However, several aspects of experimental data on the non-coenzymatic function of thiamine focused on its relationships with hormonal factors. On the one hand, thiamine and dopamine showed a close relationship in biosynthesis processes. Thiamine biosynthesis involved two independent pathways: synthesis of the thiazole and production of the pyrimidine moieties of thiamine, which are then coupled to form thiamine. L-tyrosine acts as an indispensable factor in the biosynthesis of the thiazole moiety of thiamine. L-tyrosine is the common precursor of the biosyntheses of both dopamine and thiamine. Tyrosine hydroxylase is the rate-limiting enzyme of catecholamine biosynthesis: It converts the L-tyrosine into L-dopa, a precursor of dopamine. Thiamine deficiency decreased tyrosine hydroxylase in the brain. These observations suggest that thiamine influences dopamine synthesis through its interactions with both L-tyrosine and tyrosine hydroxylase. Indeed, thiamine deficiency reduced synthesis of dopamine and decreased catecholamine turnover (dopamine + noradrenaline) in the hypothalamus and other brain regions. Moreover, cerebrospinal fluid (CSF) levels of thiamine decreased in patients with Parkinson’s disease.
Parkinson’s disease patients under levodopa therapy had significantly higher CSF levels of thiamine diphosphate and total thiamine than those not treated with this drug.
Discover the impact of thiamine deficiency on 17β-estradiol's modulation of dopamine D2 receptors. Explore the effects of bromocriptine mesylate and sulpiride on water, sugar, alcohol, and food consumption in thiamine-deficient female rats. Gain insights into the interplay between thiamine and...
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