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Benfotiamine blocks
three major pathways of hyperglycemic damage and prevents experimental
diabetic retinopathy.
Hammes HP, Du X, Edelstein D,
Taguchi T, Matsumura T, Ju Q, Lin J, Bierhaus A, Nawroth P, Hannak D,
Neumaier M, Bergfeld R, Giardino I, Brownlee M.
Medical
Clinic V, School of Clinical Medicine, Mannheim, Germany.
Three
of the major biochemical pathways implicated in the pathogenesis of
hyperglycemia induced vascular damage (the hexosamine pathway, the
advanced glycation end product (AGE) formation pathway and the
diacylglycerol (DAG)-protein kinase C (PKC) pathway) are activated by
increased availability of the glycolytic metabolites
glyceraldehyde-3-phosphate and fructose-6-phosphate. We have discovered
that the lipid-soluble thiamine derivative benfotiamine can inhibit
these three pathways, as well as hyperglycemia-associated NF-kappaB
activation, by activating the pentose phosphate pathway enzyme
transketolase, which converts glyceraldehyde-3-phosphate and
fructose-6-phosphate into pentose-5-phosphates and other sugars. In
retinas of diabetic animals, benfotiamine treatment inhibited these
three pathways and NF-kappaB activation by activating transketolase, and
also prevented experimental diabetic retinopathy. The ability of
benfotiamine to inhibit three major pathways simultaneously might be
clinically useful in preventing the development and progression of
diabetic complications.
PMID: 12592403 [PubMed - indexed for
MEDLINE]
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