Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide analysis of differentially methylated genes in the fetal pancreas of progenies born from oocytes of maternal hyperglycemia

ABSTRACT: Genome-wide analysis of differentially methylated genes in the fetal pancreas of progenies born from oocytes of maternal hyperglycemia

PROVIDER: PRJNA622519 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11465407_1.fastq.gz	Fastqsanger.gz
	SRR11465407_2.fastq.gz	Fastqsanger.gz
	SRR11465408_1.fastq.gz	Fastqsanger.gz
	SRR11465408_2.fastq.gz	Fastqsanger.gz
	SRR11465409_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

Genome-wide analysis of differentially methylated genes in the fetal pancreas of progenies born from oocytes of maternal hyperglycemia

Project description:MeDIP-seq was performed to identify the epigenetic alterations in the fetal pancreas of progenies born from oocytes of maternal hyperglycemia.

2023-03-27 | GSE147904 | GEO

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

Hyperglycemia-independent neonatal streptozotocin-induced retinopathy (NSIR) in rats

Project description:Chemicals, such as MNU (N-methyl-N-nitrosourea) and NaIO3 (sodium iodate), are widely used to induce retinal degeneration in rodents. Streptozotocin (STZ) is an analog of N-acetyl glucosamine in which an MNU moiety is linked to a hexose and has a special toxic effect on insulin-producing pancreatic β-cells. It is commonly used to induce hyperglycemia to model diabetes. While intracerebroventricular injection of STZ can produce Alzheimer's disease independent of hyperglycemia, most retinal studies using STZ focus on the effects of hyperglycemia on the retina, but whether STZ has any impact on retinal cells independent of hyperglycemia is unknown. We aimed to investigate the role of cytotoxicity of STZ in rat retina. Intravitreal (5ug or 10ug) or subcutaneous (30mg/kg) injection of STZ at the early stage of newborn rats couldn’t induce hyperglycemia but caused NSIR (neonatal STZ-induced retinopathy), including reduced ERG amplitudes, retinal rosettes and apoptosis, cell cycle arrest, microglial activation, and delayed retinal angiogenesis. STZ did not affect the early-born retinal cell types but significantly reduced the late-born ones. Short-term and long-term hyperglycemia had no significant effects on the NSIR phenotypes. RNA sequencing revealed that STZ induces oxidative stress and activates the p53 pathway of retinal cells. Locally or systemically, STZ injection after P8 couldn’t induce NSIR when all retinal progenitors exit the cell cycle. Thus, NSIR in rats is independent of hyperglycemia but due to STZ’s direct cytotoxic effects on retinal progenitor cells. NSIR is a typical reaction to STZ-induced retinal oxidative stress and DNA damage. This significant finding suggests that NSIR may be a valuable model for studying retinal progenitor DNA damage-related diseases, potentially leading to new insights and treatments.

2024-07-16 | GSE272311 | GEO

Misgurnus anguillicaudatus breed:F1 progenies

Project description:Misgurnus anguillicaudatus breed:F1 progenies Raw sequence reads

| PRJNA317549 | ENA

Hyponutrition during pregnancy after insemination alters the progenies’ behavior and DNA methylation of their brain

Project description:Recent epidemiological studies suggest that hyponutritional stress during fetal period increase risks of adult-onset diseases, such as type 2 diabetes and mental diseases. Rodent models have demonstrated that hyponutrition during pregnancy alters epigenetic status of neuronal genes in the fetal brains; this implicate fatal environment contributes to susceptibility to mental disorders. However, in these studies, progenies were generated with natural mating and effects of hyponutrition during egg formation have not been eliminated. Therefore, we conducted experiments in order to finely evaluate the hyponutritional effects during fatal life using in vitro fertilization. We divided three experimental groups such as control diet (CD (AIN93G)), protein-restricted diet (PR), and PR diet with supplemental folic acid (FA) and compared body weight of mother and progenies, clinical-blood biochemistry, DNA methylation and gene-expression pattern in adult brain of the progenies, behavioral phenotypes of the progenies, and DNA methylation profile in brain of the progenies. The progenies of the PR group and the FA group exhibited increased activity in the home cage, decreased contact to a novel object, and decreased social behavior compared with the CD group. Increased home-cage activity in the PR group was rescued in the FA group. The progenies of the PR group and the FA group showed different patterns of mRNA expression and genomic methylation in the brain compared with the CD group. These results suggest that hyponutrition after insemination sufficiently induced phenotypic and epigenetic changes in the progenies. In addition, supplemental nutrition to mothers should rescue the epigenetic and phenotypic changes induced with hyponutrition.

2017-03-08 | GSE79847 | 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

Human pluripotent stem cell (hPSC)-derived progenies

Project description:Human pluripotent stem cell (hPSC)-derived progenies

| PRJNA695005 | ENA

Chronic hyperglycemia impairs metabolic switching of human myotubes

Project description:Skeletal muscle of insulin resistant individuals is characterized by lower fasting lipid oxidation and reduced ability to switch between lipid and glucose oxidation. The purpose of the present study was to examine if impaired metabolic switching could be induced by chronic hyperglycemia. Human myotubes were treated with or without chronic hyperglycemia (HG) (20 mmol/l glucose for 4 days), and the metabolism of [14C]oleic acid (OA) and [14C]glucose was studied. Acute glucose (5mmol/l) suppressed OA oxidation by 50% in normoglycemic (NG) (5.5 mmol/l glucose) cells. Myotubes exposed to chronic hyperglycemia showed a significantly reduced OA uptake and oxidation to CO2, whereas acid-soluble metabolites were increased. Glucose suppressibility, the ability of acute glucose to suppress lipid oxidation, was significantly reduced to 21%, while adaptability, the capacity to increase lipid oxidation with increasing fatty acid availability, was unaffected. Glucose uptake and oxidation was significantly reduced by about 40%. Substrate oxidation in presence of mitochondrial uncouplers showed that net and maximal oxidative capacities were significantly reduced after hyperglycemia, and the concentration of ATP was reduced by 25%. However, none of the measured mitochondrial genes were downregulated nor was mitochondrial content. Microarray showed that no genes were significantly regulated by chronic hyperglycemia. Addition of chronic lactate reduced both glucose and OA oxidation to the same extent as hyperglycemia, and this effect was specific for lactate. In conclusions, chronic hyperglycemia reduced substrate oxidation in skeletal muscle cells and impaired the metabolic switching. The effect is most likely due to an induced mitochondrial dysfunction.

2009-12-24 | GSE19620 | GEO

Gene methylation profiles in offspring born before vs. after maternal bariatric surgery

Project description:Evaluate differences in gene methylation levels between offspring born after maternal bariatric surgery and their siblings born before surgery Offspring born after maternal bariatric surgery (AMS, N=25) vs. offspring born before maternal surgery (BMS, N=25)

2013-05-16 | E-GEOD-44798 | biostudies-arrayexpress

Gene expression profile in offspring born before vs. after maternal bariatric surgery

Project description:Evaluate differences in gene expression levels between offspring born after maternal bariatric surgery and their siblings born before surgery Offspring born after maternal bariatric surgery (AMS, N=23) vs. offspring born before maternal surgery (BMS, N=23)

2013-05-16 | E-GEOD-44407 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data