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G. Rindi - One of the best experts on this subject based on the ideXlab platform.
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Thiamine uptake in human intestinal biopsy specimens including observations from a patient with acute Thiamine deficiency
The American Journal of Clinical Nutrition, 1997Co-Authors: Umberto Laforenza, C. Patrini, C Alvisi, A Faelli, Anna Licandro, G. RindiAbstract:Mucosal biopsy specimens obtained by routine endoscopy from 108 human subjects, including one patient with Thiamine deficiency, were incubated at 37°C in oxygenated calcium-free Krebs-Ringer solution (pH 7.5) containing tritiated Thiamine and [ 14 C]dextran as a marker of adherent mucosal water. The amount of labeled Thiamine taken up was measured radiometrically. In subjects with no clinical evidence of Thiamine deficiency. 1) Thiamine uptake by duodenal mucosa had a hyperbolic time course. reaching equilibrium at 10 min; 2) Thiamine concentrations > colon stomach); and 4) Thiamine uptake was competitively inhibited in the duodenum by Thiamine analogs, albeit with a different order of potency compared with rats, and was blocked by 2,4-dinitrophenol. In the Thiamine-deficient patient, the duodenal saturable uptake was increased, with higher K m and J max values. In conclusion, physiologic concentrations of Thiamine were transported in human small intestine by a specific mechanism dependent on cellular metabolism, whose transporters appear to be down-regulated.
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Thiamine transport by erythrocytes and ghosts in Thiamine-responsive megaloblastic anaemia
Journal of Inherited Metabolic Disease, 1992Co-Authors: G. Rindi, V. Poggi, C. Patrini, B. Vizia, D. Casirola, U. LaforenzaAbstract:A 9-year study of Thiamine metabolism and cellular transport was performed in two patients with Thiamine-responsive megaloblastic anaemia associated with diabetes mellitus and sensorineural deafness, in their relatives, and in age-matched controls from the same area. The ratios between the content of Thiamine and that of its phosphoesters in erythrocytes were within the normal range, whereas the absolute values of Thiamine and Thiamine compounds were reduced by about 40% as compared to controls. Thiamine pyrophosphokinase activity was about 30% lower than in controls. Thiamine treatment restored the levels of Thiamine and Thiamine compounds to normal values, whereas kinase was unaffected. Both the saturable (specific, predominant at low, < 2 µmol/L, physiological concentrations of Thiamine) and the non-saturable component of Thiamine transport were investigated. Erythrocytes and ghosts from patients exhibited no saturable component, this abnormality being specific for the patients and not shared by their parents. It is concluded that the cells from Thiamine-responsive megaloblastic anaemia patients contain low levels of Thiamine compounds, probably due to their inability to take up and retain physiological concentrations of Thiamine, as a result of the lack of the saturable, specific component of transport and reduced Thiamine pyrophosphokinase.
U. Laforenza - One of the best experts on this subject based on the ideXlab platform.
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Thiamine transport by erythrocytes and ghosts in Thiamine-responsive megaloblastic anaemia
Journal of Inherited Metabolic Disease, 1992Co-Authors: G. Rindi, V. Poggi, C. Patrini, B. Vizia, D. Casirola, U. LaforenzaAbstract:A 9-year study of Thiamine metabolism and cellular transport was performed in two patients with Thiamine-responsive megaloblastic anaemia associated with diabetes mellitus and sensorineural deafness, in their relatives, and in age-matched controls from the same area. The ratios between the content of Thiamine and that of its phosphoesters in erythrocytes were within the normal range, whereas the absolute values of Thiamine and Thiamine compounds were reduced by about 40% as compared to controls. Thiamine pyrophosphokinase activity was about 30% lower than in controls. Thiamine treatment restored the levels of Thiamine and Thiamine compounds to normal values, whereas kinase was unaffected. Both the saturable (specific, predominant at low, < 2 µmol/L, physiological concentrations of Thiamine) and the non-saturable component of Thiamine transport were investigated. Erythrocytes and ghosts from patients exhibited no saturable component, this abnormality being specific for the patients and not shared by their parents. It is concluded that the cells from Thiamine-responsive megaloblastic anaemia patients contain low levels of Thiamine compounds, probably due to their inability to take up and retain physiological concentrations of Thiamine, as a result of the lack of the saturable, specific component of transport and reduced Thiamine pyrophosphokinase.
Edouard Delacoux - One of the best experts on this subject based on the ideXlab platform.
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Thiamine Deficiency in Hepatitis C Virus and Alcohol-Related Liver Diseases
Digestive Diseases and Sciences, 2002Co-Authors: Stéphane Lévy, Edouard Delacoux, Christian Hervé, Serge ErlingerAbstract: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.
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Comparison of erythrocyte transketolase activity with Thiamine and Thiamine phosphate ester levels in chronic alcoholic patients
Clinica Chimica Acta, 1995Co-Authors: Cailleau Hervé, P. Beyne, Ph Lettéron, Edouard DelacouxAbstract:The effect of chronic alcoholism on biochemical evaluation of Thiamine status was studied by the concomitant determination of erythrocyte transketolase (ETK) activity, its relative increase by in vitro addition of Thiamine diphosphate (TDP effect) and the direct measurement of Thiamine and its phosphate esters by high performance liquid chromatography. Thirty-eight percent of alcoholic subjects showed a Thiamine deficiency with decreased Thiamine diphosphate concentrations compared with healthy subjects (90.8 ± 25.7 nmol/l vs. 176 ± 28.0 nmol/l, respectively, mean ± S.D., P < 0.001). Thiamine diphosphate concentrations were highly correlated with total Thiamine concentrations and TDP effect (respectively r = 0.99 and 0.79, n = 85, P < 0.001). No abnormality in Thiamine phosphorylation related to chronic alcoholism was noted. Finally, 47% of these deficient alcoholic patients had normal ETK activity. We concluded that, if indirect evaluation of Thiamine status is to be chosen, the determination of ETK activity should be associated with TDP effect since the latter has been shown to be highly linked to total Thiamine and Thiamine diphosphate in erythrocytes. Furthermore, the direct measurement of Thiamine and its phosphate esters was a more sensitive and specific index of Thiamine nutrition. © 1995.
C. Patrini - One of the best experts on this subject based on the ideXlab platform.
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Thiamine uptake in human intestinal biopsy specimens including observations from a patient with acute Thiamine deficiency
The American Journal of Clinical Nutrition, 1997Co-Authors: Umberto Laforenza, C. Patrini, C Alvisi, A Faelli, Anna Licandro, G. RindiAbstract:Mucosal biopsy specimens obtained by routine endoscopy from 108 human subjects, including one patient with Thiamine deficiency, were incubated at 37°C in oxygenated calcium-free Krebs-Ringer solution (pH 7.5) containing tritiated Thiamine and [ 14 C]dextran as a marker of adherent mucosal water. The amount of labeled Thiamine taken up was measured radiometrically. In subjects with no clinical evidence of Thiamine deficiency. 1) Thiamine uptake by duodenal mucosa had a hyperbolic time course. reaching equilibrium at 10 min; 2) Thiamine concentrations > colon stomach); and 4) Thiamine uptake was competitively inhibited in the duodenum by Thiamine analogs, albeit with a different order of potency compared with rats, and was blocked by 2,4-dinitrophenol. In the Thiamine-deficient patient, the duodenal saturable uptake was increased, with higher K m and J max values. In conclusion, physiologic concentrations of Thiamine were transported in human small intestine by a specific mechanism dependent on cellular metabolism, whose transporters appear to be down-regulated.
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Thiamine transport by erythrocytes and ghosts in Thiamine-responsive megaloblastic anaemia
Journal of Inherited Metabolic Disease, 1992Co-Authors: G. Rindi, V. Poggi, C. Patrini, B. Vizia, D. Casirola, U. LaforenzaAbstract:A 9-year study of Thiamine metabolism and cellular transport was performed in two patients with Thiamine-responsive megaloblastic anaemia associated with diabetes mellitus and sensorineural deafness, in their relatives, and in age-matched controls from the same area. The ratios between the content of Thiamine and that of its phosphoesters in erythrocytes were within the normal range, whereas the absolute values of Thiamine and Thiamine compounds were reduced by about 40% as compared to controls. Thiamine pyrophosphokinase activity was about 30% lower than in controls. Thiamine treatment restored the levels of Thiamine and Thiamine compounds to normal values, whereas kinase was unaffected. Both the saturable (specific, predominant at low, < 2 µmol/L, physiological concentrations of Thiamine) and the non-saturable component of Thiamine transport were investigated. Erythrocytes and ghosts from patients exhibited no saturable component, this abnormality being specific for the patients and not shared by their parents. It is concluded that the cells from Thiamine-responsive megaloblastic anaemia patients contain low levels of Thiamine compounds, probably due to their inability to take up and retain physiological concentrations of Thiamine, as a result of the lack of the saturable, specific component of transport and reduced Thiamine pyrophosphokinase.
Hiroshi Nishimura - One of the best experts on this subject based on the ideXlab platform.
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Mutation thi81 causing a deficiency in the signal transduction of Thiamine pyrophosphate in Saccharomyces cerevisiae.
FEMS microbiology letters, 1997Co-Authors: Hiroshi Nishimura, Yuko Kawasaki, Kazuto Nosaka, Yoshinobu KanekoAbstract:We isolated a strain carrying a recessive constitutive mutation (thi81) for the expression of Thiamine metabolism in Saccharomyces cerevisiae. The thi81 mutant exhibits significant Thiamine transport, Thiamine-repressible acid phosphatase (T-rAPase) activities and significant activities of enzymes involved in Thiamine biosynthesis which are repressed in the wild-type strain in medium supplemented with Thiamine (2×10−7 M). The thi81 mutant exhibited the same level of Thiamine pyrophosphokinase activity and intracellular Thiamine pyrophosphate concentration as the wild-type strain in medium supplemented with exogenous Thiamine. The mutant strain constitutively produced PHO3 mRNA encoding T-rAPase in medium supplemented with Thiamine. These results suggest that the thi81 mutant lacks a negative factor involved in the regulation of the genes encoding proteins involved in yeast Thiamine metabolism.
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A constitutive Thiamine metabolism mutation, thi80, causing reduced Thiamine pyrophosphokinase activity in Saccharomyces cerevisiae.
Journal of bacteriology, 1991Co-Authors: Hiroshi Nishimura, Yuko Kawasaki, Kazuto Nosaka, Yoshinobu Kaneko, Akio IwashimaAbstract:We identified a strain carrying a recessive constitutive mutation (thi80-1) with an altered Thiamine transport system, Thiamine-repressible acid phosphatase, and several enzymes of Thiamine synthesis from 2-methyl-4-amino-5-hydroxymethylpyrimidine and 4-methyl-5-beta-hydroxyethylthiazole. The mutant shows markedly reduced activity of Thiamine pyrophosphokinase (EC 2.7.6.2) and high resistance to oxyThiamine, a Thiamine antagonist whose potency depends on Thiamine pyrophosphokinase activity. The intracellular Thiamine pyrophosphate content of the mutant cells grown with exogenous Thiamine (2 x 10(-7) M) was found to be about half that of the wild-type strain under the same conditions. These results suggest that the utilization and synthesis of Thiamine in Saccharomyces cerevisiae is controlled negatively by the intracellular Thiamine pyrophosphate level.
