Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Hyperglycemia Alters the Fetal Islet Transcriptome and Leads to Progeny Islet Dysfunction

ABSTRACT: Hyperglycemia Alters the Fetal Islet Transcriptome and Leads to Progeny Islet Dysfunction

PROVIDER: PRJNA485184 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7661940_1.fastq.gz	Fastqsanger.gz
	SRR7661940_2.fastq.gz	Fastqsanger.gz
	SRR7661941_1.fastq.gz	Fastqsanger.gz
	SRR7661941_2.fastq.gz	Fastqsanger.gz
	SRR7661936_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Hyperglycemia Alters the Fetal Islet Transcriptome and Leads to Progeny Islet Dysfunction

Project description:The overall goal of this project is to identify transcriptome alteration in fetal islets exposed to transient maternal hyperglycemia from GD20 to GD22.

2019-08-01 | GSE118323 | GEO

The effect of extreme hyperglycemia on islet cell expression program

Project description:The effect of extreme hyperglycemia on islet cell expression program

| PRJNA862348 | ENA

Hyperglycemia induced microRNAs in endothelial dysfunction

Project description:Hyperglycemia is a hallmark in prediabetes and type 2 diabetes mellitus (T2DM) which increases risk of micro and macrovascular complications such as diabetic retinopathy, diabetic nephropathy (microvascular complications), and peripheral vascular disease, cerebrovascular disease and cardiovascular diseases (macrovascular complications). Endothelial cells are affected in both cases. In this study, we investigated the miRNA expression changes in HUVECs during different glucose treatment (5mM, 10mM, 25mM and 40mM glucose) at various time intervals (6, 12, 24 and 48hrs). The results of miRNA microarray showed there is a correlation between hyperglycemia induced endothelial dysfunction and miRNA expression. In silico prediction showed that the following pathways: Regulation of actin cytoskeleton, PI3K-Akt signaling pathway, Apoptosis, Neurotrophin signaling pathway, and Insulin signaling pathway, were dysregulated during hyperglycemia. Majority of the pathways are related to apoptosis. 10 miRNAs (miR-26a-5p, -26b-5p, 29b-3p, 29c-3p, 125b-1-3p, -130b-3p, - 140-5p, -221-3p, -192-5p, and -320a,) showed increased expression with increasing concentration of glucose treatment. miR-26a-5p, -29b-3p, - 140-5p, -221-3p, and -192-5p are involves in endothelial apoptosis. Our study revealed miRNAs (miR-29b-3p and – 192-5p) with known mRNA targets (BCL2 and MCL1) showed expression pattern inversely correlating with their respective target mRNAs. Therefore these miRNAs could involve in the endothelial dysfunction due to hyperglycemia.

2016-05-23 | GSE74296 | GEO

Dysfunction of the circadian clock in the renal tubule leads to enhanced renal gluconeogenesis and exacerbated hyperglycemia in diabetes

Project description:In diabetes, the kidney contributes to the development of diabetic hyperglycemia by increasing glucose reabsorption from the primary urine and by upregulating gluconeogenesis in the proximal tubule. However, these two processes are also controlled by the circadian clock, a mechanism that synchronizes a large number of specific renal functions with environmental daily cycles. Here, we investigated the (patho)physiological role of intrinsic renal tubule circadian clocks in the diabetic kidney. We demonstrate that diabetic mice devoid of the circadian transcriptional regulator BMAL1 in the renal tubule exhibit additional enhancement of renal gluconeogenesis, exacerbated hyperglycemia, increased glucosuria, polyuria and renal hypertrophy. Collectively, our results suggest that diabetic hyperglycemia can be worsened by dysfunction or misalignment of intrinsic renal circadian clocks.

2022-05-27 | GSE178319 | GEO

Transcription profiling of pancreatic islet implanted transgenic (expressing survivini) in mice

Project description:Transgenic mice were generated that expressed the inhibitor of apoptosis and mitotic regulator survivin in pancreatic islet beta cells. Control non-transgenic or transgenic islets were then used in a model of islet transplantation in diabetic recipient mice and tested for their ability to correct hyperglycemia and allow long-term engraftment of tranplanted islets in vivo. Control or transgenic islets were analyzed by chip microarray for potential transcriptional changes associated with transgenic expression of survivin, in vivo.

2006-01-16 | E-MEXP-536 | biostudies-arrayexpress

The effect of extreme hyperglycemia on islet cell expression program

Project description:Our in vivo Insulin-rtTA;TET-DTA mouse model of severe hyperglycemia revealed that proloned exposure to very high glucose levels inhibits cell cycle entry and progression of pancreatic beta cells. To investigation of the molecular mechanisms responsible for this observation we performed ex vivo experiment on wild-type ICR mouse islets mimiking the in vivo conditions and subjected them to RNAseq analysis.

2022-07-29 | GSE209751 | GEO

ARID1A loss in pancreas leads to islet developmental defect and metabolic disturbance ,Islet cell ChIP-Seq HDAC6 arid1a

Project description:ARID1A loss in pancreas leads to islet developmental defect and metabolic disturbance ,Islet cell ChIP-Seq HDAC6 arid1a

| PRJNA910559 | ENA

Gene expression profile at single cell level of islet cells from normoglycemic or hyperglycemic mice

Project description:The purpose of the experiment was to investigate the heterogeneity of islet cell response, especially beta-cells to hyperglycemia induced by severe insulin resistance in mice.

2023-09-21 | GSE234770 | GEO

Dysfunction of the circadian clock in the renal tubule leads to enhanced renal gluconeogenesis and exacerbated hyperglycemia in diabetes

Project description:Dysfunction of the circadian clock in the renal tubule leads to enhanced renal gluconeogenesis and exacerbated hyperglycemia in diabetes

| PRJNA738480 | ENA

Paternal high-fat diet elicits early-onset se-specific islet inflammation in rat progeny

Project description:Progressive β–cell failure and apoptosis, resultant of innate immune system activation1,2 is gaining traction as a converging point for type 1 (T1D) and type 2 (T2D). Islet inflammation (insulitis), a hallmark of T1D, occurs typically during the initiation phase of the disease, subsequently orchestrating an autoimmune assault against β–cells. Whether this is a primary event or a consequence of glucotoxicity or lipotoxicity is undetermined3 but metabolic stress is demonstrated to prompt islet inflammation1,2. Here we show that paternal consumption of high fat diet (HFD) invoked distinct immuno-inflammatory transcriptional response in the pancreatic islets of their weanling daughters, in contrast to compensatory changes in the sons. Importantly, these changes occurred in conjunction with transition in islet repertoire resembling the spectrum of T2D, along with progressive development of β–cell dysfunction4. Note, these females were lean, normolipidaemic and insulin sensitive4. These findings provide experimental support for the notion that islet inflammation could be an antecedent event in T2D, leading to β–cell secretory defect, repair/regeneration and apoptosis. Importantly, these effects were transmitted via paternal nutrient stress to offspring.

2021-12-29 | GSE89138 | GEO

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