by Mark Lin

Created on: December 18, 2008

The first vitamin in the B group is known as thiamine, also called B1, which plays vital roles in the metabolism. Frist of all, the vitamin thiamine is a cofactor for the enxyome pyruvate dehydrogenase, a vital enzyme in the glycolytic pathway. The enzyme regulates how much energy is produced in the form of ATP (adenosine triphosphate) by limiting the amount of acetyl CoAs produced. The reaction is irreversable, with pyruvate dehydrogenase guarding the gates. Second of all, the enzyme thiamine also serves as the cofactor for the enzyme transketolase, which functions in the hexose monophosphate shunt, also known as the glucose-6-phosphate pathway. The aim of the pathway is to produce the NADPH, which may be used in red blood cells to eliminate the reactive free radicals from the erythrocyte cytoplasm, but is also utilized in white blood cells to produce free radicals, which in turn kills off the harmful microorganisms ingested. Malfunctioning of this enzyme may result in hemolytic anemia due to excessive hemolysis of the red blood cells. This phenomenom isn observed due to the inabilities to eliminate the free radicals. Just the contrary may be observed in white blood cells. Lack of NADPH results in decreased generation of free radicals, which in turn affects the productivity of the halide myeloperoxidase system of defence. The system is considered the most effective oxygen-dependent method of microorganism elimination. The defect may be manifested by recurrent infection by various microbes, such as streptococcal bacteria, various viruses and fungi, etc. Last of all, thiamine constitutes a part of the enzyme alpha-ketoglutarate dehydrogenase, an enzyme of the citric acid cycle, also known as the tricarboxylic acid cycle. In the reaction catalyzed, the reactant alpha ketoglutarate is converted into the product succinyl CoA, with the side-production of a molecule of carbon dioxide and a reducing equivalent in the form of NADH. Malfunctioning of this enzyme can lead to the accumulation of the reactant alpha-ketoglutarate in the mitochondrial matrix, leading to complete block in the citric acid cycle. The defect is manifested by weakness of the limbs and certain neural disfunctioning, such as malaise, confusion, etc. As discussed above, vitamin B1 serves as a cofactor in the enzymes pyruvate dehydrogenase, alpha-ketoglutarte dehydrogenase, and transketolase, with abnormalities manifested in the ways described above.

The deficiency of the vitamin thiamine can also be manifested in other ways than described above. First of all, a condition known as wet beriberi may develop. Wet beriberi is manifested clinically by high cardiac outputs, frequently accompanied by arryhthmias of the atriums and ventricles. If the deficiency were allowed to be left untreated for a certain duration, the cardiac defects may become permenant and progress ultimately into congestive heart disease. Second of all, the Wercicke-Korsakoff syndrome covers the neural portion of the defects manifested. The syndrome may be characterized by paralysis of the eye muscles (ophthalamoplegia), ataxia (wasting), psychosis, etc. One may contribute the nerual findings to the fact that the nervous tissues must meet their enormous energy demands in order to funciton properly. Such requirement is deprived due to the inactivity of the enzymes pyruvate dehydrogenase and alpha-ketoglutarate. To conclude, some other symptoms are as listed above.

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