Transketolase, Thiamine, and Nucleotide Metabolism

There's a lot of research in relation to diabetes that shows some effects of lipid-soluble prodrugs of vitamin B1 (thiamine) on augmenting transketolase activity past the point that can be achieved with thiamine by itself. Here's a representative article: http://diabetes.diabetesjournals.org/cgi/content/full/52/8/2110. I don't think high-dose thiamine has much of an effect in humans. The main idea with that article was that the animals' thiamine loss in the urine was increased because of diabetes-induced glomerular hyperfiltration, essentially. There are some problems with the thiamine prodrugs, drugs that include benfotiamine, fursultiamine (thiamine tetrahydrofurfuryl disulfide), and sulbutiamine (?). I think that's the name of the third one, but the drugs are rather reactive and might be expected to form mixed disulfides with albumin, etc. The main issue is that enhancing transketolase activity can only do so much to overcome a crippled oxidative arm of the pentose phosphate pathway. It's interesting, though, to see the effect that transketolase activity can have on nucleotide metabolism. Although there's plenty of legitimate research on the effects of exogenous ribose, in combination with nucleotides, on nucleotide metabolism and glycolysis, here's an obscure, German-language article showing that lipid-soluble thiamine prodrugs might have effects that are sort of similar to the effects of pyrimidine nucleotides:

http://www.ncbi.nlm.nih.gov/pubmed/9064269

Magnesium is required for thiamine diphosphate binding to transketolase and is likely, along with low-dose vitamin B1, to be a more reasonable, adjunctive approach to maintaining transketolase activity. This type of approach shouldn't be expected to do much by itself but would be expected to decrease the likelihood that adverse effects would occur with something like ribose in combination with exogenous nucleotides.