N-3 polyunsaturated fatty acids effectively protect against neural tube defects in diabetic mice induced by streptozotocin

2021 ◽  
Author(s):  
Kelei Li ◽  
Yan Shi ◽  
Suqin Zhu ◽  
Xianfeng Shao ◽  
Huiying Li ◽  
...  

Folate cannot prevent all neural tube defects (NTD), indicating other pathogenesis still exists except for folate deficiency. Maternal diabetes mellitus during pregnancy can increase the risk of offspring NTD. Our...

2020 ◽  
Vol 26 (11) ◽  
pp. 837-849
Author(s):  
Maria Schindler ◽  
Dirk Dannenberger ◽  
Gerd Nuernberg ◽  
Mareike Pendzialek ◽  
Katarzyna Grybel ◽  
...  

Abstract During the first days of development the preimplantation embryo is supplied with nutrients from the surrounding milieu. Maternal diabetes mellitus affects the uterine microenvironment, leading to a metabolic adaptation processes in the embryo. We analysed embryonic fatty acid (FA) profiles and expression of processing genes in rabbit blastocysts, separately in embryoblasts (EBs) and trophoblasts (TBs), to determine the potential consequences of maternal diabetes mellitus on intracellular FA metabolism. Insulin-dependent diabetes was induced by alloxan in female rabbits. On Day 6 post coitum, FA profiles in blastocysts (EB, TB and blastocoel fluid) and maternal blood were analysed by gas chromatography. The expression levels of molecules involved in FA elongation (fatty acid elongases, ELOVLs) and desaturation (fatty acid desaturases, FADSs) were measured in EB and TB. Maternal diabetes mellitus influenced the FA profile in maternal plasma and blastocysts. Independent from metabolic changes, rabbit blastocysts contained a higher level of saturated fatty acids (SFAs) and a lower level of polyunsaturated fatty acids (PUFAs) compared to the FA profile of the maternal plasma. Furthermore, the FA profile was altered in the EB and TB, differently. While SFAs (palmitic and stearic acid) were elevated in EB of diabetic rabbits, PUFAs, such as docosahexaenoic acid, were decreased. In contrast, in the TB, lower levels of SFAs and higher levels of oleic acid were observed. EB and TB specific alterations in gene expression were found for ELOVLs and FADSs, key enzymes for FA elongation and desaturation. In conclusion, maternal diabetes mellitus alters embryonic FA metabolism differently in EB and TB, indicating a lineage-specific metabolic adaptive response.


2021 ◽  
Vol 224 (2) ◽  
pp. S188-S189
Author(s):  
Stacey Gold ◽  
Catherine Lopez ◽  
Jessica L. Quistorff ◽  
Sarah Downs ◽  
Sara Iqbal ◽  
...  

2008 ◽  
Vol 17 (23) ◽  
pp. 3675-3685 ◽  
Author(s):  
K. A. Burren ◽  
D. Savery ◽  
V. Massa ◽  
R. M. Kok ◽  
J. M. Scott ◽  
...  

Hypertension ◽  
2019 ◽  
Vol 73 (1) ◽  
Author(s):  
Joana Oliveira Miranda ◽  
Rui João Cerqueira ◽  
Henrique Barros ◽  
José Carlos Areias

Intrauterine fetal conditions can have lifelong cardiovascular effects. The impact of maternal diabetes mellitus on children’s cardiovascular profile is not well established. The goal of this study was to explore the association between maternal diabetes mellitus and offspring’s blood pressure (BP) ≤10 years of age. Generation XXI is a prospective birth cohort, which enrolled 8301 mother-offspring pairs, including 586 (7.1%) children of diabetic mothers. The associations between maternal diabetes mellitus and BP at 4, 7, and 10 years of age was modeled using linear regression. A mixed-effects model was built to assess differences in BP variation over time. Path analysis was used to quantify effects of potential mediators. Maternal diabetes mellitus was associated with higher BP in offspring at the age of 10 (systolic: β, 1.48; 95% CI, 0.36–2.59; and diastolic: β, 0.86; 95% CI, 0.05–1.71). This association was independent of maternal perinatal characteristics, and it was mediated by child’s body mass index and, to a lesser extent, by gestational age, type of birth, and birth weight (indirect effect proportion, 73%). No significant differences in BP were found at 4 and 7 years of age. Longitudinal analysis showed an accelerated systolic BP increase on maternal diabetes mellitus group (β, 1.16; 95% CI, 0.03–2.28). These finding were especially relevant in males, suggesting sex differences in the mechanisms of BP prenatal programing. Our results provide further evidence that maternal diabetes mellitus is associated with high BP late in childhood, demonstrating a significant role of child’s body mass in the pathway of this association.


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