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pubmed-article:16645728pubmed:abstractTextThe spontaneous hypertensive rat (SHR) is a widely studied model of hypertension that exhibits metabolic abnormalities, which share features with the human metabolic syndrome. Genetic linkage studies have revealed a defective CD36 gene, encoding a membrane fatty acid (FA) transporter, in hyperinsulinemia of the SHR. However, there is no unifying mechanism that can explain these phenotypes as a consequence of a defective CD36 gene. Impaired fatty acid uptake is compensated by increased glucose uptake. We hypothesized that (1) the abundant intracellular glucose is not oxidized proportionally and (2) the correction of the uncoupling of glucose oxidation to its cellular entry might be effective against the pathophysiology of CD36-defective SHR. Therefore, we attempted to activate glucose oxidation with the repletion of thiamine, a coenzyme for multiple steps of glucose metabolism.lld:pubmed
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pubmed-article:16645728pubmed:articleTitleThiamine attenuates the hypertension and metabolic abnormalities in CD36-defective SHR: uncoupling of glucose oxidation from cellular entry accompanied with enhanced protein O-GlcNAcylation in CD36 deficiency.lld:pubmed
pubmed-article:16645728pubmed:affiliationThird Division, Department of Internal Medicine, Osaka Medical College, Osaka, Japan. in3024@poh.osaka-med.ac.jplld:pubmed
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