicular compartments. Electrical stimulation, which causes periodic variations of the level of ACh and ATP, also caused significant changes in thiamine esters. In addition, related changes of the vitamin and the transmitter were observed under other conditions, suggesting a functional link between the metabolism of thiamine and that of ACh in cholinergic nerve terminals.

Acetylcholine↗
PubMed1992

Blood and serum thiamin and thiamin phosphate esters concentrations in patients with alcohol dependence syndrome before and after thiamin treatment.

The blood and serum concentrations of free thiamin and its three phosphate esters were determined concomitantly by a new high-performance liquid chromatography (HPLC) method in 30 patients with alcohol dependence syndrome on admission to hospital and 24 hr after thiamin injection. We studied 24 men and 6 women; mean age, 50 years (range 21 to 69); mean ethanol consumption during the last 30 days, 164 +/- 119 g/day. A control group included 40 healthy volunteers (25 men, 15 women), of whom 10 were given the same thiamin injection as were the patients. Thiamin monophosphate was significantly reduced in the patients compared with controls before treatment (men 2.9 +/- 2.3 and 5.9 +/- 3.1 nmol/liter) and after (8.1 +/- 5.1 and 19.5 +/- 8.1 nmol/liter). On admission, free thiamin and thiamin diphosphate were similar in controls and in patients in whole blood (B) and serum (S) and increased similarly after treatment (mean B-thiamin diphosphate in male patients: 149 +/- 64 to 238 +/- 88 nmol/liter, in controls: 179 +/- 40 to 289 +/- 18 nmol/liter). However, seven patients had extremely high free thiamin values. The phosphorylation ratio was lower in patients than in controls (p less than 0.05), before and after treatment. Finally, the mean B-diphosphate was lower in patients not taking vitamins (116 +/- 48 nmol/liter and 172 +/- 57 nmol/liter) and in patients with polyneuropathy (118 +/- 54 nmol/liter and 173 +/- 52 nmol/liter), compared with the other patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Distribution of thiamine, thiamine phosphates, and thiamine metabolizing enzymes in neuronal and glial cell enriched fractions of rat brain.

The distribution of thiamine, thiamine phosphoesters, and the thiamine pyrophosphate synthetizing [thiamine-pyrophosphokinase (TPKase)] as well as hydrolyzing [thiamine pyrophosphatase (TPPase) and thiamine monophosphatase (TMPase)] enzymes was determined in neuronal and glial enriched fractions prepared from rat brain. Nucleoside diphosphatases [inosine diphosphatase (IDPase) and uridine diphosphatase (UDPase)] and nucleoside monophosphatases [uridine monophosphatase (UMPase) and inosine monophosphatase (IMPase)] were also determined. Thiamine and thiamine mono- and pyrophosphate were present in neuronal enriched fractions at concentrations 2.8, 3.6, and 4.6 times higher than in glial fractions. TMPase was found only in glial enriched fractions, whereas the levels of TPKase, UMPase, IMPase, IDPase, UDPase, and TPPase were 2.0-, 2.2-, 1.3-, 2.8-, 3.7-, and 20.8-fold higher in neuronal than in glial fractions.

Animals↗
PubMed1990

Thiamine, thiamine phosphates and thiamine metabolizing enzymes in synaptosomes of rat brain.

Thiamine and thiamine mono-, pyro- and triphosphate were found at detectable levels in synaptosomes isolated from whole rat brain. Synaptosomes prepared from whole brain, cerebellum and medulla were also found to contain uridine and inosine mono- and diphosphatases as well as the thiamine pyrophosphate synthetizing and hydrolyzing enzymes, but no thiamine monophosphatase. By isoelectric focusing on thin layer polyacrylamide gel of Triton X-100 homogenates of synaptosomes, thiamine pyrophosphatase activity could be separated into 10 bands with different isoelectric points. The contents of thiamine compounds and enzymes in synaptosomes were generally lower than those found in neuronal cell bodies.

Animals↗
PubMed1982

Effects of treatment with thiamin antagonists, oxythiamin and pyrithiamin and of thiamin excess of the levels and distribution of thiamin in rat tissues.

Levels of thiamin and its derivatives in brain, heart and liver were determined in control, thiamin-deficient, pyrithiamin-treated and oxythiamin-treated rats at various times after the start of treatment. With 10 micrograms of thiamin/100 g/day subcutaneously, rats rapidly lost thiamin from the tissues until growth maintenance levels were reached. Oxythiamin had a minimal further effect on tissue thiamin while pyrithiamin caused further marked reduction. With higher levels of thiamin intake, tissue thiamin levels increased with intakes of up to 150-200 micrograms/100 g/day after which they did not show any further significant increase. Levels of pyrithiamin above 50 microgram/100 g/day for 20 days had only minimal further effect upon tissue thiamin levels over that with 50 micrograms.

Animals↗
PubMed1976

Glycolytic metabolism in cultured cells of the nervous system. IV. The effects of thiamine deficiency on thiamine levels, metabolites and thiamine-dependent enzymes on the C-6 glioma and C-1300 neuroblastoma cell lines.

C-6 glioma and C-1300 neuroblastoma cells were cultured in thiamine deficient and control media. Thiamine levels, transketolase and pyruvate decarboxylase activities, and high energy phosphate metabolites were all measured in deficient and control cells. Thiamine levels in the deficient cells were found to be below the level of detectability. Pyruvate decarboxylase activity was more susceptible to thiamine deficiency in both cell lines than transketolase. In spite of the large decrease in pyruvate decarboxylase activity, high energy phosphate metabolites were not decreased in either cell line. These data indicate that C-6 glioma and C-1300 neuroblastoma cells have the capacity to maintain normal energy metabolites in the presence of large changes in thiamine levels and thiamine dependent enzyme activity.

Cell Line↗
PubMed1986

Oral treatment of polioencephalomalacia and subclinical thiamine deficiency with thiamine propyl disulphide and thiamine hydrochloride.

Thiaminase type I production by Bacillus thiaminolyticus and activity in vitro were repressed by the primary substate thiamine and by thiamine monophosphate and thiamine propyl disulphide. At thiamine concentrations of 300-3000 mumol/l production of active enzyme by B. thiaminolyticus, and activity of purified enzyme, were totally repressed. Growth of B. thiaminolyticus was inhibited by thiamine propyl disulphide at 3000 mumol/l. Activity of purified thiaminase was lost when incubated with ruminal fluid from healthy thiaminase free sheep. Enzyme activity was also lost when exposed to mildly alkaline conditions but was stimulated and stabilized against heat denaturation if treated with dithiothreitol. Thiaminase activities in the ruminal fluids of cases of ovine polioencephalomalacia were repressed within 2 h of oral administration of thiamine propyl disulphide. Blood pyruvate levels and transketolase activities were restored to normal following treatment. Treated animals recovered clinically and were returned to pasture.

Administration, Oral↗
PubMed2003

Simultaneous liquid chromatographic assessment of thiamine, thiamine monophosphate and thiamine diphosphate in human erythrocytes: a study on alcoholics.

An isocratic HPLC procedure for the assessment of thiamine (T), thiamine monophosphate (TMP) and thiamine diphosphate (TDP) in human erythrocytes is described. Several aspects of the procedure make it suitable for both clinical and research purposes: limits of detection and quantification of 1 and 2.5 nmol/l, respectively, recovery of 102% on average (range 93-112%), intra- and inter-day precisions within 5 and 9%, respectively, total elution time 15 min. This analytical methodology was applied to a case-control study on erythrocyte samples from 103 healthy subjects and 36 alcohol-dependent patients at risk of thiamine deficiency. Mean control values obtained were: T=89.6+/-22.7 nmol/l, TMP=4.4+/-6.6 nmol/l and TDP=222.23+/-56.3 nmol/l. T and TDP mean values of alcoholics were significantly lower than those of control cases: T=69.4+/-35.9 nmol/l (P<0.001) and TDP=127.4+/-62.5 nmol/l (P<10(-5)). The diagnostic role of TDP was evaluated and a significant role for thiamine was established in the study of alcohol related problems.

Adolescent↗
PubMed1984

Nervous tissue thiamine metabolism in vivo. I. Transport of thiamine and thiamine monophosphate from plasma to different brain regions of the rat.

The transport of thiamine (T) and thiamine monophosphate (TMP) across the blood-brain barrier was measured in vivo in the rat. Different doses of [14C]T (15-550 nmol) and [14C]TMP (11-110 nmol) were injected into the femoral vein. The content of T and its phosphoesters in blood and brain tissue (cerebellum, pons, medulla and cerebral cortex) 20 s after the injection was determined radiometrically after electrophoretic separation. Blood flow and blood volume in the same regions of the brain was also determined. Both T and TMP entered rapidly the cerebral tissue, where they were found chemically unmodified. The cerebral tissue extracted less than 7% of plasma T. At physiological plasma T concentrations, the rate of transport ranged from 0.43 to 0.65 nmol X g-1 X h-1 with only minor differences among the various regions. T was transported into the nervous tissue by two separate mechanisms: one saturable, that at physiological plasma T levels accounted for 95% (cerebellum) to 91% (cerebral cortex) of the total T taken up, and one non-saturable, that was most efficient in the cerebral cortex. The Km (half-saturation constant) of the former transport mechanism ranged from 1.95 to 2.75 nmol X ml-1 in the 4 areas investigated. Vmax (maximal transport rate) values ranged from 6 to 9 nmol X g-1 X h-1, the highest value being found in the cerebellum. The overall transport rate of TMP was on average 5-10 times as low as that of T and also showed a saturable and a non-saturable component. Both components were slower than those observed for T.

Animals↗
PubMed1974

Inhibition of thiamine pyrophosphate utilization by thiamine or its monophosphate in Escherichia coli.

The growth of a thiamine pyrophosphate auxotroph of Escherichi coli was inhibited by either thiamine or thiamine monophosphate, and the growth of a thiamine monophosphate auxotroph was inhibited by thiamine. The thiamine pyrophosphate-dependent oxidation of pyruvate was inhibited by thiamine with whole cells of the thiamine pyrophosphate auxotroph but not with cell extracts prepared from the same organism. In addition, the thiamine pyrophosphate uptake of the thiamine pyrophosphate auxotroph was inhibited by either thiamine or thiamine monophosphate. Although the thiamine pyrophosphate uptake of a revertant, selected for prototrophy from the thiamine monophosphate auxotroph, was inhibited by thiamine to an extent comparable to that observed with the thiamine monophosphate auxotroph, its growth was no longer inhibited by thiamine. A possible mechanism for the inhibition by thiamine and thiamine monophosphate in the utilization of thiamine pyrophosphate is discussed.

Anaerobiosis↗
PubMed2000

Thiamine for Alzheimer's disease.

BACKGROUND: Vitamin B1 (thiamine) plays an important role in Wernicke-Korsakoff syndrome (a form of amnesia caused by brain damage occurring in long-term alcoholics who rely mainly on alcohol for nutrition). The acute syndrome is normally reversible but may proceed to profound dementia, although its progress can be stopped by a timely injection of a large dose of thiamine. There have been suggestions that thiamine may have a beneficial effect in Alzheimer's disease. OBJECTIVES: The objective of this systematic review is to evaluate evidence of the effect of thiamine for Alzheimer's disease. SEARCH STRATEGY: The Cochrane Controlled Trials Register and the CDCIG Register were searched using the terms 'thiamine*, alzheimer* and vitamin* B1'. Other sources were also searched. SELECTION CRITERIA: All unconfounded, double-blind, randomized trials in which treatment with thiamine was administered for more than a day and compared to placebo in patients with dementia of the Alzheimer's type. DATA COLLECTION AND ANALYSIS: Data were extracted independently by two reviewers, pooled if appropriate and possible, and the pooled odds ratios (95% CI) or the average differences (95% CI) were estimated. No intention-to-treat data were available to be used. MAIN RESULTS: Few data were available for review. The data were compatible with thiamine producing harm, no change or improvement. For measures of cognition, the effect of thiamine was non-significantly worse than placebo on the Mini Mental State Examination score (0-30; high=good) at 12 months: WMD -4.3 (95% CI: -14.4 - +5.8) and at time points 3, 6 and 9 months. Change from baseline analyses showed placebo to be significantly better than thiamine at all time points beyond three months; WMD -4.8 (95% CI: -6.0 to -3.6) at 12 months. There was no statistically significant difference in the test of Verbal Fluency and the Boston Naming Test. These analyses were based only on those who completed the study and not on intention-to-treat analyses. There were no results presented for withdrawal by treatment group. Data on measures of functional autonomy, behaviour, quality of life, dependency, or effect on carer were not available. REVIEWER'S CONCLUSIONS: This review finds no evidence that thiamine is a useful treatment for the symptoms of Alzheimer's disease. The data are so poor and sparse that it is difficult to state almost anything of its effect in Alzheimer's disease. Thiamine cannot be recommended for patients with Alzheimer's disease.

Alzheimer Disease↗
PubMed1999

The effects of maternal thiamine nutrition on thiamine status of the offspring in broiler chickens.

The response of broiler chickens to a wide range of dietary supplementation of thiamine to broiler breeder diet was studied in order to understand the effects of maternal thiamine nutrition on the status of thiamine indices in the offspring. Thiamine, and thiamine pyrophosphate (TPP) content, and alpha-ketoglutarate dehydrogenase (KGDH) activity were measured in hearts from 20 day old chicken embryos and from chickens at 1, 7, 14, and 21 days of age and in blood at 21 days of age. Total thiamine content in the heart of day old chicks was higher in comparison to 20 day old embryos. Maternal supplementation of thiamine increased heart thiamine in the offspring (p < 0.001), and increased the activity of KGDH in the hearts of day old chicks (p < 0.001), but not in the embryo. The TPP content in the heart increased in response to both maternal and offspring thiamine supplementation (p < 0.001), however the effect of broiler thiamine supplementation was largely independent from the maternal effect. The effect of maternal thiamine nutrition on the offspring's heart KGDH activity was apparent, but the responses to broiler supplementation were dependent largely on the maternal effect. Blood TPP content was not affected by maternal thiamine supplementation (p = 0.39), but thiamine supplementation in the offspring diets increased blood TPP (p < 0.001). Both maternal and offspring thiamine supplementation increased blood free base thiamine content (both p < 0.001). It is concluded from this study that maternal thiamine nutrition affects thiamine status indices and thiamine metabolism of the offspring.

Aging↗
PubMed1981

Thiamin transport by rat small intestine "in vitro": influence of endogenous thiamin content of jejunal tissue.

The relationship between thiamin intestinal transport and phosphorylation in vitro was investigated using everted jejunal sacs from normal rats, rats affected with dietary thiamin deficiency at different degrees and relative pair-fed controls; recovered rats, i.e. severely thiamin-deficient animals, 6 hours after the intravenous injection of 1 mg of thiamin chloride/100 g body weight. The sacs were incubated at 37 degrees for 30 min with 0.2 microM 14C-labeled thiamin. During incubation, the endogenous phosphorylated thiamin undergoes a dephosphorylation, which is lowest in thiamin deficient rats. The jejunal sacs from all experimental groups take up and phosphorylate labeled thiamin: the rate is inversely proportional to the endogenous cellular content of phosphorylated thiamin. The net transport of labeled thiamin is enhanced in thiamin-deficient rats. The labeled thiamin net transport after incubation is linearly related to the labeled phosphorylated thiamin content of intestinal tissue. Thiamin repletion of severely thiamin-deficient rats restore the normal levels of endogenous free and phosphorylated thiamin in the intestinal within 6 hours. In addition after incubation, the labeled phosphorylated thiamin content reverts to the levels of the control, while thiamin net transport remains high.

Animals↗
PubMed1989

Identity of soluble thiamine-binding protein with thiamine repressible acid phosphatase in Saccharomyces cerevisiae.

Two secretory glycoproteins of S. cerevisiae, a soluble thiamine-binding protein and a thiamine-repressible acid phosphatase, were shown to be repressed to a similar extent by excess thiamine in the growth medium. Thiamine-repressible acid phosphatase was co-purified throughout the purification of the soluble thiamine-binding protein. Purified and deglycosylated soluble thiamine-binding proteins exhibited both thiamine-binding and acid phosphatase activities on non-denaturing polyacrylamide gel electrophoresis. Heat treatment of the purified soluble thiamine-binding protein caused a decrease in both activities with a similar inactivation profile. Two thiamine-repressible acid phosphatase-defective mutants isolated were found to be also defective in soluble thiamine-binding activity. The uptake of [14C]thiamine phosphate esters, such as thiamine monophosphate and thiamine pyrophsphate, was remarkably impaired in the mutant cells, whereas the uptake of [14C]thiamine by the mutant was almost the same with that by the parent strain. From these results, it was concluded that the soluble thiamine-binding protein is identical to the thiamine-repressible acid phosphatase in S. cerevisiae, which is involved in the hydrolysis of exogenous thiamine phosphate esters in the periplasmic space prior to the uptake of their thiamine moiety by yeast cells.

Acid Phosphatase↗