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Mice model for 15q11-13 duplication syndrome show late onset obesity and altered lipid metabolism

ABSTRACT: To investigate the gene expression change in the white adipose tissue (WAT) of patDp/+ mice compared with wild type mice, the whole genome microarray profiling was performed. Total RNA from WAT of young adult stage mice (9-10 weeks old) was extracted and subject to microarray analysis. Expression change of sfrp5 gene was further validated by real-time PCR, suggesting this gene might contribute to the obesity in patDp/+ mice. We measured the gene expression change in WAT of young adult stage mice. Three patDp/+ mice and threewild type mice were used in the experiment.

ORGANISM(S): Mus musculus

SUBMITTER: Xiaoxi Liu

PROVIDER: E-GEOD-58191 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Mice model for 15q11-13 duplication syndrome show late onset obesity and altered lipid metabolism

Project description:To investigate the gene expression change in the white adipose tissue (WAT) of patDp/+ mice compared with wild type mice, the whole genome microarray profiling was performed. Total RNA from WAT of young adult stage mice (9-10 weeks old) was extracted and subject to microarray analysis. Expression change of sfrp5 gene was further validated by real-time PCR, suggesting this gene might contribute to the obesity in patDp/+ mice.

2015-05-01 | GSE58191 | GEO

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2012-04-24 | E-GEOD-37514 | biostudies-arrayexpress

Identification of CD44 downstream target genes

Project description:CD44 expression has been shown to be enhanced in the liver and white adipose tissue (WAT) during obesity, suggesting a possible regulatory role for CD44 in metabolic syndrome. To study this hypothesis, we compared the gene expression profiles in liver and in WAT between WT and CD44 knockout (CD44KO) mice fed a high-fat diet (HFD) for 21 weeks. This analysis demonstrated that several genes associated with triglyceride synthesis and accumulation, including Mogat2, Cidea, Cidea, Apoa4, and Elovl7, were decreased in the livers of CD44KO mice compared to WT mice. Many genes encoding pro-inflammatory chemokines and chemokine receptors also were decreased in the livers of CD44KO mice. Analysis with WAT showed that genes associated with triglyceride accumulation, including Fasn, Elovl6 and Mogat2, were increased in WAT of CD44KO(HFD) mice compared to WT(HFD) mice. Moreover, many genes associated with inflammation, including cytokines (Cxcl14, Cxcl12, Il33, and Il2), cytokine receptors (Ccr1, Il6ra, Il10rb), trypases (Tpsb2, Tpsab1, Tpsg1), and cellular matrix proteins (Integrin ?4 (Itga4), ItgaM, Itgb2), were decreased in WAT of CD44(HFD) compared to WT(HFD) mice. This study indicates that CD44 plays a critical role in regulating several aspects of metabolic syndrome. Liver and white adipose tissue (WAT) total RNAs were purified from 5 WT and 5 CD44 knockout mice fed with a high-fat diet for 21 weeks. Then, samples were applied on Agilent mouse genome chips.

2013-06-01 | E-GEOD-43104 | biostudies-arrayexpress

Effect of ablation of Sfrp5 on gene expression in gonadal white adipose tissue

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Cardiac over-expression of Med13, non-cardiac tissue analysis

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RNA-seq of ventricle and fat tissues of male and female cardiac myocyte-specific estrogen receptor KO mice

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Multilayered Omics Revealsl Sex- and Depot-Dependent Adipose Progenitor Cell Heterogeneity

Project description:White adipose tissue (WAT) harbors functionally diverse subpopulations of adipose progenitor cells that differentially impact tissue plasticity in a sex- and depot-dependent manner. To date, the molecular basis of this cellular heterogeneity has not been fully defined. Here, we describe a multilayered omics approach to dissect adipose progenitor cell heterogeneity from in three dimensions: progenitor subpopulation, sex, and anatomical localization. We applied state-of-the-art mass spectrometry methods to quantify 4870 proteins in eight different stromal cell populations from perigonadal and inguinal WAT of male and female mice and acquired transcript expression levels of 15477 genes using RNA-seq. Notably, our data highlight the molecular signatures defining sex differences in PDGFR+ preadipocyte differentiation and identify regulatory pathways that functionally distinguish adipose tissue PDGFRb+ subpopulations. The data are freely accessible as a resource at "Pread Profiler. Together, the multilayered omics analysis provides unprecedented insights into adipose stromal cell heterogeneity.

2023-03-11 | PXD023829 | Pride

Nuclear receptor, RORa plays a critical role in obesity-associated inflammation, hepatic steatosis, and insulin resistance

Project description:We demonstrated that RORa-deficient staggerer mice (RORasg/sg) fed with a high fat diet (HFD) showed reduced adiposity and hepatic triglyceride levels compared to wild type (WT) littermates and were resistant to the development of hepatic steatosis, adipose-associated inflammation, and insulin resistance. Gene expression profiling showed that many genes involved in triglyceride synthesis and storage, including Cidec, Cidea, and Mogat1, were expressed at much lower levels in liver of RORasg/sg mice. In addition to reduced lipid accumulation, inflammation was greatly diminished in white adipose tissue (WAT) of RORasg/sg mice fed with a HFD. The infiltration of macrophages and the expression of many immune-response and pro-inflammatory genes, including those encoding various chemo/cytokines, toll-like receptors, and TNF signaling proteins, were significantly reduced in RORasg/sg WAT. Moreover, RORasg/sg mice fed with a HFD were protected from the development of insulin resistance. Together, these results indicate that RORa plays a critical role in the regulation of several aspects of metabolic syndrome. Therefore, RORa may provide a novel therapeutic target in the management of obesity and associated metabolic diseases. Liver and white adipose tissue (WAT) total RNAs were purified from 5 WT and 5 RORasg/sg (natural deletion of RORa gene in mice) mice fed with a high fat diet for 6 weeks. Then samples were applied on Agilent mouse genome chip.

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