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GSE100388
Mus musculus
15 Downloadable Samples
Description
To elucidate the bioactive property of the dietary antioxidant curcumin, we examined tissue distribution and the gene expression- and lipidomic-profiles in epididymal white adipose tissue (eWAT) of the diet-induced obese mice. Dietary intake of curcumin (0.1% W/W) didnt affect the eWAT weight and the plasma lipid levels but reduced the levels of lipid peroxidation marker in eWAT. Curcumin was a slightly accumulated in eWAT and altered the gene expression associated with eukaryotic translation initiation factor 2 (EIF2) signaling. Curcumin suppressed the endoplasmic reticulum (ER) stress-related eIF2 phospholyration, the accumulation of macrophages and the expression of oxidative stress-sensitive transcription factor NF-B p65 and leptin, whereas anti-inflammatory effect wasnt enough to reduce the TNF- and IFN- levels. Lipidomic- and gene expression analysis suggests that curcumin reduced the contents of some diacylglyverols (DAGs) and DAG derived glycerophospholipids by suppressing the expressions of lipogenesis-related glycerol-3-phosphate acyltransferase 1 and lipolysis-related adipose triglyceride lipase.
Publication Title
Dietary Intake of Curcumin Improves eIF2 Signaling and Reduces Lipid Levels in the White Adipose Tissue of Obese Mice.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 23 Downloadable Samples
Description
Cardiac hypertrophy can lead to heart failure, and is induced either by physiological stimuli eg postnatal development, chronic exercise training or pathological stimuli eg pressure or volume overload. Majority of new therapies for heart failure has mixed outcomes. A combined mouse model and oligo-array approach are used to examine whether phosphoinositide 3-kinase (p110-alpha isoform) activity is critical for maintenance of cardiac function and long-term survival in a setting of heart failure. The significance and expected outcome are to recognise genes involved in models of heart failure ie pathological- vs physiology-hypertrophy, and examine the molecular mechanisms responsible for such activity.
Publication Title
PI3K(p110 alpha) protects against myocardial infarction-induced heart failure: identification of PI3K-regulated miRNA and mRNA.
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