GSE73436: Chronic Activation of γ2 AMPK Induces Obesity and Reduces Beta Cell Function

Gene Expression Data Explorer
Info Gene counts are sourced from ARCHS4, which provides uniform alignment of GEO samples. You can learn more about ARCHS4 and its pipeline here.
Enter gene symbol:

Select conditions below to toggle them from the plot:

GROUP CONDITION SAMPLES
Brain
GSM1893680 GSM1893681 GSM1893682 GSM1893683 GSM1893684
GSM1893675 GSM1893676 GSM1893677 GSM1893678 GSM1893679
GSM1893685 GSM1893686
Description

Submission Date: Sep 25, 2015

Summary: Despite significant advances in our understanding of the biology determining systemic energy homeostasis, the treatment of obesity remains a medical challenge. Activation of AMP-activated protein kinase (AMPK) has been proposed as an attractive strategy for the treatment of obesity and its complications. AMPK is a conserved, ubiquitously expressed, heterotrimeric serine/threonine kinase whose short-term activation has multiple beneficial metabolic effects. Whether these translate into long-term benefits for obesity and its complications is unknown. Here, we observe that mice with chronic AMPK activation, resulting from mutation of the AMPK γ2 subunit, exhibit ghrelin signalling-dependent hyperphagia, obesity and impaired pancreatic islet insulin secretion. Humans bearing the homologous mutation manifest a congruent phenotype. Our studies highlight that long-term AMPK activation can have adverse metabolic consequences with implications for pharmacological strategies seeking to chronically activate AMPK systemically to treat metabolic disease.

GEO Accession ID: GSE73436

PMID: 27133129

Description

Submission Date: Sep 25, 2015

Summary: Despite significant advances in our understanding of the biology determining systemic energy homeostasis, the treatment of obesity remains a medical challenge. Activation of AMP-activated protein kinase (AMPK) has been proposed as an attractive strategy for the treatment of obesity and its complications. AMPK is a conserved, ubiquitously expressed, heterotrimeric serine/threonine kinase whose short-term activation has multiple beneficial metabolic effects. Whether these translate into long-term benefits for obesity and its complications is unknown. Here, we observe that mice with chronic AMPK activation, resulting from mutation of the AMPK γ2 subunit, exhibit ghrelin signalling-dependent hyperphagia, obesity and impaired pancreatic islet insulin secretion. Humans bearing the homologous mutation manifest a congruent phenotype. Our studies highlight that long-term AMPK activation can have adverse metabolic consequences with implications for pharmacological strategies seeking to chronically activate AMPK systemically to treat metabolic disease.

GEO Accession ID: GSE73436

PMID: 27133129

Visualize Samples

Info Visualizations are precomputed using the Python package scanpy on the top 5000 most variable genes.

Precomputed Differential Gene Expression

Info 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 Gene Expression Analysis
Info Differential expression signatures can be computed using DESeq2 or characteristic direction.
Select differential expression analysis method:
Bulk RNA-seq Appyter

This pipeline enables you to analyze and visualize your bulk RNA sequencing datasets with an array of downstream analysis and visualization tools. The pipeline includes: PCA analysis, Clustergrammer interactive heatmap, library size analysis, differential gene expression analysis, enrichment analysis, and L1000 small molecule search.