Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome analysis of islets from diabetes-resistant and diabetes-prone obese mice reveals novel gene regulatory networks involved in beta cell compensation and failure

ABSTRACT: We carried out genome-wide transcriptome analysis of islets to investigate the gene expression landscape of ob/ob and db/db mouse models at 6 and 16 weeks of age. The purpose of this study is to determine the changes in the islet transcriptomic landscape that mediate the processes of beta cell compensation and failure in ob/ob and db/db mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE169275 | GEO | 2021/12/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Mouse-adapted SARS-CoV-2 infected Lungs from wild type or genetically obese mice

Project description:Lung samples were generated from male mice of C57BL/6J(B6), C57BL/6JHamSlc-ob/ob (ob/ob) and C57BLKS/J-db/db on 3 days post infection of mouse-adapted SARS-CoV-2

2023-05-15 | E-MTAB-12617 | biostudies-arrayexpress

Lung samples from obese mice with or without mouse-adapted SARS-CoV-2 infection

Project description:Lung samples were generated from male mice of C57BL/6JHamSlc-ob/ob (ob/ob) and C57BLKS/J-db/db on 3 days post infection of mouse-adapted SARS-CoV-2 or non-infected condition

2023-05-15 | E-MTAB-12618 | biostudies-arrayexpress

Single-cell RNA sequencing of pancreatic islets from obese mice with different diabetes risk reveals diabetes-susceptible β cell clusters

Project description:Single-cell RNA sequencing of pancreatic islets from 18-week-old male New Zealand Obese (NZO/HIBomDife) and B6.V-Lepob/ob (OB) mice were fed a standard diet or a carbohydrate-enriched diet for 2 additional days (+CH / -CH).

2022-07-07 | GSE159211 | GEO

Transcriptome analysis of islets from diabetes-resistant and diabetes-prone obese mice reveals novel gene regulatory networks involved in beta cell compensation and failure

Project description:Transcriptome analysis of islets from diabetes-resistant and diabetes-prone obese mice reveals novel gene regulatory networks involved in beta cell compensation and failure

| PRJNA716068 | ENA

Transcription profiling of adipose tissue, liver, skeletal muscle, and pancreatic islets from nondiabetic and diabetic obese mice to understand susceptibility to diabetes.

Project description:Obesity is a strong risk factor for the development of type 2 diabetes. We have previously reported that in adipose tissue of obese (ob/ob) mice, the expression of adipogenic genes is decreased. When made genetically obese, the BTBR mouse strain is diabetes susceptible and the C57BL/6J (B6) strain is diabetes resistant. We used DNA microarrays and RT-PCR to compare the gene expression in BTBR-ob/ob versus B6-ob/ob mice in adipose tissue, liver, skeletal muscle, and pancreatic islets. Our results show: 1) there is an increased expression of genes involved in inflammation in adipose tissue of diabetic mice; 2) lipogenic gene expression was lower in adipose tissue of diabetes-susceptible mice, and it continued to decrease with the development of diabetes, compared with diabetes-resistant obese mice; 3) hepatic expression of lipogenic enzymes was increased and the hepatic triglyceride content was greatly elevated in diabetes-resistant obese mice; 4) hepatic expression of gluconeogenic genes was suppressed at the prediabetic stage but not at the onset of diabetes; and 5) genes normally not expressed in skeletal muscle and pancreatic islets were expressed in these tissues in the diabetic mice. We propose that increased hepatic lipogenic capacity protects the B6-ob/ob mice from the development of type 2 diabetes. Diabetes 52:688â700, 2003 Experiment Overall Design: Four B6-ob/ob and four BTBR-ob/ob male mice at 14 weeks of age were used in the microarray study. RNA samples from two individuals were pooled for each tissue, and each pooled RNA sample was applied to an Affymetrix MGU74AV2 array. Because of the scarcity of islets in the BTBR-ob/ob mice, 4 additional mice were pooled to obtain islet RNA from these animals. Sixteen MGU74Av2 arrays (2 strains X 4 tissues X 2 replicates = 16 arrays) were used to monitor the expression level of â12,000 genes or ESTs.

2007-08-31 | E-GEOD-2899 | biostudies-arrayexpress

Gene expression in diabetes-prone (NZO/HiBomDife) and diabetes-resistant (C57BL/6.V-Lepob/ob) mouse strains

Project description:Mouse strains like NZO and B6-ob/ob differ in their susceptibility to diet-induced diabetes. Comparison of the islet transcriptomes leads to genes that are either involved in protection or apoptosis of pancreatic islet cells upon carbohydrate challenge. Genes being upregulated in NZO can be seen as drivers of beta cell failure, while genes upregulated in B6-ob/ob are most likely involved in beta cell protection.

2018-02-19 | GSE64956 | GEO

Profiling pancreatic islets from obese db/db and lean control db/+ mice

2013-03-22 | GSE31953 | GEO

Profiling pancreatic islets from obese db/db and lean control db/+ mice

Project description:This program addresses the molecular basis of beta-cell failure associated with the development of type 2 diabetes in the db/db mice. Specifically, which genes are differentially expressed in pancreatic islets of the db/db mice compared to the control db/+ mice? The db/db mice islets profiling data was analyzed by identifying genes that were up- and down-regulated at selected p value and fold change in the islets of db/db mice compared to the corresponding db/+ controls.

2013-03-22 | E-GEOD-31953 | biostudies-arrayexpress

Enriched Alternative Splicing in Islets of Diabetes-Susceptible Mice

Project description:Mouse strains like NZO and B6-ob/ob differ in their susceptibility to diet-induced diabetes. Comparison of the islet transcriptomes already revealed different biological processes, here we focused on alternative splicing events as one possible mechanism.

2021-09-04 | GSE183247 | GEO

Endogenous advanced glycation end products in pancreatic islets after short-term carbohydrate intervention in obese, diabetes-prone mice.

Project description:Diet-induced hyperglycemia is described as one major contributor to the formation of advanced glycation end products (AGEs) under inflammatory conditions, crucial in type 2 diabetes progression. Previous studies have indicated high postprandial plasma AGE-levels in diabetic patients and after long-term carbohydrate feeding in animal models. Pancreatic islets play a key role in glucose metabolism; thus, their susceptibility to glycation reactions due to high amounts of dietary carbohydrates is of special interest. Therefore, diabetes-prone New Zealand Obese (NZO) mice received either a carbohydrate-free, high-fat diet (CFD) for 11 weeks or were additionally fed with a carbohydrate-rich diet (CRD) for 7 days. In the CRD group, hyperglycemia and hyperinsulinemia were induced accompanied by increasing plasma 3-nitrotyrosine (3-NT) levels, higher amounts of 3-NT and inducible nitric oxide synthase (iNOS) within pancreatic islets. Furthermore, N-ε-carboxymethyllysine (CML) was increased in the plasma of CRD-fed NZO mice and substantially higher amounts of arg-pyrimidine, pentosidine and the receptor for advanced glycation end products (RAGE) were observed in pancreatic islets. These findings indicate that a short-term intervention with carbohydrates is sufficient to form endogenous AGEs in plasma and pancreatic islets of NZO mice under hyperglycemic and inflammatory conditions.

| S-EPMC6411991 | biostudies-literature

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