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Successful discontinuation of insulin treatment after gestational diabetes is shown to be a case of MODY due to a glucokinase mutation

100%
Talapatra I., Kalavalapalli S., Robinson J., Ellard S., Tymms D.
Open Medicine
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2008
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vol. 3
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issue 2
225-228
EN
We describe a woman who first presented with gestational diabetes at 26 weeks gestation and was managed with insulin. Following delivery of a healthy baby she had an abnormal OGTT (oral glucose tolerance test) 6 weeks post partum and was managed with diet. In her second pregnancy she was diagnosed with gestational diabetes at 10 weeks and required insulin. Following delivery she was again managed on diet alone. Four years later, during her third pregnancy, she was managed with insulin from the outset. She remained on insulin post partum and for several years. Later her two younger children, aged 11 years and 7 years, were found to have GCK mutation causing MODY (Maturity Onset Diabetes Of the Young) subtype glucokinase. Following this she underwent molecular genetic testing and was also shown to have the GCK mutation. She was gradually taken off insulin and is now managed on diet alone with excellent glycaemic control. Her two children are under regular follow up care and on no medication for diabetes.
2
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Exposure to Maternal Diabetes in Utero and DNA Methylation Patterns in the Offspring

88%
West N. A., Kechris K., Dabelea D.
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vol. 1
1-9
EN
Perturbations in early life environments, including intrauterine exposure to maternal gestational diabetes (GDM), are hypothesized to lead to metabolic imprinting resulting in increased risk of cardiometabolic outcomes later in life. We aimed to 1) identify candidate genes and biological pathways associated with differentially methylated regions (DMRs) in relation to exposure to GDM in utero and, 2) using mediation analysis, more definitively investigate the potential for mediation of the effect of exposure to maternal diabetes in utero on cardiometabolic traits in childhood risk through our identified DMRs. Genome-wide methylation analysis of peripheral blood mononuclear cell’s DNA was conducted in 21 healthy children, ages 8-12 years. P-values from multiple linear regression analyses for >27,000 CpG sites were ranked to identify DMRs between the exposure groups. Among the top 10 ranked DMRs, we identified several genes, including NPR1, PANK1, SCAND1, and GJA4, which are known to be associated with cardiometabolic traits. Gene enrichment analysis of the top 84 genes, each with p<=0.005, identified the ubiquitin proteasome system (UPS) as the most enriched biological pathway (p = 0.07). The UPS pathway reflects biological processes known to be associated with endothelial function, inflammation, lipid metabolism, insulin resistance and b-cell apoptosis, whose derangements are central to the pathogenesis of cardiometabolic diseases. Increased methylation of PYGO1 and CLN8 had the greatest relative mediation effect (RME = 87%, p=0.005 and RME=50%, p=0.01) on the impact of exposure to maternal diabetes in utero on VCAM-1 levels in the offspring. Multiple candidate genes and the UPS were identified for future study as possible links between exposure to maternal gestational diabetes in utero and adverse cardiometabolic traits in the offspring. In particular, increased methylation of PYGO1 and CLN8 may be biological links between intrauterine exposure to maternal diabetes and significantly increased VCAM-1 levels in the offspring.
3
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Ventricular septal defects in function of maternal sociodemographic aspects

63%
Vereczkey A., Kósa Z., Csáky-Szunyogh M., Urbán R., Czeizel A.
Open Medicine
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2012
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vol. 7
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issue 4
511-522
EN
The objective of our project is to reveal the possible etiological factors of different congenital cardiovascular abnormalities. In this study, we evaluated single ventricular septal defect (VSD) after surgical correction or with lethal outcome. The birth outcomes of these cases in the function of maternal socio-demographic features were evaluated. Data are based on 1,659 VSD cases, 2,534 matched controls and 38,151 all controls without any defects, in addition in the mothers of 19,393 malformed controls with other isolated defects in the population-based large dataset of the Hungarian Case-Control Surveillance of Congenital Abnormalities. VSD had mild female excess with a higher rate of preterm birth and mainly low birth weight indicating intrauterine growth restriction of affected fetuses, particularly in males and full-term or average weighted cases. The mothers of cases with VSD had lower socioeconomic status and higher rate of smoking and particularly drinking habit. The evaluation of medically recorded pregnancy complications showed an association of gestational diabetes with a higher risk of VSD. In conclusion, the association of small localized size of VDS and obvious fetal growth restriction needs further explanation in these cases, while gestational diabetes, lower socioeconomic status and adverse lifestyle of pregnant women may have a role in the origin of VSD.
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