Does genetic variability in the fructosamine-3-kinase play a role in the progression of diabetic nephropathy, morbidity and mortality of diabetics?

Varování

Publikace nespadá pod Ústav výpočetní techniky, ale pod Lékařskou fakultu. Oficiální stránka publikace je na webu muni.cz.

Autoři	PÁCAL Lukáš TANHÄUSEROVÁ Veronika SVOJANOVSKÝ Jan KRUSOVÁ Darja ŠTĚPÁNKOVÁ Soňa OLŠOVSKÝ Jindřich BĚLOBRÁDKOVÁ Jana ŘEHOŘOVÁ Jitka SMRŽOVÁ Jana KAŇKOVÁ Kateřina
Rok publikování	2010
Druh	Konferenční abstrakty
Fakulta / Pracoviště MU	Lékařská fakulta
Citace
Popis	Fructosamines are products of non-enzymatic glycation formed in accelerated rate during hyperglycemia. As precursors of advanced glycation end-products (AGEs) fructosamines supposedly contribute to the development of glucotoxic injury. Mechanism of enzymatic deglycation of proteins in vivo by fructosamine-3-kinase (FN3K) was described recently. The -385A/G (rs3859206) and 900C/G (rs1056534) single nucleotide polymorphisms (SNPs) in the FN3K gene were found to have potential functional impact.The aim was to study relationship between polymorphisms in FN3K gene, progression of diabetic nephropathy (DN) and cardiovascular morbidity and mortality of diabetics. Based on our results, we can not identify high FN3K deglycating activity as a protective factor, on the contrary higher rate of 3-deoxyglucosone formation may counterbalance putative protection by providing substrate for Arg-directed glycation and AGE formation.
Související projekty:	Genetická variabilita enzymů pentózového cyklu jako faktor modulující nástup a progresi diabetické nefropatie