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GEO accession GSE263483 is currently private and is scheduled to be released on Dec 30, 2025.

ABSTRACT: GEO accession GSE263483 is currently private and is scheduled to be released on Dec 30, 2025.

PROVIDER: PRJNA1097628 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28590210_1.fastq.gz	Fastqsanger.gz
	SRR28590210_2.fastq.gz	Fastqsanger.gz
	SRR28590211_1.fastq.gz	Fastqsanger.gz
	SRR28590211_2.fastq.gz	Fastqsanger.gz
	SRR28590212_1.fastq.gz	Fastqsanger.gz

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TET-dependent signaling of β-cell underlies intrauterine hyperglycemia-induced glucose intolerance in offspring [RRBS]

Project description:Epidemiologically, gestational diabetes mellitus (GDM) increases offspring’s diabetes risk. Intrauterine hyperglycemia (IHG) is a typical characteristic of GDM, impairing offspring’s glucose tolerance and insulin secretion, but the underlying mechanisms remain unclear. Here, we found IHG downregulates DNA demethylases Tet2/3 in fetal pancreatic islets. Pancreas-specific Tet2/3 double knockout (DKO) recapitulates the IHG effects.

2025-12-31 | GSE288093 | GEO

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

Project description:Studies on human and animals suggest associations between gestational diabetes mellitus (GDM) with impaired cognitive performance in offspring. Using a mouse model of diabetes during pregnancy, we found that intrauterine hyperglycemia exposure resulted in memory impairment in both the first filial (F1) males and the second filial (F2) males from the F1 male offspring. The effects of intrauterine hyperglycemia exposure on F1 and F2 hippocampus gene expression were also examined.

2021-08-25 | GSE147039 | GEO

TET-dependent signaling of β-cell underlies intrauterine hyperglycemia-induced glucose intolerance in offspring [scRNA-seq]

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Single-cell profiling of liver in offspring with intrauterine hyperglycemia reveals acute-phase response deficiency

Project description:Gestational diabetes mellitus (GDM) has long-term effects on the offspring health. Among these chronic diseases, inflammatory profiles play important roles in their development. Assessment for inflammatory status of GDM offspring is limited. Thus, the single cell RNA sequencing (scRNA-seq) was conducted to delineate the inflammatory characteristics of offspring with intrauterine hyperglycemia (IHG). scRNA-seq analysis of mice liver revealed myeloid polarization and multiple lineages developmental retardationwas identified in IHG offspring. Proinflammatory potential of myeloid cells seemed to be deeply imprinted in the liver of adult offspring with IHG.

2025-10-21 | GSE289783 | GEO

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.

2025-12-30 | GSE263483 | GEO

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

Epigenetic reprogramming of sperm in F1 adult male mice with intrauterine hyperglycemia exposure

Project description:Birth cohort studies and experimental investigations in animals link gestational diabetes mellitus (GDM) with impaired cognitive performance in the first filial generation (F1). We found that intrauterine hyperglycemia exposure resulted in behavior abnormality and cognitional functional disorder of both F1- and F2-GDM male mice. Methylome of sperm of F1 adult male mice from control pregnant mice (F1-C) and GDM pregnant mice (F1-GDM) revealed differentially methylated genes enriched in neurodevelopmental process.

2021-08-25 | GSE142502 | GEO

Intrauterine hyperglycemia exposure per se altered metabolic functions in F2 offspring via reprogramming F1 PGCs

Project description:Intrauterine hyperglycemia has been linked to an elevated risk of diabetes in next and further generations. Existing reports about transmission effects of intrauterine hyperglycemia have included both intrauterine and postnatal metabolic exposure factors, the impact of intrauterine hyperglycemia per se has not been separately assessed. To investigate effect of intrauterine hyperglycemia exposure per se on further generations, we selected non-phenotypic F1-GDM and F2-GDM male mice to examin metabolic changes in next generation and performed a methylome on day 13.5 primordial germ cells (PGCs) of F1-GDM male fetus to explore its underlying mechanism. We found that intrauterine hyperglycemia exposure per se resulted in obesity, insulin resistance and/or glucose intolerance in F2 male mice, and no changes in F3 male mice. Methylome of day 13.5 PGCs of F1-GDM male fetus revealed differently methylation genes enriched in obesity and diabetic pathogenesis. Methylation validation of targeted gene Fyn showed consistent hypo-methylation status in F1 PGCs, F1 fetal testis, sperm of F1/N-GDM mice, and somatic cells of F2-GDM male mice. While fetal testis of F2-GDM mice showed no alteration in Fyn methylation. Our data indicates that intrauterine hyperglycemia exposure per se contributes to metabolic changes in F2 but not F3 generation, by altering methylation erasure in PGCs of F1 generation.

2017-12-20 | GSE108319 | GEO

Intrauterine hyperglycemia impairs primordial germ cell development and fertility by sex-specific epigenetic reprogramming interference in mice offspring [ATAC-seq]

Project description:Adverse intrauterine environments, such as hyperglycemia, impair the sexual reproduction and species continuous, yet the underlying mechanisms remain poorly understood. In this study, we demonstrated that intrauterine hyperglycemia significantly disrupted primordial germ cell (PGC) development, especially in female offspring and thus reduced fertility. Using Oct4-EGFP transgenic mice with intrauterine hyperglycemia exposure, we revealed that hyperglycemia compromised sexually specific chromatin accessibility and DNA methylation reprogramming during PGC development. Particularly, in female PGCs, hyperglycemia leads to the aberrant retention of chromatin accessibility at pluripotency gene promoters such as Nanog and Tfap2c, inhibiting proper gene silencing and blocking the initiation of meiosis, which ultimately hinders oocyte maturation. Conversely, male PGCs exhibit less severe changes in chromatin accessibility and gene transcription. Intriguingly, the global DNA methylation reconstruction is impaired in male PGCs, particularly in key imprinted gene regions, suggesting potential developmental ramifications for later stages and even subsequent generations. Particularly, our findings indicate that intrauterine hyperglycemia adversely affects sex differentiation in PGCs by disrupting the expression of critical sex-determining transcription factors. Collectively, these findings highlight how intrauterine hyperglycemia interferes with sex-specific epigenetic reprogramming during PGC development, leading to abnormal germ cell development, reduced fertility, and adverse intergenerational effects.

2025-07-28 | GSE286574 | GEO

Intrauterine hyperglycemia impairs primordial germ cell development and fertility by sex-specific epigenetic reprogramming interference in mice offspring [RNA-seq]

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