E-MTAB-9213
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-9213 | ExpressionAtlas | 2021-03-22
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:RNA-Seq of pancreatic islets from whole body knockout of lncRNA Pax6os1 mice
| PRJEB38857 | ENA
Project description:RNA-Seq was performed on pancreatic islets from four transgenic mouse strains affecting LKB1 and AMPK. A conditional LKB1 knockout strain was generated. Double conditional knockouts for AMPK alpha1 and AMPK alpha2 were also generated. These conditional strains were crossed with RIP-Cre (driven by rat insulin promoter) or Ins1-Cre mice to generate LKB1 knockout and AMPK double knockout strains.
2014-10-25 | E-MTAB-2791 | biostudies-arrayexpress
Project description:RNA-Seq of pancreatic islets from beta cell-specific Pax6 knockout mice
| PRJEB20579 | ENA
Project description:Objective: Disturbances in NAD+ metabolism have been described as a hallmark for multiple metabolic and age-related diseases, including type 2 diabetes. While alterations in pancreatic -cell function are critical determinants of whole-body glucose homeostasis, the role of NAD+ metabolism in the endocrine pancreas remains poorly explored. Here, we aimed to evaluate the role of nicotinamide riboside (NR) metabolism in maintaining NAD+ levels and pancreatic -cell function in pathophysiological conditions. Methods: Whole body and pancreatic -cell-specific NRK1 knockout (KO) mice were metabolically characterized in situations of high-fat feeding and aging. We also analyzed pancreatic -cell function and gene expression. Results: We first demonstrate that NRK1, the essential enzyme for the utilization of NR, is substantially expressed in pancreatic -cells. While NR treatment did not alter glucose-stimulated insulin secretion in pancreatic islets from young healthy mice, NRK1 knockout mice displayed glucose intolerance and compromised -cells response to a glucose challenge upon high-fat feeding or aging. Interestingly, β cells dysfunction stemmed from the functional failure of other organs, such as liver and kidney, and the associated changes in circulating peptides and hormones, as mice lacking NRK1 exclusively in β-cells did not show altered glucose homeostasis. Conclusions: This work unveils a new physiological role for NR metabolism in the maintenance of glucose tolerance and pancreatic -cell function in high-fat feeding or aging conditions.
2025-01-31 | GSE208552 | GEO
Project description:Whole proteomic analysis was conducted on isolated mouse pancreatic islets from both WT and C3ar1 KO mice.
2025-05-07 | PXD062327 | Pride
Project description:To explore the underlying mechanism for the regulatory role of SIRT3 in pancreatic islets under standard and high fat diet feeding, we conducted RNA sequencing on the isolated islets from standard diet and high fat diet-fed wild type and pancreatic beta cell selective Sirt3 knockout mice (four groups in total). Three biological replicates were performed for each group.
2022-08-15 | GSE156345 | GEO
Project description:RNA-seq data of founder mice pancreatic islets
2021-07-27 | GSE180364 | GEO
Project description:AIMS/HYPOTHESIS: Manoeuvres aimed at increasing beta cell mass have been proposed as regenerative medicine strategies for diabetes treatment. Raf-1 kinase inhibitor protein 1 (RKIP1) is a common regulatory node of the mitogen-activated protein kinase (MAPK) and nuclear factor κB (NF-κB) pathways and therefore may be involved in regulation of beta cell homeostasis. The aim of this study was to investigate the involvement of RKIP1 in the control of beta cell mass and function. METHODS: Rkip1 (also known as Pebp1) knockout (Rkip1 (-/-)) mice were characterised in terms of pancreatic and glucose homeostasis, including morphological and functional analysis. Glucose tolerance and insulin sensitivity were examined, followed by assessment of glucose-induced insulin secretion in isolated islets and beta cell mass quantification through morphometry. Further characterisation included determination of endocrine and exocrine proliferation, apoptosis, MAPK activation and whole genome gene expression assays. Capacity to reverse a diabetic phenotype was assessed in adult Rkip1 (-/-) mice after streptozotocin treatment. RESULTS: Rkip1 (-/-) mice exhibit a moderately larger pancreas and increased beta cell mass and pancreatic insulin content, which correlate with an overall improvement in whole body glucose tolerance. This phenotype is established in young postnatal stages and involves enhanced cellular proliferation without significant alterations in cell death. Importantly, adult Rkip1 (-/-) mice exhibit rapid reversal of streptozotocin-induced diabetes compared with control mice. CONCLUSIONS/INTERPRETATION: These data implicate RKIP1 in the regulation of pancreatic growth and beta cell expansion, thus revealing RKIP1 as a potential pharmacological target to promote beta cell regeneration. Pancreatic gene expression of Rkip-1 (Raf kinase inhibitor 1) knockout (KO) and wild type (WT) mice, including three biological replicates in each group.
2012-11-19 | E-GEOD-31150 | biostudies-arrayexpress
Project description:Reactive oxygen species (ROS) have been implicated as mediators of pancreatic β-cell damage. While β-cells are thought to be vulnerable to oxidative damage, we have shown, using inhibitors and acute depletions, that thioredoxin reductase, thioredoxin, and peroxiredoxins are the primary mediators of antioxidant defense in β-cells. However, the role of this antioxidant cycle in maintaining redox homeostasis and β-cell survival in vivo remains unclear. Here, we generated mice with a β-cell specific knockout of thioredoxin reductase 1 (Txnrd1.fl/fl; Ins1.Cre/+, βKO). Despite blunted glucose-stimulated insulin secretion, knockout mice maintain normal whole body glucose homeostasis. Unlike pancreatic islets with acute Txnrd1 inhibition, βKO islets do not demonstrate increased sensitivity to continuous ROS. RNA-sequencing analysis revealed that Txnrd1-deficient β-cells have increased expression of Nuclear factor erythroid 2-related factor 2 (Nrf2)-regulated genes, and altered expression of genes involved in heme and glutathione metabolism, suggesting an adaptive response. Txnrd1-deficient β-cells also have decreased expression of factors controlling β-cell function and identity which may explain the mild functional impairment. Together, these results suggest that Txnrd1-knockout β-cells compensate for loss of this essential antioxidant pathway by increasing expression of Nrf2-regulated antioxidant genes, allowing for protection from excess ROS at the expense of normal β-cell function and identity.
2022-07-05 | GSE200965 | GEO
Project description:The short chain fatty acid (SCFA) receptor (free fatty acid receptor-3; FFAR3) is expressed in pancreatic beta cells; however, its role in insulin secretion is not clearly defined. Here, we examined the role of FFAR3 in insulin secretion. Using islets from global knockout FFAR3 (Ffar3-/-) mice, we explored the role of FFAR3 and ligand-induced FFAR3 signaling on glucose stimulated insulin secretion. RNA sequencing was also performed to gain greater insight into the impact of FFAR3 deletion on the islet transcriptome. First exploring insulin secretion, it was determined that Ffar3-/- islets secrete more insulin in a glucose-dependent manner as compared to wildtype (WT) islets. Next, exploring its primary endogenous ligand, propionate, and a specific agonist for FFAR3, signaling by FFAR3 inhibited glucose-dependent insulin secretion, which occurred through a Gαi/o pathway. To help understand these results, transcriptome analyses by RNA-sequencing of Ffar3-/- and WT islets observed multiple genes with well known roles in islet biology to be altered by genetic knockout of FFAR3. Our data shows that FFAR3 signaling mediates glucose stimulated insulin secretion through Gαi/o sensitive pathway. Future studies are needed to more rigorously define the role of FFAR3 by in vivo approaches. Analysis of total RNA from 3 biological replicates of pancreatic islets isolated from free fatty acid receptor 3 knockout (Ffar3 KO) and wildtype (Ffar3 WT) male mice
2016-07-03 | E-GEOD-67991 | biostudies-arrayexpress