Thiamine mononitrateThiamine pyrophosphate (TPP)
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Thiamine

Thiamine or thiamin, also known as vitamin B1, is a colorless compound with chemical formula C12H17N4OS. It is soluble in water and insoluble in alcohol. Thiamine decomposes if heated. more...

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Thiamine pyrophosphate (TPP) is a coenzyme for pyruvate dehydrogenase, α-ketoglutarate dehydrogenase and transketolase. The first two of these enzymes function in the metabolism of carbohydrates, while transketolase functions in the pentose phosphate pathway to synthesize NADPH and the pentose sugars deoxyribose and ribose. Systemic thiamine deficiency can lead to myriad problems including neurodegeneration, wasting, and death. Well-known syndromes caused by lack of thiamine due to malnutrition or a diet high in thiaminase-rich foods include Wernicke-Korsakoff syndrome and beriberi, diseases also common in chronic abusers of alcohol.

Genetic diseases of thiamine transport are rare but serious. Thiamine Responsive Megaloblastic Anemia with diabetes mellitus and sensorineural deafness (TRMA) is an autosomal recessive disorder caused by mutations in the gene SLC19A2, a high affinity thiamine transporter. TRMA patients do not show signs of systemic thiamine deficiency, suggesting redundancy in the thiamine transport system. This has led to the discovery of a second high affinity thiamine transporter, SLC19A3.

Thiamine was first discovered by Umetaro Suzuki in Japan when researching how rice bran cured patients of Beriberi. He named it aberic acid.

The only known cases of thiamine overdose occurred with thiamine injections.


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Thiamine deficiency in hepatitis C virus and alcohol-related liver diseases - Brief Article
From Alternative Medicine Review, 6/1/02 by S Levy

Levy S, Herve C, Delacoux E, Erlinger S. Dig Dis Sci 2002;47:543-548.

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 erythrocytc 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.

COPYRIGHT 2002 Thorne Research Inc.
COPYRIGHT 2002 Gale Group

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