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Plasma thiamine

Thiamine is absorbed by a pathway that is saturable at concentrations of 0.5-1.0 jumol/L. Oral doses in excess of 10 mg do not significantly increase blood or urine concentrations of vitamin Bi. In the human, absorption occurs predominantly in the jejunum and ileum. Some ferns, shellfish, fish, and species of bacteria contain thiami-nase, which cleaves the pyrimidine ring from the thiazole ring. This enzyme causes thiamine deficiency in cattle. In plasma, thiamine is transported bound to albumin and, to a small extent, other proteins. TPP is synthesized in the liver by thiamine pyrophosphokinase. [Pg.915]

Techniques using HPLC and fluorescent detection are now the standard for direct quantification of thiamine in blood (Lynch and Young 2000). Plasma contains less than 10% of whole blood thiamine (in the form of T" and TMP) and levels are strongly influenced by recent food consumption (Tallaksen et al. 1993). Following thiamine intake, plasma thiamine levels peak at 50 minutes (range 20-120 minutes) and return to baseline within 12 hours (Tallaksen et al. 1993). Thus, a fasting state is often recommended to increase accuracy of plasma thiamine measures. However, measurements in whole blood or erythrocytes are preferred as plasma measures suffer from poor sensitivity and specificity. [Pg.265]

Gold, M., Flauser, R.A., and Chen, M.F., 1998. Plasma thiamine deficiency associated with Alzheimer s disease but not Parkinson s disease. Metabolic... [Pg.278]

Lee, D.C., Chu, J., Satz, W., and Silbergleit, R., 2000. Low plasma thiamine levels in elder patients admitted through the emergency department. Academy of Emergency Medicine. 7 1156-1159. [Pg.279]

McLaren, D.S., Docherty, M.A., and Boyd, D.H., 1981. Plasma thiamin pyrophosphate and erythrocyte transketolase in chronic alcoholism. The American Journal of Clinincal Nutrition. 34 1031-1033. [Pg.280]

Vognar, L., and Stoukides, J., 2009. The role of low plasma thiamin levels in eognitively impaired elderly patients presenting with acute behavioral disturbances. Journal of the American Geriatrics Society. 57 2166-2168. [Pg.283]

Fig. 3. Intracellular transport route of the SFV spike glycoproteins from the endoplasmic reticulum (ER), over the Golgi apparatus, to the plasma membrane (PM). The cis cisternae do not react positively for add phosphatase or thiamin pyrophosphatase, and do not label with ridn in thin frozen sections. The medial cisternae do not react positively for thiamin pyrophosphatase or acid phosphatase, but label with ridn. The trans cisternae are positive for all of these markers. Fig. 3. Intracellular transport route of the SFV spike glycoproteins from the endoplasmic reticulum (ER), over the Golgi apparatus, to the plasma membrane (PM). The cis cisternae do not react positively for add phosphatase or thiamin pyrophosphatase, and do not label with ridn in thin frozen sections. The medial cisternae do not react positively for thiamin pyrophosphatase or acid phosphatase, but label with ridn. The trans cisternae are positive for all of these markers.
The transport of amino acids at the BBB differs depending on their chemical class and the dual function of some amino acids as nutrients and neurotransmitters. Essential large neutral amino acids are shuttled into the brain by facilitated transport via the large neutral amino acid transporter (LAT) system [29] and display rapid equilibration between plasma and brain concentrations on a minute time scale. The LAT-system at the BBB shows a much lower Km for its substrates compared to the analogous L-system of peripheral tissues and its mRNA is highly expressed in brain endothelial cells (100-fold abundance compared to other tissues). Cationic amino acids are taken up into the brain by a different facilitative transporter, designated as the y system, which is present on the luminal and abluminal endothelial membrane. In contrast, active Na -dependent transporters for small neutral amino acids (A-system ASC-system) and cationic amino acids (B° system), appear to be confined to the abluminal surface and may be involved in removal of amino acids from brain extracellular fluid [30]. Carrier-mediated BBB transport includes monocarboxylic acids (pyruvate), amines (choline), nucleosides (adenosine), purine bases (adenine), panthotenate, thiamine, and thyroid hormones (T3), with a representative substrate given in parentheses [31]. [Pg.30]

Infusions of thiamine at two different rates during Intravenous injections of a constant dose of I produced sequentially slower removal of I from plasma.163 The half-time for the rapid phase of removal of I from plasma was 4.2 min in the control runs it was Increased to 8.4 min during the infusion of thiamine at both rates. [Pg.309]

Thiamine- and pyridoxal-phoshates human blood/plasma deproteination PRP ion-pair PRP post-Flu 67... [Pg.259]

L13. Lou, H. C., Correction of increased plasma pyruvate and plasma lactate levels using large doses of thiamine in patients with Kearns-Sayre syndrome. Arch. Neurol. 38, 469 (1981). [Pg.122]

The transport system is saturated at relatively low concentrations of thiamin (about 2 /xmol per L), thus limiting the amount of thiamin that can be absorbed. As a result, increasing test doses of thiamin from 2.5 to 20 mg have only a negligible effect on the plasma concentration of thiamin or on urinary excretion. By contrast, the absorption of lipid-soluble aUithiamin derivatives is not apparendy saturable, and they can be used to achieve high blood concentrations of thiamin. [Pg.151]

Both free thiamin and thiamin monophosphate circulate in plasma about 60% of the total is the monophosphate. Under normal conditions, most is bound to albumin when the albumin binding capacity is saturated, the excess is rapidly filtered at the glomerulus and excreted in the urine. Although a significant amount of newly absorbed thiamin is phosphorylated in the Uver, aU tissues can take up both thiamin and thiamin monophosphate, and are able to phosphorylate them to thiamin diphosphate and thiamin triphosphate. In most tissues, it is free thiamin that is the immediate precursor of thiamin diphosphate, which is formed by a pyrophosphokinase both the p-and y-phosphates of ATP are incorporated. Thiamin monophosphate arises mainly as a result of sequential hydrolysis of thiamin triphosphate and thiamin diphosphate. [Pg.151]

Thiamin that is not bound to plasma proteins is rapidly filtered at the glomerulus. Diuresis increases the excretion of the vitamin, and patients who are treated with diuretics are potentially at risk of thiamin deficiency. Some of the diuretics used in the treatment of hypertension may also inhibit cardiac (and other tissue) uptake of thiamin, thus further impairing thiamin status, which may be a factor in the etiology of heart failure (Suter and Vetter, 2000). [Pg.152]

The role of thiamin diphosphate in pymvate dehydrogenase means that, in deficiency, there is impaired conversion of pymvate to acetyl GoA, and hence impaired entry of pymvate into the citric acid cycle. Especially in subjects on a relatively high carbohydrate diet, this results in increased plasma concentrations oflactate and pymvate, which may lead to life-threateninglactic acidosis. [Pg.164]

The increase in plasma lactate and pyruvate after a test dose of glucose was used historically as a means of assessing thiamin nutritional status (Section 6.5). [Pg.165]

In experimental animals and in depletion studies, measurement of the concentration of thiamin in plasma or whole blood provides an indication of the progression of deficiency. The normal method is by the formation of thiochrome, which is fluorescent ordy free thiamin, and not the phosphates, undergoes... [Pg.167]

Erythrocytes and leukocytes contain mainly thiamin diphosphate, whereas plasma contains free thiamin and thiamin monophosphate. The concentration of thiamin diphosphate in erythrocytes is normally between 110 and 330 nmol per L of packed cells. The total thiamin concentration in erythrocytes is about 4- to 5-fold higher than in plasma and that in leukocytes is 10-fold higher again. [Pg.168]

Reggiani C, Patrini C, and Hindi G (1984) Nervous tissue thiamine metabolism in vivo. 1. Transport of thiamine and thiamine monophosphate from plasma to different brain regions of the rat. Brain Research 293,319-27. [Pg.448]

Clomethiazole is structurally related to vitamin B 1 (thiamine) and is a hypnotic, sedative and anticonvulsant. It is comparatively free from hangover it can cause nasal irritation and sneezing. Dependence occurs and use should always be brief. When taken orally, it is subject to extensive hepatic first-pass metabolism (which is defective in the elderly and in liver damaged alcoholics who get higher peak plasma concentrations), and the usual t) is 4 h (with more variation in the old than the young) it may also be given i.v. [Pg.403]

At one time it was thought that plasma pyruvate levels could be used to assess thiamin status. Plea.se rat Inna li .c this test. State how it would work. Then eKplain how the test could be influenced by factors other than thiamin status. (Sec Chong, 1970.)... [Pg.608]

Tallaksen, C. M., Bobmer, I., Karisen, J., and Bell, H. (1997). Determii ation of thiamin and its phosphate esters in human blood, plasma, and urine. F.nzumoi. 279, Part I,... [Pg.666]

The severity of the symptoms of thiamin deficiency has been associated with energy intake. The consumption of large doses of glucose has been foimd to induce an unusual rise in plasma pyruvate and lactate, as well as neurological symptoms, in thiamin deficient humans. Because of this association, the thiamin requirement is sometimes expressed on a per energy intake basis. [Pg.608]


See other pages where Plasma thiamine is mentioned: [Pg.706]    [Pg.309]    [Pg.310]    [Pg.706]    [Pg.105]    [Pg.167]    [Pg.167]    [Pg.608]    [Pg.609]    [Pg.609]   
See also in sourсe #XX -- [ Pg.1093 ]




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