Clinical Application of Blood Transketolase Determinations

Dreyfus, P

doi:10.1056/nejm196209202671204

Cited by 199 publications

(46 citation statements)

References 5 publications

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“…Whole blood transketolase activity and the thiamine pyrophosphate (TPP) effect were measured by the technique of Dreyfus (20). Brain thiamine (combined free and phosphorylated moieties) was assayed by the method of Lewin and Wei (21) in which the thiochrome produced is read fluorometrically.…”

Section: Methodsmentioning

confidence: 99%

Encephalopathy of thiamine deficiency: studies of intracerebral mechanisms

Dw¹,

Schenker²,

Cook³

1968

J. Clin. Invest.

164

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A B S T R A C T Thiamine-deficient encephalopathy is characterized by morphologic lesions in the brainstem and less extensively in the cerebellum, but the early neurologic signs reverse rapidly and fully with thiamine, indicating a metabolic disorder. The suggested causal mechanisms of the encephalopathy involve two thiamine-dependent enzymes: (a) impairment of pyruvate decarboxylase activity with decreased cerebral energy (ATP) synthesis, and (b) reduction of transketolase activity with possible impairment of the hexose monophosphate shunt and subsequent decrease in NADPH formation. The latter may be important in maintaining glutathione in a reduced form (GSH), which apparently functions by keeping enzymes in a reduced (active) conformation.To examine some of these postulated mechanisms, in this study we measured pyruvate decarboxylase and transketolase activity, lactate, ATP and GSH levels in the cerebral cortex, cerebellum, and brainstem, and thiamine concentration in whole brain of rats with diet-induced low thiamine encephalopathy. Pair-fed and normally fed asymptomatic control animals were similarly investigated. To assess the functional importance of some of our results, we repeated the studies in rats, immediately (16-36 hr) The data obtained led to the following conclusions: (a) Brain contains a substantial reserve of thiamine in that thiamine level has to fall to below 20% of normal before the onset of overt encephalopathy and an increase in brain thiamine to only 26%o of normal results'in rapid reversal of neurologic signs. (b) Both cerebral transketolase and pyruvate decarboxylase activities are impaired in low thiamine encephalopathy and the abnormality in the pyruvate decarboxylase is reflected in a rise in brain lactate. These biochemical abnormalities occur primarily in the brainstem and cerebellum, the sites of the morphologic changes. (c) Although the fall in cerebral transketolase is about twofold greater than that of pyruvate decarboxylase activity during encephalopathy, both enzymes rise on reversal of neurologic signs and the degree of the transketolase rise is slight. Accordingly, this study cannot ascertain the relative functional importance of these two pathways in the induction of the encephalopathy. The data suggest, however, that the depression of transketolase is not functionally important per se, but may only be an index of some other' critical aspect of the hexose monophosphate shunt. (d) The normal cerebral ATP concentration and small GSH fall during encephalopathy, with little GSH rise on reversal of neurologic signs, suggest that a depletion of neither substance is instrumental in inducing thiaminedeficient encephalopathy.

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Section: Methodsmentioning

confidence: 99%

Encephalopathy of thiamine deficiency: studies of intracerebral mechanisms

Dw¹,

Schenker²,

Cook³

1968

J. Clin. Invest.

164

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“…The 'stimulating effect' of thiamin pyrophosphate (TPP effect) in the transketolase enzyme activity (Brin et al, 1960;Dreyfus, 1962;Chong and Ho. 1970;Basu et al 1974b) is increasingly being used for assessing thiamin status.…”

Section: Resultsmentioning

confidence: 99%

The ‘Thiamin-Sparing’ Effect of Ascorbic Acid

Basu¹,

Jenner²,

Williams³

1976

Ann Nutr Metab

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The thiamin status of 16 female geriatric patients was investigated by means of the thiamin pyrophosphate stimulating effect (TPP effect) on the thiamin pyrophosphate-dependent transketolase enzyme activity. These patients had values for the TPP effect which were greater than the suggested normal limit of 10%, and these results indicated that they had some degree of thiamin deficiency. The TPP effect was, however, significantly reduced and excretory levels of thiamin were significantly increased in these patients by oral supplementation with ascorbic acid for 1 week, the dose being 1 g daily. Oral supplementation with a loading dose of ascorbic acid also resulted in an increased urinary level of thiamin in a group of healthy subjects.

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“…Die Blutkörperchensenkungsgeschwindigkeit wurde nach Westergren gemessen. Der Vitamin BrStatus wurde bestimmt durch die Messung der Transketolase-Aktivität (ETK) in den Erythrozyten mit (ETK+) und ohne (ETK0) Beigabe von Thiamin-Pyrophosphat unter standardisierten Bedingungen in einer Modifikation der Methoden von Dreyfuss (1962) und Schouten etal. (1964) unter Bildung des Quotienten aETK aus ETK+ und ETK0.…”

Section: Labordatenunclassified

Nebenwirkungen von Antiepileptika bei Langzeitmedikation

Krause

1988

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Clinical Application of Blood Transketolase Determinations

Cited by 199 publications

References 5 publications

Encephalopathy of thiamine deficiency: studies of intracerebral mechanisms

Encephalopathy of thiamine deficiency: studies of intracerebral mechanisms

The ‘Thiamin-Sparing’ Effect of Ascorbic Acid

Nebenwirkungen von Antiepileptika bei Langzeitmedikation

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