Dysfunctional protection against advanced glycation due to thiamine metabolism abnormalities in gestational diabetes
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu klinické zkoušky, časopisecké články, práce podpořená grantem
PubMed
27287225
DOI
10.1007/s10719-016-9688-9
PII: 10.1007/s10719-016-9688-9
Knihovny.cz E-zdroje
- Klíčová slova
- Advanced glycation end products, Gestational diabetes mellitus, Oral glucose tolerance test, Pregnancy, Thiamine,
- MeSH
- dospělí MeSH
- erytrocyty metabolismus MeSH
- gestační diabetes krev MeSH
- lidé MeSH
- membránové transportní proteiny krev MeSH
- následné studie MeSH
- produkty pokročilé glykace krev MeSH
- těhotenství MeSH
- thiaminpyrofosfát krev MeSH
- transketolasa krev MeSH
- Check Tag
- dospělí MeSH
- lidé MeSH
- těhotenství MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- klinické zkoušky MeSH
- práce podpořená grantem MeSH
- Názvy látek
- membránové transportní proteiny MeSH
- produkty pokročilé glykace MeSH
- SLC19A2 protein, human MeSH Prohlížeč
- SLC19A3 protein, human MeSH Prohlížeč
- thiaminpyrofosfát MeSH
- transketolasa MeSH
While the pathogenic role of dicarbonyl stress and accelerated formation of advanced glycation end products (AGEs) to glucose intolerance and to the development of diabetic complications is well established, little is known about these processes in gestational diabetes mellitus (GDM), a condition pathogenically quite similar to type 2 diabetes. The aims of the present study were (i) to determine plasma thiamine and erythrocyte thiamine diphosphate (TDP) and transketolase (TKT) activity in pregnant women with and without GDM, (ii) to assess relationships between thiamine metabolism parameters and selected clinical, biochemical and anthropometric characteristics and, finally, (iii) to analyse relationship between variability in the genes involved in the regulation of transmembrane thiamine transport (i.e. SLC19A2 and SLC19A3) and relevant parameters of thiamine metabolism. We found significantly lower plasma BMI adjusted thiamine in women with GDM (P = 0.002, Mann-Whitney) while levels of erythrocyte TDP (an active TKT cofactor) in mid-trimester were significantly higher in GDM compared to controls (P = 0.04, Mann-Whitney). However, mid-gestational TKT activity - reflecting pentose phosphate pathway activity - did not differ between the two groups (P > 0.05, Mann-Whitney). Furthermore, we ascertained significant associations of postpartum TKT activity with SNPs SLC19A2 rs6656822 and SLC19A3 rs7567984 (P = 0.03 and P = 0.007, resp., Kruskal-Wallis). Our findings of increased thiamine delivery to the cells without concomitant increase of TKT activity in women with GDM therefore indicate possible pathogenic role of thiamine mishandling in GDM. Further studies are needed to determine its contribution to maternal and/or neonatal morbidity.
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