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PubMed1980

Mechanisms of thiamin deficiency in chronic alcoholism.

In the United States and other developed countries thiamin deficiency is often related to chronic alcoholism. A number of mechanisms may be involved in the pathogenesis of thiamin deficiency in the alcoholic population. An important cause is inadequate intake of thiamin. Moreover, there may be decreased converstion of thiamin to the active coenzyme, reduced hepatic storage of the vitamin in patients with fatty metamorphosis, ethanol inhibition of intestinal thiamin transport, and impaired thiamin absorption secondary to other states of nutritional deficiency. The present discussion focuses on the mechanism of ethanol-related thiamin malabsorption. Under normal conditions thiamin transport in animals and humans is biphasic. At low or physiological thiamin concentrations, transport is a saturable, carrier-mediated, active process; but at higher concentrations, the transport of thiamin is predominantly passive. Ethanol reduces the rate of intestinal absorption and the net transmural flux of thiamin. Furthermore, ethanol inhibits only the active and not the passive component of thiamin transport by impeding the cellular exit of thiamin across the basolateral or serosal membrane. The impairment of thiamin movement out of the enterocyte correlates with a fall in the activity of Na-K ATPase. Bound to the basolateral membrane, Na-K ATPase is believed to be involved in the kinetics of active transport. Ethanol also increases the fluidity of enterocyte brush border and basolateral membranes. Since ethanol increases membrane fluidity it is possible that tahe impairment of thiamin transport and the diminution of Na-K ATPase activity may be related, at least partly, to a physical perturbation of the enterocyte membrane.

Alcoholism↗
PubMed2005

Erythrocyte thiamine (Th) esters: a major factor of the alcohol withdrawal syndrome or a candidate marker for alcoholism itself?

AIMS: Thiamine (Th) deficiency is a major problem in alcoholics. In this study, the relationship of alcohol withdrawal syndrome (AWS) to Th and its esters, as well as the diagnostic power of Th and its esters were investigated. PATIENTS AND METHODS: Th and its esters were assessed in a series of chronic alcoholics (and in controls) using an improved method. RESULTS: No association was found between AWS severity and Th and its esters, while the diagnostic power of thiamine diphosphate (TDP) and Th was very high. TDP was the most significant among the parameters under study, confirming that erythrocyte TDP is a suitable marker of alcoholism: TDP sensitivity across subjects was 84.1%, specificity 85.4%, positive predictive value 82.4%, and negative predictive value 88.0%.

Adult↗
PubMed1999

Dietary thiamin level influences levels of its diphosphate form and thiamin-dependent enzymic activities of rat liver.

This study was prompted by our incomplete understanding of the mechanism responsible for the clinical benefits of pharmacological doses of thiamin in some patients with maple syrup urine disease (MSUD) and the question of whether thiamin diphosphate (TDP), a potent inhibitor of the activity of the protein kinase that phosphorylates and inactivates the isolated branched-chain alpha-ketoacid dehydrogenase (BCKDH) complex, affects the activity state of the complex. Rats were fed a chemically-defined diet containing graded levels of thiamin (0, 0.275, 0.55, 5.5, and 55 mg thiamin/kg diet). Maximal weight gain was attained over a 3-wk period only in rats fed diets with 5.5 and 55 mg thiamin/kg. Feeding rats the thiamin-free diet for just 2 d caused loss of nearly half of the TDP from liver mitochondria. Three more days caused over 70% loss, an additional 3 wk, over 90%. Starvation for 2 d had no effect, suggesting a mechanism for conservation of TDP in this nutritional state. Mitochondrial TDP was higher in rats fed pharmacological amounts of thiamin (55 mg thiamin/kg diet) than in rats fed adequate thiamin for maximal growth. Varying dietary thiamin had marked but opposite effects on the activities of alpha-ketoglutarate dehydrogenase (alpha-KGDH) and BCKDH. Thiamin deficiency decreased alpha-KGDH activity, increased BCKDH activity, and increased the proportion of BCKDH in the active, dephosphorylated, state. Excess dietary thiamin had the opposite effects. TDP appears to be more tightly associated with alpha-KGDH than BCKDH in thiamin-deficient rats, perhaps denoting retention of alpha-KGDH activity at the expense of BCKDH activity. Thus, thiamin deficiency and excess cause large changes in mitochondrial TDP levels that have a major influence on the activities of the keto acid dehydrogenase complexes.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗
PubMed1990

Blood thiamine and thiamine phosphate concentrations in excessive drinkers with or without peripheral neuropathy.

The aim of our study was to answer the following questions: (1) is thiamine deficient in chronic excessive drinkers; and (2) is peripheral neuropathy associated with thiamine deficiency or with alcohol intake itself? We performed direct assays of blood concentrations of free thiamine and thiamine phosphate in excessive drinkers with or without peripheral neuropathy and in control subjects. We found no difference in free thiamine concentrations between excessive drinkers with and without neuropathy, and no difference in free thiamine concentrations between the two groups of excessive drinkers and the control group. By contrast, a deficiency in thiamine phosphate was observed in each group of excessive drinkers compared to the control group. This was reflected in blood concentrations of total thiamine which were also lower in excessive drinkers than in controls. Finally, the thiamine phosphate: free thiamine ratio was slightly but significantly lower in the two groups of excessive drinkers than in the control group. Both groups of excessive drinkers showed typical moderate liver disease of alcoholic origin. In conclusion, the free thiamine fraction was not diminished in this group of alcoholic hospital inpatients. Thiamine deficiency would not therefore appear to play a determining role in the onset of peripheral neuropathy. In contrast, the phosphorylated fraction was slightly reduced, probably owing to the liver disease in these subjects. Contrary to studies using indirect assay techniques, our results suggest that thiamine deficiency is either slight or absent in chronic drinkers.

Adult↗