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Benfotiamine alleviates diabetes-induced cerebral oxidative damage independent of advanced glycation end-product, tissue factor and tnf-alpha.

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Benfotiamine is believed to enhance in humans the activity of the enzyme transketolase, which converts harmful glucose metabolites at the cellular level into harmless chemicals, preventing damage, especially to the endothelial cells which line the small arteries and capillaries of the kidneys and retinas.

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On the other hand, benfotiamine had better bioavailability than fursultiamine in increasing the blood levels of free thiamine and tpp.

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High doses of thiamine and benfotiamine might also prevent the diabetic kidney disease called nephropathy.

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Benfotiamine prevents increased -amyloid production in hek cells induced by high glucose.

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the result is that benfotiamine can dramatically increase the levels of b1 in the blood stream, and effectively decrease or eliminate the symptoms of neuropathy.

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