Rattus norvegicus
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PROVIDER: PRJNA252928 | ENA |
REPOSITORIES: ENA
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Project description:Expression data from liver of WNIN/Ob lean and obese rats
| PRJNA252930 | ENA
Project description:Obesity is characterised by increased adipocyte size and number. Analysis of altered gene expression gives better understading about the mechanisms involved/alterted in the development of obesity in this new obese rat model. We used Microarrays to delinate the alted gene expression in adipose tissue of WNIN/Ob obese rats Retroperitioneal adipose tissue was collected from 4 month old WNIN/Ob lean and obese rats (n=2 per phenotype) for RNA extraction and hybridization on Affymatrix Rat gene 1ST arrays.
2014-06-18 | E-GEOD-58575 | biostudies-arrayexpress
Project description:In mammals, expansion of adipose tissue mass induces accumulation of adipose tissue macrophages (ATMs). We isolated CD11c- (FB) and CD11c+ (FBC) perigonadal ATMs from SVCs of lean (C57BL/6J Lep +/+) and obese leptin-deficient (C57BL/6J Lep ob/ob) mice. We used expression microarrays to generate transcription profiles of perigonadal ATMs from lean (C57BL/6J Lep +/+) and obese (C57BL/6J Lep ob/ob) mice. Profiling purified FBs and FBCs, we identified 521 transcripts whose expression was differentially (nominal p-value < 0.01) expressed between FBs from lean and obese mice and 1509 genes whose expression was differentially (nominal p-value <0.01) expressed between FBC from lean and obese mice
2013-12-18 | GSE53403 | GEO
Project description:In mammals, expansion of adipose tissue mass induces accumulation of adipose tissue macrophages (ATMs). We isolated CD11c- (FB) and CD11c+ (FBC) perigonadal ATMs from SVCs of lean (C57BL/6J Lep +/+) and obese leptin-deficient (C57BL/6J Lep ob/ob) mice. We used expression microarrays to generate transcription profiles of perigonadal ATMs from lean (C57BL/6J Lep +/+) and obese (C57BL/6J Lep ob/ob) mice. Profiling purified FBs and FBCs, we identified 521 transcripts whose expression was differentially (nominal p-value < 0.01) expressed between FBs from lean and obese mice and 1509 genes whose expression was differentially (nominal p-value <0.01) expressed between FBC from lean and obese mice RNA was isolated from sorted FBC (F4/80+, CD11b+, CD11c+) cells and FB ( F4/80+, CD11b+, CD11c-) cells and using RNeasy micro-kits (Qiagen), using a PicoPure RNA isolation kit then amplified two-rounds. Labeled cRNA Mouse Genome 430 2.0 arrays (purified FB and FBC adipose tissue macrophages. There was a total of sixteen samples. FB and FBC populations were isolated from 4 lean and 4 obese mice.
2013-12-18 | E-GEOD-53403 | biostudies-arrayexpress
Project description:The expression of adipogenic genes is decreased in obesity and diabetes mellitus ; Samuel T. Nadler*, Jonathan P. Stoehr*, Kathryn L. Schueler*, Gene Tanimoto, Brian S. Yandell, and Alan D. Attie*,§ ; Departments of * Biochemistry, and Statistics and Horticulture, University of Wisconsin, Madison, WI, 53706; and Affymetrix, Inc., Santa Clara, CA 95051 ; Communicated by Neal L. First, University of Wisconsin, Madison, WI, July 13, 2000 (received for review April 3, 2000) ; Obesity is strongly correlated with type 2 diabetes mellitus, a common disorder of glucose and lipid metabolism. Although adipocytes are critical in obesity, their role in diabetes has only recently been appreciated. We conducted studies by using DNA microarrays to identify differences in gene expression in adipose tissue from lean, obese, and obese-diabetic mice. The expression level of over 11,000 transcripts was analyzed, and 214 transcripts showed significant differences between lean and obese mice. Surprisingly, the expression of genes normally associated with adipocyte differentiation were down-regulated in obesity. Not all obese individuals will become diabetic; many remain normoglycemic despite profound obesity. Understanding the transition to obesity with concomitant diabetes will provide important clues to the pathogenesis of type 2 diabetes. Therefore, we examined the levels of gene expression in adipose tissue from five groups of obese mice with varying degrees of hyperglycemia, and we identified 88 genes whose expression strongly correlated with diabetes severity. This group included many genes that are known to be involved in signal transduction and energy metabolism as well as genes not previously examined in the context of diabetes. Our data show that a decrease in expression of genes normally involved in adipogenesis is associated with obesity, and we further identify genes important for subsequent development of type 2 diabetes mellitus. Experiment Overall Design: For obesity study, lean samples include C57BL/6J lean, (C57BL/6J X BTBR) F1 and BTBR lean, obese sampples incluse C57BL/6J-ob/ob, (C57BL/6J X BTBR) F2-ob/ob and BTBR-ob/ob. All samples are subjected to Mu11K A and B arrays. Experiment Overall Design: For diabetes study, B6-ob/ob, (C57BL/6J X BTBR) F2-ob/ob low glucose, (C57BL/6J X BTBR) F2-ob/ob medium glucose, (C57BL/6J X BTBR) F2-ob/ob high glucose, and BTBR-ob/ob samples were analyzed for genes whose expression levels changes correlated with the plasma glucose levels in these mice. All samples are subjected to Mu11K A and B arrays.
2007-12-04 | E-GEOD-2952 | biostudies-arrayexpress
Project description:Profiling adipose tissue (eWAT) from obese ob/ob and lean control ob/+ mice
| PRJNA155293 | ENA
Project description:BACKGROUND AND AIMS: It is proposed that impaired expansion of subcutaneous adipose tissue (SAT), caused in part by an increase in adipose tissue fibrosis, redirects fatty acids to the liver and other organs, leading to ectopic lipid accumulation and insulin resistance. We therefore evaluated whether a decrease in SAT expandability, assessed by measuring SAT lipogenesis (triglyceride production), and an increase in SAT fibrogenesis (collagen production) are associated with nonalcoholic fatty liver disease (NAFLD) and insulin resistance in people with obesity. APPROACH AND RESULTS: In vivo SAT lipogenesis and fibrogenesis, the expression of SAT genes involved in extracellular matrix (ECM) formation, and insulin sensitivity were assessed in three groups stratified by adiposity, insulin sensitivity and intrahepatic triglyceride (IHTG) content: 1) healthy lean (Lean-NL; n=12); 2) obese with normal IHTG content and normal glucose tolerance (Ob-NL; n=25); and 3) obese with NAFLD and abnormal glucose metabolism (Ob-NAFLD; n=25). Abdominal SAT total triglyceride synthesis rates were greater in the Ob-NL (65.9±4.6 g/wk) and Ob-NAFLD (71.1±6.7 g/wk) than the Lean-NL group (16.2±2.8 g/wk), without a difference between the obese groups. Abdominal SAT collagen synthesis rate and the composite expression of collagen genes progressively increased from Lean-NL to Ob-NL to Ob-NAFLD and were greater in the Ob-NAFLD than the Ob-NL group (P<0.05). Collagen synthesis rate and the composite expression of collagen genes correlated with factors that regulate collagen production, including circulating insulin and fibrogenic factors in SAT (all P<0.001). CONCLUSIONS: Adipose tissue lipogenesis and expandability are not impaired in people with obesity and NAFLD. However, SAT fibrogenesis and extracellular matrix remodeling are greater in people with obesity and NAFLD than in those with obesity and normal IHTG content. ClinicalTrials.gov number: NCT02706262.
2021-10-01 | GSE159924 | GEO
Project description:ob/ob mice is an obese mice. CIDE family proteins including Cidea, Cideb and Cidec play important role in lipid metabolism. Cidea is mainly expressed in the brown adipose tissue (BAT). Cidec is mainly expressed in the BAT and white adipose tissue (WAT). We generated ob/ob/Cidea-/-/Cidec-/- mice to investigate the phenotype of fat tissue. ob/ob/Cidea-/-/Cidec-/- mice are lean when compared with ob/ob mice. The tissue weight and TAG content of BAT and WAT was extreamly decreased in ob/ob/Cidea-/-/Cidec-/- mice compared with that in ob/ob mice. We next extract the total RNA from the BAT and WAT of ob/ob and ob/ob/Cidea-/-/Cidec-/- mice, to perform microarray analysis using Mouse Gene 1.0 ST array system, Affymetrix. We then analysised the up-regulated and down regulated pathways.
2018-04-18 | GSE100989 | GEO
Project description:Obesity is risk factor for development of fatty liver. Analysis of altered gene expression gives better understading about the mechanisms involved/alterted in the development of obesity-induced fattyliver in this new obese rat model. We used Microarrays to delinate the alted gene expression in liver of WNIN/Ob obese rats Liver was collected from 4 month old WNIN/Ob lean and obese rats for RNA extraction and hybridization on Affymatrix Rat gene 1ST arrays. Four RNA samples from each phenotype were pooled and used for the study.
2014-06-18 | E-GEOD-58576 | biostudies-arrayexpress
Project description:We characterized the insulin sensitivity and multi-tissue gene expression profiles of lean and insulin resistant, obese Zucker rats untreated or treated with one of four PPARγ ligands (pioglitazone, rosiglitazone, troglitazone, and AG035029). We analyzed the transcriptional profiles of adipose tissue, skeletal muscle, and liver from the rats and determined whether ligand insulin-sensitizing potency was related to ligand-induced alteration of functional pathways. Ligand treatments improved insulin sensitivity in obese rats, albeit to varying degrees. Male Zucker fatty (fa/fa) and lean (fa/+) rats (Charles River, Wilmington, MA) were received at 6 weeks of age. Fatty rats were weight-matched upon arrival and randomly divided into one of five experimental groups. The fatty rat groups varied by the type of chow they were fed - normal chow alone or with a PPARγ ligand admixture: normal chow (fatty control, FC), rosiglitazone-treated (Rosi), pioglitazone-treated (Pio), troglitazone-treated (Tro), or AG035029-treated (AG). Lean control (LC) rats were all fed normal chow. Rats groups were maintained on the diets for 21 days. Adipose tissue (epididymal), skeletal muscle (gastrocnemius), and liver were harvested from lean (LC) and insulin resistant, obese Zucker rats untreated (FC) or treated with one of four PPARγ ligands (pioglitazone [Pio], rosiglitazone [Rosi], troglitazone [Tro], and AG035029 [AG]).
2011-02-11 | E-GEOD-21329 | biostudies-arrayexpress