Thiamine and PARP Activity

These articles imply that marginal thiamine status or thiamine depletion may increase poly(ADP-ribose) polymerase (PARP) activity:

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=198524

http://scholar.google.com/scholar?q=%22Effects+of+an+Intraperitoneal+Injection%22+NAD+thiamine&hl=en&lr=

I know that it's only implied, but ATP depletion per se can increase PARP activity, and hyperglycemia-induced oxidative stress obviously does. An increase in NAD+ levels, in the face of a supposed increase in PRPP levels (assuming thiamine doesn't tend to decrease PRPP levels), could be interpreted, in relation to PARP activity, in a number of ways. I find it sort of unlikely that normalizing thiamine status would increase PARP activity, and so the higher NAD+ levels (in the second article) would suggest a reduced consumption of newly-synthesized NAD+ levels by PARP. This was shown to occur in the livers of rats (decreased PARP levels that were accompanied by increases in NAD+ levels, in rats whose folate and B12 pools had been normalized and were no longer depleted): (James et al., 1997: http://carcin.oxfordjournals.org/cgi/content/abstract/18/2/287 pubmed: http://www.ncbi.nlm.nih.gov/pubmed/9054620?dopt=Abstract). There are other interpretations of the thiamine/PRPP study, of course, but I doubt thiamine would lead to an increase in PARP expression or activity. It's also interesting that the authors found a large infusion of niacinamide (the amide form of vitamin B3) decreased the liver thiamine content, and the authors suggested, by implication, that the niacinamide-induced increase in NAD+ levels might have depleted PRPP and led to a compensatory increase in transketolase activity-mediated deliver of ribose (thereby maintaining PRPP availability but increasing thiamine turnover). It seems like that woulnd't have occurred so rapidly, though. Maybe niacinamide interferes with the transport of thiamine or its coenzymes and leads to an increase in their efflux from cells (given the competition for transport among all of these cofactors).

I haven't meant, in past postings, to dismiss the usefulness of lipid-soluble thiamine derivatives (benfotiamine, etc.) for preventing hyperglycemia-induced inhibition of glyceraldehyde-3-phosphate dehydrogenase activity. But I'm just saying that, in the absence of some specific disease state, reasonable-dose thiamine is more conservative and is unlikely to require a person to consider the issues having to do with, for example, the competition for transporters by biotin/pantothenate/lipoate/thiamine.