Thiamin absorption

Thiamine hydrochloride absorption is sodium dependent thus, saturation limits ab.sorption to 8 to IS mg daily. Absorption is decreased in alcoholism and cirrhosis. Ftxxl affects the rate, but not the amount, absorbed. After absorption, thiamine hydrochloride is distributed to all tissues. There is limited storage of the vitamin in the body (about 30 mgl. Normally, little or no thiamine is excreted in the urine. If doses exceed physiological needs after body stores arc saturated, however, thiamine can be found in the urine as pyrimidine or as the unchanged compound. 

Following absorption, thiamin is transported to the liver where it is phosphorylated under the action of ATP to form the coenzyme thiamin diphosphate (formerly called thiamin pyrophosphate or cocarboxylase), (see Fig. T-9) although this phosphorylation occurs rapidly in the liver, it is noteworthy that all nucleated cells appear to be capable of bringing about this conversion. 

In food, thiamin occurs mainly as phosphate coenzymes and the predominant form is TDP (also called thiamin pyrophosphate and cocarboxylase). The phosphate coenzymes are broken down in the gut by phosphatases to give free thiamin for absorption. Thiamin is absorbed mainly from the upper intestine, and less thiamin is absorbed on an empty stomach than when taken with a meal. The latter could be due to the alkaline conditions in the duodenum, which are prevented by the presence of food. Absorption of up to 2 mg per meal occurs by an active saturable process involving a sodium-dependent adenosine triphosphatase and against a concentration gradient. During absorption, thiamin is phosphorylated to the monophosphate ester (TMP). Thiamin is absorbed via the portal venous system. Further phosphorylation to TDP occurs on entry into all tissues. TDP can cross the blood-brain barrier, where a portion is converted to TTP, although even in the brain, TDP is the predominant form of thiamin. A second passive absorption process operates when intakes of thiamin are >5 mg but the maximum that can be absorbed from an oral dose is 2-5 mg. 

Description of Method. The water-soluble vitamins Bi (thiamine hydrochloride), B2 (riboflavin), B3 (niacinamide), and Be (pyridoxine hydrochloride) may be determined by CZE using a pH 9 sodium tetraborate/sodlum dIhydrogen phosphate buffer or by MEKC using the same buffer with the addition of sodium dodecyl-sulfate. Detection Is by UV absorption at 200 nm. An Internal standard of o-ethoxybenzamide Is used to standardize the method. 

Milk is an excellent source of calcium, phosphorus, riboflavin (vitamin B2), thiamine (vitamin Bl) and vitamin B12, and a valuable source of folate, niacin, magnesium and zinc (Food Standards Agency, 2002). In particular, dairy products are an important source of calcium, which is vital for maintaining optimal bone health in humans (Prentice, 2004). The vitamins and minerals it provides are all bioavailable (i.e. available for absorption and use by the body) and thus milk consumption in humans increases the chances of achieving nutritional recommendations for daily vitamins and mineral intake (Bellew et al., 2000). 

Evered DF, Mallett C (1983) Thiamine absorption across human buccal mucosa in vivo. Life Sci 32 1355-1358... 

Thiamine deficiency is commonly seen in alcoholics, who may develop a complex of symptoms associated with Wernicke peripheral neuropathy and Korsakoff psychosis. Alcohol interferes with thiamine absorption from the intestine. Symptoms include ... 

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. 

Thiamine deficiency may also develop In alcoholics due to poor nutrition and poor absorption of thiamine In the gastrointestinal tract. 

Alcoholics may have both decreased intake and decreased absorption of thiamine. Liver disease can prevent the formation of the active coenzyme. 

A compound that includes an aminopyrimidine ring as well as the quaternary salt present in thiamine shows preferential inhibition of absorption of that co-factor by coccidia parasites over uptake by vertebrates. The compound is thus used in poultry where coccidiosis is an economically important disease. Condensation of ethoxymethylenemalononitrile (42-1) with the amidine (42-2) leads to the aminopyrimidine (42-4), probably via the intermediate addition-elimination intermediate (42-3). The nitrile group is then reduced to the methylamino derivative (42-5) by means of hthium aluminum hydride. Exhaustive methylation, for example by reaction with formaldehyde and formic acid, followed by methyl iodide leads to the quaternary methiodide (42-6). The quaternary salt is then displaced by bromine, and the resulting benzyhc-like cylic halide (42-7) is displaced by 2-picoline (42-8). There is thus obtained amprolium (42-9) [43]. 

N.A. Cineole, thujone, ascorbic acid, thiamine, inulin, resin, tannin.100-102 Improve appetite, digestive function, and absorption of nutrients. Antiseptic, a uterine stimulant. 

The crystal structures of thiamin-dependent enzymes (see next section) as well as modeling102 103 suggest that lactylthiamin pyrophosphate has the conformation shown in Eq. 14-21. If so, it would be formed by the addition of the ylid to the carbonyl of pyruvate in accord with stereoelectronic principles, and the carboxylate group would also be in the correct orientation for elimination to form the enamine in Eq. 14-21, step b.82 83a A transient 380- to 440-nm absorption band arising during the action of pyruvate decarboxylase has been attributed to the enamine. 

Health and Safety Factors. Malononiirilc is usually available as a solidified melt in plastic-lined drums. Remclting has to he done carefully because spontaneous decomposition can occur at elevated temperatures, particularly above lOO C. in the presence of impurities such as alkalies, ammonium, and zinc sails. Occupational exposure to malononitrile mainly occurs by inhalation of vapors and absorption through the skin. Malononitrile has a recommended workplace exposure limn of 8 mg/m Uses. Malononitrile is extensively used in the life sciences industry The most important products ate vitamin B (thiamine) and bensulfuron-melhyl. a sulfonyl urea herbicide. Most other product uses fall under the. V-containing heterocycles. 

The diphosphate ester, TPP, is the physiologically active vitamer and functions as a coenzyme (67,68). The absorption, metabolism, and physiological functions of thiamine have recently been reviewed (20,67,68). 

A. The infrared absorption spectrum of a potassium bromide dispersion of the sample, previously dried at 105° for 2 h, exhibits relative maxima at the same wavelengths as those of a similar preparation of USP Thiamine Hydrochloride Reference Standard. 

Both drugs and compounds naturally present in foods may compete with vitamins for absorption. Chlorpromazine, tricyclic antidepressants, and some antimalarial dmgs inhibit the intestinal transport and metabolism of riboflavin (Section 7.4.4) carotenoids lacking vitamin A activity compete with /S-carotene for intestinal absorption and metabolism (Section 2.2.2.2) and alcohol inhibits the active transport of thiamin across the intestinal mucosa (Section 6.2). 

Synthetic allithiamin derivatives, such as thiamin propyl and tetrahydro-furfuryl disulfides, have been used for the prevention and treatment of thiamin deficiency. Because they are lipid soluble, and are not subject to the normal control of thiamin absorption by saturation of the intestinal transport system, they have potential benefits in the treatment of thiamin-deficient alcoholics, whose absorption of thiamin is impaired. 

Dietary thiamin phosphates are hydrolyzed by intestinal phosphatases, and the resultant free thiamin is absorbed by active transport in the duodenum and proximal jejunum, with little absorption in the rest of the small intestine. 

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. 

The absorption of thiamin is impaired in alcoholics, leading to thiamin deficiency (Section 6.4.4). In vitro, tissue preparations show normal uptake of the vitamin into the mucosal cells in the presence of ethanol, but impaired transport to the serosal compartment. The sodium-potassium-dependent ATPase of the basolateral membrane responsible for the active efQux of thiamin into the serosal fluid is inhibited by ethanol (Hoyumpa et al., 1977). 

There is no evidence of any toxic effect of high intakes of thiamin, although high parenteral doses have been reported to cause respiratory depression in animals and anaphylactic shock in human beings. Hypersensitivity and contact dermatitis have been reported in pharmaceutical workers handling thiamin. As noted in Section 6.2, absorption of dietary thiamin is limited, and no more than about 2.5 mg (10 /.tmol) can be absorbed from a single dose free thiamin is rapidly filtered by the kidneys and excreted. 

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