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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 |
|---|---|---|
| Liver |
GSM978542 GSM978543 GSM978544 GSM978545 GSM978546 GSM978547
|
|
|
GSM978535 GSM978536 GSM978537 GSM978538 GSM978539 GSM978540 GSM978541
|
Submission Date: Jul 30, 2012
Summary: Objective: To study if diabetic and insulin-resistant states lead to mitochondrial dysfunction in the liver, or alternatively, if there is adaption of mitochondrial function to these states in the long-term range.
Results: High-fat diet (HFD) caused insulin resistance and severe hepatic lipid accumulation, but respiratory chain parameters were unchanged. Livers from insulin-resistant IR/IRS-1+/- mice had normal lipid contents and normal respiratory chain parameters, however showed mitochondrial uncoupling. Livers from severely hyperglycemic and hypoinsulimic, streptozotocin (STZ)-treated mice had massively depleted lipid levels, but respiratory chain abundance was unchanged. However, their mitochondria showed increased abundance and activity of the respiratory chain, which was better coupled compared to controls.
Conclusions: Insulin resistance, either induced by obesity or by genetic manipulation, does not cause mitochondrial dysfunction in the liver of mice. However, severe insulin deficiency and high blood glucose levels in mice cause an enhanced performance of the respiratory chain, probably in order to maintain the high energy requirement of the unsuppressed gluconeogenesis.
GEO Accession ID: GSE39752
PMID: 24291365
Submission Date: Jul 30, 2012
Summary: Objective: To study if diabetic and insulin-resistant states lead to mitochondrial dysfunction in the liver, or alternatively, if there is adaption of mitochondrial function to these states in the long-term range.
Results: High-fat diet (HFD) caused insulin resistance and severe hepatic lipid accumulation, but respiratory chain parameters were unchanged. Livers from insulin-resistant IR/IRS-1+/- mice had normal lipid contents and normal respiratory chain parameters, however showed mitochondrial uncoupling. Livers from severely hyperglycemic and hypoinsulimic, streptozotocin (STZ)-treated mice had massively depleted lipid levels, but respiratory chain abundance was unchanged. However, their mitochondria showed increased abundance and activity of the respiratory chain, which was better coupled compared to controls.
Conclusions: Insulin resistance, either induced by obesity or by genetic manipulation, does not cause mitochondrial dysfunction in the liver of mice. However, severe insulin deficiency and high blood glucose levels in mice cause an enhanced performance of the respiratory chain, probably in order to maintain the high energy requirement of the unsuppressed gluconeogenesis.
GEO Accession ID: GSE39752
PMID: 24291365
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.