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Series GSE132056 Query DataSets for GSE132056
Status Public on Jan 30, 2020
Title Removing a Double Bond from Ceramides Ameliorates Insulin Resistance and Hepatic Steatosis
Organism Mus musculus
Experiment type Expression profiling by high throughput sequencing
Summary Ceramides contribute to the lipotoxicity that underlies diabetes, hepatic steatosis, and heart disease. By genetically engineering mice, we deleted the enzyme dihydroceramide desaturase-1 (DES1) which inserts a conserved double bond into the backbone of ceramides and other predominant sphingolipids. Ablation of DES1 from whole animals, or tissue-specific deletion in the liver, and/or adipose tissue resolved hepatic steatosis and insulin resistance in mice caused by leptin deficiency or obesogenic diets. Mechanistic studies revealed new ceramide actions that promoted lipid uptake and storage and impaired glucose utilization, none of which could be recapitulated by (dihydro)ceramides that lacked the critical double bond. These studies suggest that inhibition of DES1 may provide a means of treating hepatic steatosis and cardiometabolic disorders.
Overall design Livers isolated from Control and Liver specific Degs1 knockout mice following either normal chow or high fat diet feeding
Contributor(s) Summers SA, Chaurasia B
Citation(s) 31273070
Submission date May 31, 2019
Last update date Jan 30, 2020
Contact name Chris Stubben
Organization name Huntsman Cancer Institute
Department University of Utah
Street address 2000 Cir of Hope Dr
City Salt Lake City
State/province Utah
ZIP/Postal code 84103
Country USA
Platforms (1)
GPL24247 Illumina NovaSeq 6000 (Mus musculus)
Samples (16)
GSM3840113 194-NCD control
GSM3840114 198-NCD control
GSM3840115 209-NCD control
BioProject PRJNA545734
SRA SRP200061

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Supplementary file Size Download File type/resource
GSE132056_counts.txt.gz 653.4 Kb (ftp)(http) TXT
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