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Transcriptomic Profiling of Neonatal Offspring Hearts from Gestational Diabetes Mellitus Rat Models

ABSTRACT: Maternal diabetes during pregnancy has been associated with an increased risk of metabolic and cardiovascular disorders in the offspring. However, the underlying mechanisms by which intrauterine hyperglycemia impairs fetal cardiovascular development remain incompletely understood. Our study aimed to characterize the intrauterine environment in the setting of maternal diabetes mellitus and to identify the associated molecular alterations in the fetal heart. A rat model of intrauterine hyperglycemia was established to investigate transcriptomic changes in the cardiac tissue of offspring.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE298866 | GEO | 2026/05/06

REPOSITORIES: GEO

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Gestational diabetes mellitus alters placental structure, efficiency, and plasticity

Project description:The hemochorial placenta provides a critical barrier at the maternal-fetal interface to modulate maternal immune tolerance and enable gas and nutrient exchange between mother and conceptus. Pregnancy outcomes are adversely affected by gestational diabetes mellitus (GDM); however, the effects of GDM on placental formation, and subsequently fetal development, are not fully understood. In this report, streptozotocin was used to induce hyperglycemia in pregnant rats for the purpose of investigating the impact of GDM on placental formation and fetal development. GDM caused placentomegaly and placenta malformation, decreasing placental efficiency and fetal size. Elevated glucose disrupted rat trophoblast stem (TS) cell differentiation in vitro. Evidence of altered trophoblast differentiation was also observed in vivo, as hyperglycemia affected the junctional zone transcriptome and interfered with intrauterine trophoblast invasion and uterine spiral artery remodeling. When exposed to hypoxia, rats with GDM showed decreased proliferation and ectoplacental cone development on gestation day (gd) 9.5 and complete pregnancy loss by gd 13.5. Furthermore, elevated glucose concentrations inhibited TS cell responses to hypoxia in vitro. Overall, these results indicate that alterations in placental development, efficiency, and plasticity could contribute to the suboptimal fetal outcomes in offspring from pregnancies complicated by GDM.

2020-07-07 | GSE144276 | GEO

Proteomics and Bioinformatics Analysis of Cardiovascular Related Proteins in Offspring Exposed to Gestational Diabetes Mellitus

Project description:Introduction Previous studies have demonstrated that exposed to the initial suboptimal intrauterine environment of gestational diabetes mellitus (GDM) may increase risk of cardiovascular disease in adulthood. Methods In order to investigate the underlying mechanisms involved in the increased risk of cardiovascular diseases in the offspring of GDM, we applied a high-throughput proteomics approach to compare the proteomic expression profile of human umbilical vessels of normal and GDM offspring. Results A total of significantly different 100 proteins were identified in umbilical vessels from GDM group compared with normal controls, among which 31 proteins were up-regulated, while 69 proteins were down-regulated. Differentially expressed proteins (DEPs) are validated using Western blotting analysis. The analysis of these differently expressed proteins (DEPs) related diseases and functions results, performed by Ingenuity Pathway Analysis (IPA) software. Based on 'Diseases and Disorders' analysis, 17 proteins (ACTA2, ADAR, CBFB, DDAH1, FBN1, FGA, FGB, FGG, GLS, GSTM1, HBB, PGM3, PPP1R13L, S100A8, SLC12A4, TPP2, VCAN) were described to be associated with Cardiovascular disease, especially in Anemia, Thrombus and Myocardial infarction. Functional analysis indicated that DEPs involved in many cardiovascular functions, especially in 'vasoconstriction of blood vessel' (related DEPs: ACTA2, DDAH1, FBN1, FGA, FGB and FGG). Upstream regulator analyses of DEPs identifies STAT3 as inhibitor of ACTA2, FGA, FGB and FGG. Conclusion The results of this study indicate that intrauterine hyperglycemia is associated with an elevated risk of cardiovascular risk in the offspring.

2021-03-20 | PXD024892 |

Effects of intrauterine hyperglycemia on offspring development in gestational diabetes mellitus based on placental transcriptomics

Project description:Gestational diabetes (GDM) refers to diabetes diagnosed as diabetes in the second or third trimester of pregnancy, but not obvious before pregnancy. It is one of the most common complications of pregnancy, which can lead to perinatal asphyxia, neonatal hypoglycemia, macrosomia, cardiovascular abnormalities, obesity and other short-term and long-term adverse outcomes of the offspring. This study explores the differential expression of transcriptome between GDM and non GDM placenta, and explores the impact of subtle metabolic changes in the placenta on fetal growth and development during GDM in pregnant women.

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Epigenetic signatures of gestational diabetes mellitus on ATP5A1, PRKCH, SLC17A4 and HIF3A cord blood methylation

Project description:Background: Intrauterine exposure to gestational diabetes mellitus (GDM) confers a lifelong increased risk for metabolic and other complex disorders to the offspring. GDM-induced epigenetic modifications modulating gene regulation and persisting into later life are generally assumed to mediate these increased disease risks. To identify candidate genes for fetal programming, we compared genome-wide methylation patterns of fetal cord bloods (FCBs) from GDM and control pregnancies. Methods and Results: Using Illumina's 450K methylation arrays and following correction for multiple testing, 65 CpG sites (52 of which are associated with genes) displayed significant methylation differences between GDM and control samples. Three of four candidate genes, ATP5A1, PRKCH, and SLC17A4, from our methylation screen and one, HIF3A, from the literature were validated by bisulfite pyrosequencing. The GDM effect on FCB methylation was more pronounced in women with insulin-dependent GDM who had a more severe metabolic phenotype than women with dietetically treated GDM. However, the effect remained significant after adjustment for the maternal BMI and gestational week in a multivariate regression model. Conclusions: Our study supports an association between maternal GDM and the epigenetic status of the exposed offspring. Consistent with a multifactorial disease model, the observed FCB methylation changes are of small effect size but affect multiple genes/loci. The identified genes are primary candidates for transmitting GDM effects to the next generation. They also may provide useful biomarkers for the diagnosis and prognosis of adverse prenatal exposures and assessing the success of interventions during pregnancy.

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Project description:Effects of intrauterine hyperglycemia on offspring development in gestational diabetes mellitus based on placental transcriptomics

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Maternal hyperglycemia induces alterations in hepatic amino acid, glucose and lipid metabolism of neonatal offspring: Multi-omics insights from a diabetic pig model

Project description:Intrauterine exposure to disturbed maternal glucose metabolism is associated with adverse consequences for the offspring. Hepatic disorders in affected offspring emerge in early development; thus, detection of disease biomarkers at an early stage may elucidate the underlying mechanisms of maternal hyperglycemia-induced metabolic disease and improve timely diagnosis and treatment strategies. To systematically study the molecular consequences of maternal hyperglycemia, we used data independent acquisition (DIA) proteomics and compared the molecular profiles of liver of three days old wild-type piglets born to a transgenic hyperglycemic pig model with those of wild-type piglets born to normoglycemic mothers.

2023-07-10 | PXD040305 | Pride

Gene expression in the F1 and F2 mouse hippocampus with intrauterine hyperglycemia exposure

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2021-08-25 | GSE147039 | GEO

Effects of GDM involves alterations in gene specific DNA methylation

Project description:Gestational diabetes mellitus(GDM) will bring health issues for offspring. The offspring of diabetic mothers often reveal high birth weight and are prone to have obesity, hypertension and dyslipidemia. It was implied that the phenotype of offspring might be influenced by intrauterine environment and planned in utero already in addition to the genetic influences.M-bM-^@M-^XProgrammingM-bM-^@M-^Y refers to the process whereby a stimulus at a critical window of development has long-term effects. A large body of studies investigated the adverse intrauterine environment was correlated with poor fetal growth and increased risk of Type 2 diabetes in the adulthood. Epigenetic mechanism has been proposed to involve in the link between environmental and nutritional factors and gene expression regulation. DNA methylation is one of the major epigenetic modifications. We hypothesized that DNA methylation changes could participate in the gene expression related to glucose intolerance in the offspring. Furthermore, DNA methylation might also determine the transgenerational disease transmission. comparison of intrauterine hyperglycemia exposed rats vs. control rats for genome-wide DNA methylation changes

2015-02-10 | E-GEOD-65779 | biostudies-arrayexpress

Methylation arrays (MethylationEPIC) of cord and peripheral whole blood from children born to mothers with obesity or gestational diabetes, with longitudinal follow-up during their first year of life

Project description:Epidemiological studies have associated maternal metabolic conditions such as obesity and gestational diabetes with poor health outcomes in the offspring. Epigenetic mechanisms may help explain the intrauterine influence that mothers have on their offspring during pregnancy. Here, using Illumina's MethylationEPIC array technology, we have longitudinally profiled the blood methylomes of children born to mothers with obesity and obesity with gestational diabetes, and healthy controls, during the first year of life (measurements at 0, cord blood; 6 and 12 months, peripheral blood).

2023-03-01 | E-MTAB-12728 | biostudies-arrayexpress

Gestational diabetes and human amniocytes

Project description:Context: Context: Gestational diabetes (GDM) has profound effects on the intrauterine metabolic milieu and is linked to obesity and diabetes in offspring, but the mechanisms driving these effects remain largely unknown. Alterations gene expression in amniocytes exposed to GDM in utero may identify potential mechanisms leading to metabolic dysfunction later in life. Objective: Objective: To profile changes in the transcriptome in human amniocytes exposed to GDM Methods: A nested case-control study was performed in second trimeseter amniocytes matched for offspring sex, maternal race/ethnicity, maternal age, gestational age at amniocentesis, gestational age at birth and gestational diabetes status. Sex-specific RNA-sequencing was completed and gene expression changes were identified. Results: Expression of interferon-stimulated genes was increased in GDM amniocytes accounting for 6 of the top 10 altered genes (q<0.05). Enriched biological pathways in GDM anmiocytes included pathways involving inflammation, the interferon response, fatty liver disease, monogenic diabetes and atherosclerosis. Conclusion: In a unique repository of human amniocytes exposed to GDM in utero, trancriptome analysis identified enrichment of inflammation and interferon-related pathways.

2020-05-15 | GSE150621 | GEO

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