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Raw gene Expression data is sourced from GEO, and the appropriate db package for mapping probes to gene symbols was sourced from the Bioconductor AnnotationData packages.
You can read more about microarray data here.
Select conditions below to toggle them from the plot:
| GROUP | CONDITION | SAMPLES |
|---|---|---|
| Pancreatic Beta Cells |
GSM401525 GSM401526 GSM401527
|
|
|
GSM401528 GSM401529 GSM401530
|
Submission Date: May 11, 2009
Summary: Peroxisome proliferator-activated receptor beta/delta protects against obesity by reducing dyslipidemia and insulin resistance via effects in various organs, including muscle, adipose tissue, liver, and heart. However, nothing is known about the function of PPAR-beta in pancreas, a prime organ in the control of glucose metabolism. To gain insight into so far hypothetical functions of this PPAR isotype in insulin production, we specifically ablated Ppar-beta in pancreas. The mutated mice developed a chronic hyperinsulinemia, due to an increase in both beta-cell mass and insulin secretion. Gene expression profiling indicated a broad repressive function of PPAR-beta impacting the vesicular compartment, actin cytoskeleton, and metabolism of glucose and fatty acids. Analyses of insulin release from the islets revealed an increased second-phase glucose-stimulated insulin secretion. Higher levels of PKD, PKC-delta and diacyglycerol in mutated animals lead to an enhanced formation of trans-Golgi network (TGN)-to-plasma-membrane transport carriers in concert with F-actin disassembly, which resulted in increased insulin secretion and its associated systemic effects. Taken together, these results provide evidence for PPAR-beta playing a repressive role on beta-cell growth and insulin exocytosis, which shed new light on its anti-obesity action.
GEO Accession ID: GSE16048
PMID: 23093780
Submission Date: May 11, 2009
Summary: Peroxisome proliferator-activated receptor beta/delta protects against obesity by reducing dyslipidemia and insulin resistance via effects in various organs, including muscle, adipose tissue, liver, and heart. However, nothing is known about the function of PPAR-beta in pancreas, a prime organ in the control of glucose metabolism. To gain insight into so far hypothetical functions of this PPAR isotype in insulin production, we specifically ablated Ppar-beta in pancreas. The mutated mice developed a chronic hyperinsulinemia, due to an increase in both beta-cell mass and insulin secretion. Gene expression profiling indicated a broad repressive function of PPAR-beta impacting the vesicular compartment, actin cytoskeleton, and metabolism of glucose and fatty acids. Analyses of insulin release from the islets revealed an increased second-phase glucose-stimulated insulin secretion. Higher levels of PKD, PKC-delta and diacyglycerol in mutated animals lead to an enhanced formation of trans-Golgi network (TGN)-to-plasma-membrane transport carriers in concert with F-actin disassembly, which resulted in increased insulin secretion and its associated systemic effects. Taken together, these results provide evidence for PPAR-beta playing a repressive role on beta-cell growth and insulin exocytosis, which shed new light on its anti-obesity action.
GEO Accession ID: GSE16048
PMID: 23093780
Visualize Samples
Visualizations are precomputed using the Python package scanpy on the top 5000 most variable genes.
Precomputed Differential Gene Expression
Differential expression signatures are automatically computed using the limma R package.
More options for differential expression are available to compute below.
Signatures:
Select conditions:
Control Condition
Perturbation Condition
Only conditions with at least 1 replicate are available to select
Differential expression signatures can be computed using DESeq2 or characteristic direction.