Thiamine vitamin b

Thiamine plays a critical role in energy metabolism. It is highly soluble in water and stable to both heat and oxidation at pH < 5.0. The structural formula of thiamine is shown in Figure 7.1.

Because of its structure, thiamine can form ester linkages with various acid groups, allowing for the formation of its active forms (thiamine pyrophosphate [TPP],


Suggested B Vitamin Intakes for Uncomplicated Critically Ill Patients as Compared to Recommended Dietary Allowances (RDA) for Healthy Men and Women


Suggested B Vitamin Intakes for Uncomplicated Critically Ill Patients as Compared to Recommended Dietary Allowances (RDA) for Healthy Men and Women


Critically Ill

RDA (men)

RDA (women)

Vitamin B1

10 mg/day

1.5 mg/day

1.1 mg/day

Vitamin B2

10 mg/day

1.7 mg/day

1.3 mg/day


200 mg/day

19.0 mg/day

15.0 mg/day

Vitamin B6

20 mg/day

2.0 mg/day

1.6 mg/day

Pantothenic acid

100 mg/day

5.0-7.0 mg/day

same as men

Vitamin B12

20 |gm/day

2.0 |gm/day

2.0 | gm/day


5 mg/day

30.0-100.0 |gm/day

same as men

Folic acid

2 mg/day

200 | gm/day

180 |gm/day

thiamine monophosphate [TMP], and thiamine triphosphate [TTP]). There are three enzymes that are known to participate in the formation of these phosphate esters:

  1. Thiamine pyrophosphokinase catalyzes the formation of TPP from thiamine and adenosine triphosphate (ATP).
  2. TPP-ATP phosphoryl transferase catalyzes the formation of TTP from TPP and ATP.
  3. Thiamine pyrophosphatase hydrolyzes TPP to form TMP.

The percentages of the three active forms of thiamine found in the body are 80% TPP, 10% TTP, and 10% TMP and thiamine. Higher concentrations are found in the skeletal muscle (50%), heart, liver, kidneys, and brain.3

The absorption of thiamine takes place in the upper part of the small intestine (i.e., duodenum). Oral thiamine is well absorbed and rapidly converted to its phosphorylated forms. It was shown that when the upper section of the small intestine is removed due to ulcers or injury, thiamine absorption is significantly affected by alkaline pH found in the lower intestinal tract. After absorption, thiamine is carried by the hepatic portal system to the liver. In normal adults, 20 to 30% of thiamine in the plasma is protein bound in the form of TPP. The biological






FIGURE 7.1 Vitamin Bj (thiamine).

half-life of 14C-thiamine in the body is 9 to 18 d.4 Because thiamine is not stored in large amounts in any tissue, a continuous supply from the diet is necessary.

Thiamine deficiency in animals and humans affects the cardiovascular, muscular, nervous, and gastrointestinal systems, with end results including cardiac failure, muscular weakness, peripheral and central neuropathy, and gastrointestinal malfunction. This broad-based impact is primarily due to the fact that thiamine is required for the conversion of glucose to pyruvate with the help of the coenzyme NAD (nicotinamide adenine dinucleotide). Thiamine pyrophosphate plays a vital role in the energy metabolism of the cells by first converting pyruvate to acetyl coenzyme and CO2 and also promoting the conversion of a five-carbon compound of tricar-boxylic acid (TCA) to a four-carbon compound. It is clear that the main metabolic function of thiamine is in oxidative decarboxylation. Clinically, thiamine deficiency has been shown to cause beriberi, heart disease and, in alcoholics, Wernicke-Korsakoff syndrome. Polyneuropathy is a common problem with this deficiency, because failure of energy metabolism predominantly affects neurons and their functions in selected areas of the central nervous system.

Thiamine deficiency is more common in the elderly. It is also noted to occur in alcoholics. It has been postulated that thiamine deficiency that is induced by excess alcohol intake or liver disease may affect levels of apoenzyme transketolase or its cofactor binding and, thus, prevent the formation of TPP. However, it has been observed that in well-nourished alcoholics, sufficient amounts of thiamine are maintained in the organs, and there is no abnormality in the maintenance of appropriate concentrations of phosphorylated species of thiamine. Acute thiamine deficiency was recently reported in foreign workers who complained of weakness and lower limb edema. One worker died of refractory metabolic acidosis and shock.5 Thiamine deficiency is also more common in subjects taking diuretics, because thiamine is readily excreted in the urine.6

Various biochemical tests are available to detect thiamine deficiency. These include urinary thiamine excretion, thiamine concentrations in cerebral spinal fluid (CSF), erythrocyte transketolase activity (ETKA) and thiamine pyrophosphate effect (TPPE) on ETKA. Presently, there are no known data that indicate that thiamine has toxic effects when large amounts are consumed in the diet or via long-term supplementation.

Thiamine is present in a variety of animal and vegetable food products; however, the best sources are yeast, lean pork, and legumes. A number of compounds are known to be thiamine antagonists or antithiamine factors. These include alcohols, polyphenols, flavonoids, and thiaminase (a heat-labile enzyme found in certain foods).7 Alcohol has been shown to inhibit intestinal ATP-ase, which is involved in thiamine absorption.8 The RDA for thiamine in the United States is 0.5 mg/1000 kcal/day.8

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