Detailed Information on Publication Record
2018
Transketolase Activity but not Thiamine Membrane Transport Change in Response to Hyperglycaemia and Kidney Dysfunction
CHALÁSOVÁ, Katarína, Lukáš PÁCAL, Anna PLESKAČOVÁ, Lucia KNOPFOVÁ, Jitka ŘEHOŘOVÁ et. al.Basic information
Original name
Transketolase Activity but not Thiamine Membrane Transport Change in Response to Hyperglycaemia and Kidney Dysfunction
Authors
CHALÁSOVÁ, Katarína (703 Slovakia, belonging to the institution), Lukáš PÁCAL (203 Czech Republic, guarantor, belonging to the institution), Anna PLESKAČOVÁ (203 Czech Republic, belonging to the institution), Lucia KNOPFOVÁ (203 Czech Republic, belonging to the institution), Jitka ŘEHOŘOVÁ (203 Czech Republic), Marie TOMANDLOVÁ (203 Czech Republic, belonging to the institution), Josef TOMANDL (203 Czech Republic, belonging to the institution) and Kateřina KAŇKOVÁ (203 Czech Republic, belonging to the institution)
Edition
EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY & DIABETES, STUTTGART, JOHANN AMBROSIUS BARTH VERLAG MEDIZINVERLAGE HEIDELBERG GMBH, 2018, 0947-7349
Other information
Language
English
Type of outcome
Článek v odborném periodiku
Field of Study
30202 Endocrinology and metabolism
Country of publisher
Germany
Confidentiality degree
není předmětem státního či obchodního tajemství
Impact factor
Impact factor: 1.927
RIV identification code
RIV/00216224:14110/18:00106913
Organization unit
Faculty of Medicine
UT WoS
000430440200008
Keywords in English
Thiamine; transketolase; pentose phosphate pathway; diabetes; chronic kidney disease; diabetic nephropathy
Tags
International impact, Reviewed
Změněno: 26/3/2019 10:32, Soňa Böhmová
Abstract
V originále
Aim Pentose phosphate pathway (PPP) with key enzyme transketolase (TKT), represents a potentially 'protective' mechanism in hyperglycaemia. Diabetic kidney disease (DKD), a common complication of both type 1 and type 2 diabetes associated with significant morbidity and mortality, represents the most common cause of chronic kidney disease (CKD). We hypothesized that protective PPP action in diabetes and eventually even more severely in concomitant DKD might be compromised by limited intracellular availability of an active TKT cofactor thiamine diphosphate (TDP). Methods Effect of hyperglycaemia on gene expression and protein levels of key PPP loci was studied in vitro using human cell lines relevant to diabetes (HUVEC and HRGEC) and (together with measurement of TKT activity, plasma thiamine and erythrocyte TDP concentration) in vivo in diabetic vs. non-diabetic subjects with comparable renal function (n = 83 in total). Results Hyperglycaemia significantly decreased protein levels of RFC-1, THTR1, THTR2 and TKT (P < 0.05) in vitro. Analysis of blood samples from CKD patients with and without diabetes and from controls did not reveal any difference in gene expression and protein levels of thiamine transporters while TKT activity and TDP in erythrocytes gradually increased with decreasing kidney function being highest in patients with CKD3-4 of both diabetic and non-diabetic aetiology. Hyperglycaemia and uremic serum mimicking CKD in diabetes did not affect TKT activity in vitro (P < 0.05). Conclusion Both in vitro and human experiments showed decrease or unchanged expression, respectively, of thiamine transporters induced by hyperglycaemia while TKT activity in parallel with intracellular TDP was increased in CKD patients with or without diabetes. Therefore, lack of adaptive increase of thiamine transmembrane transport allowing further increase of TKT activity might contribute to compromised PPP function in diabetes and CKD and to the development of glycotoxic injury.
Links
| NV16-28040A, research and development project |
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