Originally posted by Timothy at Sci.life-extension
Ann N Y Acad Sci. 2005 Jun;1043:777-83.
High-dose thiamine therapy counters dyslipidemia and advanced glycation
of plasma protein in streptozotocin-induced diabetic rats.
Karachalias N, Babaei-Jadidi R, Kupich C, Ahmed N, Thornalley PJ.
Department of Biological Sciences, University of Essex, Wivenhoe Park,
Colchester, Essex CO4 3SQ, UK. t...@essex.ac.uk.
The streptozotocin-induced (STZ) diabetic rat experimental model of
diabetes on insulin maintenance therapy exhibits dyslipidemia, mild
thiamine deficiency, and increased plasma protein advanced glycation
end products (AGEs). The reversal of thiamine deficiency by high-dose
thiamine and S-benzoylthiamine monophosphate (benfotiamine) prevented
the development of incipient nephropathy. Recently, we reported that
high-dose thiamine (but not benfotiamine) countered diabetic
dyslipidemia. To understand further the differences between the effects
of thiamine and benfotiamine therapy, we quantified the levels of the
AGEs in plasma protein. We found hydroimidazolone AGE residues derived
from glyoxal and methylglyoxal, G-H1 and MG-H1, were increased 115% and
68% in STZ diabetic rats, with respect to normal controls, and were
normalized by both thiamine and benfotiamine; whereas
N-carboxymethyl-lysine (CML) and N-carboxyethyl-lysine (CEL) residues
were increased 74% and 118% in STZ diabetic rats and were normalized by
thiamine only. The lack of effect of benfotiamine on plasma CML and CEL
residue concentrations suggests there may be important precursors of
plasma protein CML and CEL residues other than glyoxal and
methylglyoxal. These are probably lipid-derived aldehydes.
PMID: 16037305 [PubMed - in process]
http://www.ncbi.nlm......ve&db=PubMed...
http://www.ncbi.nlm......ve&db=PubMed...