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Biochemical and enzymatic aspects of tryptophan-niacin metabolism were studied in 15 adult alcoholic pellagra patients and in 14 controls.

In addition to the clinical signs of niacin deficiency, most of the pellagra patients had other signs of malnutrition. Plasma tryptophan in pellagra patients was 2.07 +/- 1.27 mumol/dl, and in the controls 4.84 +/- 2.21 mumol/dl (p less than 0.001…

The metabolism of ethanol to acetaldehyde in the liver proceeds via alcohol dehydrogenase (ADH) and the microsomal ethanol-oxidizing system (MOS), whereas catalase plays no significant role.

ADH is an enzyme of the cytosol, requires NAD+ as cofactor and exhibits a pH optimum in the alkaline range. The Km of ADH is about 2 mM for ethanol (equivalent to 0.1%). Thus, the enzyme is alrea…

We have created a number of recombinant Hep G2 cell lines, designated VA cells, that constitutively express alcohol dehydrogenase.

Oxidation of ethanol by the VA cells results in the production and accumulation of acetaldehyde, and a dramatic increase in the nicotinamide adenine dinucleotide, reduced (NADH)/nicotinamide adenine dinucleotide (NAD(+)) ratio (redox-state).


We previously examined the effect of alcohol on muscle energy metabolism in chronic alcoholics by using 31P-magnetic resonance spectroscopy.

Measurements of intracellular pH and PCr index [PCr/(PCr + Pi)] during resting, hand grasping, and recovery in the left flexor digitorum superficialis muscle of alcoholics with neurological signs showed a marked decrease and delayed recovery of …

The metabolic effects of ethanol are due to a direct action of ethanol or its metabolites, changes in the redox state occurring during its metabolism, and modifications of the effects of ethanol by nutritional factors.

Ethanol causes hyperglycemia or hypoglycemia depending on whether glycogen stores are adequate, inhibits protein synthesis, and results in fatty liver and in elevation…

In clinical medicine, severe keto- or lactic acidosis associated with vomiting, nausea, abdominal pain, tachycardia or pathological respiration, has been described in chronic alcoholics.

This study reports on fatalities of chronic alcoholics where the cause of death could not be determined by thorough autopsy, histology and toxicology including determination of alcohol concentration.…

OBJECTIVE: Emergency physicians frequently treat ethanol-intoxicated trauma patients. In patients with apparently minor injuries, the presence of metabolic acidosis is often attributed to serum ethanol. We tested whether there is justification for the bias that ethanol reliably explains the acidosis commonly seen in alcohol-intoxicated patients.

METHODS: Prospective, observational. I…

Liver disease in the alcoholic is due not only to malnutrition but also to ethanol's hepatotoxicity linked to its metabolism by means of the alcohol dehydrogenase and cytochrome P450 2E1 (CYP2E1) pathways and the resulting production of toxic acetaldehyde.

In addition, alcohol dehydrogenase-mediated ethanol metabolism generates the reduced form of nicotinamide adenine dinucleotide (N…

Three decades of research in ethanol metabolism have established that alcohol is hepatotoxic not only because of secondary malnutrition but also through metabolic disturbances associated with the oxidation of ethanol.

Some of these alterations are due to redox changes produced by the NADH generated via the alcohol dehydrogenase (ADH) pathway which in turn affects the metabolism of li…

The primary enzymatic steps in ethanol metabolism to acetaldehyde, acetate and CO2 + water have been known for many decades, but only a few clinical implications were recognized, such as the risk of malnutrition due to use of alcohol as a source of calories, and the use of disulfiram and other ALDH blockers in the treatment of alcoholism.

In the last four decades, however, further un…

Alcoholic fatty liver is a potentially pathologic condition which can progress to steatohepatitis, fibrosis, and cirrhosis if alcohol consumption is continued.

Alcohol exposure may induce fatty liver by increasing NADH/NAD(+) ratio, increasing sterol regulatory element-binding protein-1 (SREBP-1) activity, decreasing peroxisome proliferator-activated receptor-alpha (PPAR-alpha) activ…

It is evident that ethanol by itself or one of its metabolites produces alterations in transport, metabolism and disposition of carbohydrates.

Ethanol acts via changes in the redox state of co-factors; e.g. ethanol-induced hypoglycemia is due, partly, to the inhibition of hepatic gluconeogenesis by ethanol as a consequence of the increased NADH/NAD ratio in patients whose glycogen sto…

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