Thiamine excretion

A small amount of thiamin is excreted in the urine unchanged, accounting for about 3% of a test dose, together with small amounts of thiamin monophosphate and thiamin diphosphate. As discussed in Section 6.5.1, this can be used to assess thiamin nutritional status. One of the major excretory products is thiochrome cyclization to thiochrome is the basis of the normal method of determining thiamin so, most reports of thiamin excretion are actually of thiamin plus thiochrome. In addition, small amounts of thiamin disulfide, formed by the oxidation of thiamin thiol, are also excreted. 

Urinary thiamine excretion Erythrocyte thiamine concentration Erythrocyte glutathione reductase activity Erythrocyte flavin... 

Oldham, H.G., Davis, M.V., and Roberts, L.J., 1946. Thiamine excretions and blood levels of young women on diets containing varying levels of the B... 

Nutritional status assessment for thiamine is generally carried out by assaying the total thiamine in whole blood or erythrocytes, or by measuring the activity of erythrocyte transketolase before and after incubation with exogenous thiamine pyrophosphate. The latter serves as the sensitive index of thiamine nutritional status (Brin 1980). In addition to the enzymatic test, a measure of urinary thiamine in relation to dietary intake has been the basis for balance studies to assess the adequacy of intake. When thiamine excretion is low, a larger portion of the test dose is retained, indicating a tissue s need for thiamine. A high excretion indicates tissue saturation. In the deficient state, excretion drops to zero. Plasma pyruvate and lactate concentrations have also been used to assess thiamine status. 

Human beings and laboratory animals receiving a diet adequate in thiamine excrete the vitamin in the urine. When extra thiamine is administered the excretion also increases. But always only part of the ingested thiamine reappears in the urine as such. The remainder must be broken down in the body, but how this happens is completely obscure. 

Thiamine is excreted in the urine, the amount being dependent on dietary intake and the relative saturation of the tissue stores. Determination of thiamine excretion in the urine, especially after a test dose of thiamine has been administered, is one of the methods used in evaluating nutritive status relative to this vitamin. After intramuscular injection of 1 mg. of thiamine, persons who are adequately nourished excrete at least 100 fig. in the subsequent 4 hr., whereas patients with signs of thiamine deficiency usually excrete less than 50 /xg. during this period. Estimation of the concentration of thiamine in blood has also been used in nutritional appraisal. Mean... 

Diuretics, long-term Accelerate thiamin excretion and... 

Subject Thiamin Intake 7 Per day Free Thiamin Excretion in Stools 7 per day ... 

Thiamine requirements vary and, with a lack of significant storage capabiHty, a constant intake is needed or deficiency can occur relatively quickly. Human recommended daily allowances (RDAs) in the United States ate based on calorie intake at the level of 0.50 mg/4184 kj (1000 kcal) for healthy individuals (Table 2). As Httle as 0.15—0.20 mg/4184 kJ will prevent deficiency signs but 0.35—0.40 mg/4184 kJ are requited to maintain near normal urinary excretion levels and associated enzyme activities. Pregnant and lactating women requite higher levels of supplementation. Other countries have set different recommended levels (1,37,38). 

P. M. West, Excretion of thiamin and biotin by the roots of higher plants. Nature (London) /44 1050 (1939). 

Excretion of thiamine appears to vary from individual to individual,23 and some other data are available regarding the other better-known B vitamins.24 The differences in the excretion of nicotinic acid-like compounds strongly suggest the existence of individual pattems.25,26 The urinary excretion of vitamin B12, folic acid, and the citrovorum factor by different individuals, even on controlled diets, was found to vary through rather wide ranges (2- to 9-fold) though the study was not concerned with individual differences and individual patterns were not established. 27... 

One recent study has been made involving attempts to assess thiamine needs on the basis of excretion.53 Eight normal women were investigated. For six out of eight, 500 pg. of thiamine per 1000 Cal. was judged adequate. A lower level, 300 pg., was judged inadequate... 

Vitamin deficiency of Bj leads to the disease known as Beriberi. However, nowadays in the Western hemisphere, vitamin Bj deficiency is mainly found as a consequence of extreme alcoholism. In fact, the vitamin absorption by the gut is decreased and its excretion is increased by alcohol. Alcohol also inhibits the activation of vitamin Bj to its coenzyme form, thiamine pyrophosphate ester (TPP). There is no evidence of adverse effects of oral intake of thiamine [417]. The main food sources of vitamin Bj are lean pork, legumes, and cereal grains (germ fraction). It is soluble in water and stable at higher temperature and at pH lower than 5.0, but it is destroyed rapidly by boiling at pH 7.0 or above. 

Pharmacokinetics Metabolized to thiamine pyrophosphate (active) in the liver. At dietary levels thiamine is completely distributed to tissues. At pharmacologic doses, excess thiamine is excreted in urine. 

After being found to be healthy on a thorough physical examination accompanied by a broad range of laboratory examinations, 22 men were used in studies of the renal clearance of I, after intravenous injection at 5 mg/kg under a variety of conditions.161 Alkaliniza-tion of the urine to a pH above 7.5 by administration of bicarbonate and acidification of the urine to a pH below 5.0 by administration of ammonium chloride both reduced urinary excretion of I. When 200 mg of thiamine was Injected intramuscularly 20-30 min before intravenous injection of I, urinary excretion of I during the 5 h after... 

During the first 3 h after Intravenous injection of 1 that followed administration of thiamine, urinary excretion of the oxime was about 12.7% below that during the corresponding period of the control experiment during the remainder of the run, it was 62.2% above that during the same period of the control experiment. Inasmuch as intravenous injection of 900 mg of sodium jg-aminohippurate with I decreased by only 6.3% the urinary excretion of I during the first 3 h after its administration, the tubular transport mechanisms for 1 and for jg-amino-hippurate probably are different. 

Vitamins are chemically unrelated organic compounds that cannot be synthesized by humans and, therefore, must must be supplied by the diet. Nine vitamins (folic acid, cobalamin, ascorbic acid, pyridoxine, thiamine, niacin, riboflavin, biotin, and pantothenic acid) are classified as water-soluble, whereas four vitamins (vitamins A, D, K, and E) are termed fat-soluble (Figure 28.1). Vitamins are required to perform specific cellular functions, for example, many of the water-soluble vitamins are precursors of coenzymes for the enzymes of intermediary metabolism. In contrast to the water-soluble vitamins, only one fat soluble vitamin (vitamin K) has a coenzyme function. These vitamins are released, absorbed, and transported with the fat of the diet. They are not readily excreted in the urine, and significant quantities are stored in Die liver and adipose tissue. In fact, consumption of vitamins A and D in exoess of the recommended dietary allowances can lead to accumulation of toxic quantities of these compounds. 

The first water-soluble vitamin discovered was called vitamin B to distinguish it from vitamin A. Later other B vitamins were discovered and given names such as vitamin B2, B2, etc. Now the specific chemical names are used. In distinction to the fat-soluble vitamins, the water-soluble vitamins are not absorbed with fats and they are not stored in appreciable quantities in the body (with the possible exception of B12 and thiamin). Excesses of these vitamins are excreted rapidly in urine, requiring a constant dietary supply. 

Tucker, R. G. Mickelsen, 0. Keys, A. (1960) The infuence of sleep, work, diuresis, acute starvation, thiamine intake, and bed rest on human riboflavin excretion. J. Nutr. 72, 251-61. 

Metabolic abnormalities under normal conditions, such as impaired carbohydrate metabolism in thiamin deficiency (Section 6.5) or excretion of methylmalonic acid in vitamin B12 deficiency (Section 10.10.3). 

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. 

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. 

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). 

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