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

a 2010

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

PÁCAL, Lukáš, Veronika TANHÄUSEROVÁ, Jan SVOJANOVSKÝ, Darja KRUSOVÁ, Soňa ŠTĚPÁNKOVÁ et. al.

Základní údaje

Originální název

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

Autoři

PÁCAL, Lukáš, Veronika TANHÄUSEROVÁ, Jan SVOJANOVSKÝ, Darja KRUSOVÁ, Soňa ŠTĚPÁNKOVÁ, Jindřich OLŠOVSKÝ, Jana BĚLOBRÁDKOVÁ, Jitka ŘEHOŘOVÁ, Jana SMRŽOVÁ a Kateřina KAŇKOVÁ

Vydání

Diabetologia, 2010

Další údaje

Jazyk

angličtina

Typ výsledku

Konferenční abstrakt

Obor

30202 Endocrinology and metabolism

Stát vydavatele

Německo

Utajení

není předmětem státního či obchodního tajemství

Impakt faktor

Impact factor: 6.973

Organizační jednotka

Lékařská fakulta

ISSN

UT WoS

000280689700318

Klíčová slova anglicky

fructosamine-3-kinase; polymorphism; diabetic nephropathy; mortality

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 20. 4. 2011 16:03, Mgr. Lukáš Pácal, Ph.D.

Anotace

V originále

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.

Návaznosti

NR9443, projekt VaV

Název: Genetická variabilita enzymů pentózového cyklu jako faktor modulující nástup a progresi diabetické nefropatie

Investor: Ministerstvo zdravotnictví ČR, Genetická variabilita enzymů pentózového cyklu jako faktor modulující nástup a progresi diabetické nefropatie

Citovat

PÁCAL, Lukáš, Veronika TANHÄUSEROVÁ, Jan SVOJANOVSKÝ, Darja KRUSOVÁ, Soňa ŠTĚPÁNKOVÁ, Jindřich OLŠOVSKÝ, Jana BĚLOBRÁDKOVÁ, Jitka ŘEHOŘOVÁ, Jana SMRŽOVÁ a Kateřina KAŇKOVÁ. Does genetic variability in the fructosamine-3-kinase play a role in the progression of diabetic nephropathy, morbidity and mortality of diabetics? In Diabetologia. 2010. ISSN 0012-186X.

@proceedings{895659,
   author = {Pácal, Lukáš and Tanhäuserová, Veronika and Svojanovský, Jan and Krusová, Darja and Štěpánková, Soňa and Olšovský, Jindřich and Bělobrádková, Jana and Řehořová, Jitka and Smržová, Jana and Kaňková, Kateřina},
   booktitle = {Diabetologia},
   keywords = {fructosamine-3-kinase; polymorphism; diabetic nephropathy; mortality},
   language = {eng},
   title = {Does genetic variability in the fructosamine-3-kinase play a role in the progression of diabetic nephropathy, morbidity and mortality of diabetics?},
   year = {2010}
}

TY  - CONF
ID  - 895659
AU  - Pácal, Lukáš - Tanhäuserová, Veronika - Svojanovský, Jan - Krusová, Darja - Štěpánková, Soňa - Olšovský, Jindřich - Bělobrádková, Jana - Řehořová, Jitka - Smržová, Jana - Kaňková, Kateřina
PY  - 2010
TI  - Does genetic variability in the fructosamine-3-kinase play a role in the progression of diabetic nephropathy, morbidity and mortality of diabetics?
KW  - fructosamine-3-kinase
KW  - polymorphism
KW  - diabetic nephropathy
KW  - mortality
N2  - 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.
ER  -

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