Metabolic and Histological Reversibility of Thiamine Deficiency

Hakim, Antoine M.; Carpenter, Stirling; Pappius, Hanna M.

doi:10.1038/jcbfm.1983.73

Cited by 32 publications

(10 citation statements)

References 15 publications

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“…The latter, however, have been extremely difficult to prove in thiamine deficiency, and indeed seizure models in general. Finally, even though replenishment with thiamine decreases the edema seen histologically in the deficient animals, cell loss persists, in keeping with other studies indicating the incomplete reversibility of the metabolic (Hakim et al, 1983), and cognitive deficits (Victor et al, 1971) of thiamine deficiency.…”

Section: Discussionsupporting

confidence: 68%

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Regional activation of L-type voltage-sensitive calcium channels in experimental thiamine deficiency

et al. 1998

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During pyrithiamine-induced thiamine deficiency (PTD), specific regions of the brain develop histological damage. The basis of this selective vulnerability is unknown but the mechanism may involve a glutamate-mediated excitotoxic process in affected structures, leading to alterations in membrane potential and disturbances in calcium homeostasis. In this study, we have examined the volume of distribution of [3H]nimodipine, an L-type voltage-sensitive calcium channel (VSCC) antagonist, in the brain of the PTD rat. An increase in specific binding of [3H]nimodipine was detected only in the posterior thalamus at the symptomatic stage, immediately following the loss of righting reflexes (P < 0.0001). There was also an increase in nonspecific binding in the medial geniculate and inferior colliculi. Replenishment with thiamine at the symptomatic stage returned [3H]nimodipine binding to normal levels. These findings provide evidence that depolarization and activation of L-type VSCCs occur in the posterior thalamus and may contribute to the appearance of histological lesions in this structure during experimental thiamine deficiency.

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Section: Discussionsupporting

confidence: 68%

“…Regional content was measured at four coronal levels using a standardized region of interest template (Fig. 1) (Hakim, 1984;Hakim et al, 1983). This normalization minimizes between-rat variation in the subsequent statistical analysis.…”

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confidence: 99%

Regional activation of L-type voltage-sensitive calcium channels in experimental thiamine deficiency

et al. 1998

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“…It is reasonable to assume that the deficiency in both specific transport and TPKase activity could produce a sort of thiamine hypovitaminosis, causing metabolic alterations in various tissues such as the auditory pathways in the brain stem (Rinehart et al, 1949;Hakim et al, 1983;Shigematsu et al, 1990), the endocrine pancreas (Failer, 1959;Rathanaswami and Sundaresan, 1988) and the haemopoietic system (Rinehart et al,. 1948;Thornber et al, 1981), whose function is known to be greatly impaired by severe dietary thiamine deficiency.…”

Section: Discussionmentioning

confidence: 98%

Thiamine transport by erythrocytes and ghosts in thiamine‐responsive megaloblastic anaemia

Rindi

Casirola

Poggi

et al. 1991

J of Inher Metab Disea

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A 9-year study of thiamine metabolism and cellular transport was performed in two patients with thiamine-responsive megaloblastic anaemia associated with diabetes mellitus and sensorineural deafness, in their relatives, and in age-matched controls from the same area. The ratios between the content of thiamine and that of its phosphoesters in erythrocytes were within the normal range, whereas the absolute values of thiamine and thiamine compounds were reduced by about 40% as compared to controls. Thiamine pyrophosphokinase activity was about 30% lower than in controls. Thiamine treatment restored the levels of thiamine and thiamine compounds to normal values, whereas kinase was unaffected. Both the saturable (specific, predominant at low, less than 2 mumol/L, physiological concentrations of thiamine) and the non-saturable component of thiamine transport were investigated. Erythrocytes and ghosts from patients exhibited no saturable component, this abnormality being specific for the patients and not shared by their parents. It is concluded that the cells from thiamine-responsive megaloblastic anaemia patients contain low levels of thiamine compounds, probably due to their inability to take up and retain physiological concentrations of thiamine, as a result of the lack of the saturable, specific component of transport and reduced thiamine pyrophosphokinase.

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“…Thiamine deficiency impairs glucose oxidation [14,15] which is possibly reflected by a lower glucose uptake after glucose loading. Thiamine intake was, however, not associated with fasting glucose, fasting triglycerides, fasting insulin and 2-h insulin, thus an apparent effect on insulin sensitivity seems not to be involved [32,33].…”

Section: Discussionmentioning

confidence: 99%

The association of dietary fibres with glucose tolerance is partly explained by concomitant intake of thiamine: The Hoorn Study

et al. 1998

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Metabolic and Histological Reversibility of Thiamine Deficiency

Cited by 32 publications

References 15 publications

Regional activation of L-type voltage-sensitive calcium channels in experimental thiamine deficiency

Regional activation of L-type voltage-sensitive calcium channels in experimental thiamine deficiency

Thiamine transport by erythrocytes and ghosts in thiamine‐responsive megaloblastic anaemia

The association of dietary fibres with glucose tolerance is partly explained by concomitant intake of thiamine: The Hoorn Study

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