Mus musculus strain:C57BL/6 wild-type and ob/ob mice
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR179019_1.fastq.gz | Fastqsanger.gz | |||
| DRR179019_2.fastq.gz | Fastqsanger.gz | |||
| DRR179020_1.fastq.gz | Fastqsanger.gz | |||
| DRR179020_2.fastq.gz | Fastqsanger.gz | |||
| DRR179021_1.fastq.gz | Fastqsanger.gz |
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Project description:The identification of glucose-responsive genes in the skeletal muscle of WT and ob/ob mice.
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Project description:To identify novel transcriptional factors involved in dysfunctional hepatic lipids homeostasis in obesity, mRNA microarray analysis were performed to of livers of ob/ob mice, a widely used obese model, and C57BL/6J control mice. Chow-fed ob/ob and C57BL/6J mice were housed in a 12 h of light and 12 h of dark cycle and fed ad libitum a regular chow diet. Mice were sacrificed at 16:00 (Zeitgeber Time 8 during light phase). Total RNA was prepared from each liver using TRIzol (Invitrogen). Equal aliquots of total RNA from each of four mouse livers in each group were pooled and used for biotin labeling as described in the Affymetrix technical bulletin. Then the transcriptional profiles of samples were probed using the Gene-Chip Mouse Genome 430 2.0 arrays.
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Project description:Liver gene expression was compared in wild type, SHP knockout, ob/ob, and ob/ob SHP double mutant mice.
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Project description:The identification of differentially expressed genes in skeletal muscle of wild-type and ob/ob mice
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Project description:Liver gene expression was compared in wild type, SHP knockout, ob/ob, and ob/ob SHP double mutant mice. A total of eight samples were analyzed using Affymetrix arrays. Each of the four genotypes studied were assayed in duplicate.
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Project description:Proteomics of liver tissue from ob/ob and WT mice. Data accompany our paper entitled “Dynamic Regulation of N6,2′-O-dimethyladenosine (m6Am) in Obesity” scheduled for publication in Nature Communications, 2021
2021-10-27 | PXD029217 | Pride
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:Ob/ob mice were given 0, 12.5 or 25 ng/hr leptin through an osmotic pump. After 12 days, livers RNA was prepared and illumina microarrays were done. We tested whether leptin can ameliorate diabetes independent of weight loss by defining the lowest dose at which leptin treatment of ob/ob mice reduces plasma [glucose] and [insulin]. We found that a leptin dose of 12.5 ng/hour significantly lowers blood glucose and that 25 ng/hour of leptin normalizes plasma glucose and insulin without significantly reducing body weight, thus establishing that leptin exerts its most potent effects on glucose metabolism. To find possible mediators of this effect, we profiled liver mRNA using microarrays and identified IGF Binding Protein 2 as being regulated by leptin with a similarly high potency. Over-expression of IGFBP2 by an adenovirus reversed diabetes in insulin resistant ob/ob, Ay/a and diet-induced obese mice (DIO), as well as insulin deficient streptozotocin-treated mice. Hyperinsulinemic clamp studies showed a three-fold improvement in hepatic insulin sensitivity following IGFBP2 treatment in ob/ob mice. These results show that IGFBP2 can regulate glucose metabolism, a finding with potential implications for the pathogenesis and treatment of diabetes.
2009-11-25 | GSE19185 | GEO
Project description:Obesity may promote myeloid cell accumulation in liver. Intravital liver tissue imaging revealed that the number of myeloid cells attached to sinusoidal wall significantly increased in ob/ob mice. To assess the pathophysiological roll of liver sinusoidal endothelial cells (LSEC) in obese livers, we performed microarray analysis in LSEC isolated from an 8-week-old wild-type and ob/ob mouse. Pathway analysis in microarray data shows genes related to cell adhesion, chemokine signaling and leukocyte transendothelial migration are upregulated in LSEC from ob/ob.
2017-02-15 | GSE84019 | GEO
Project description:Prodynorphine-expressing neurons were targeted by eGFP-RPL10a, a transgene that is expressed under the control of the Pdyn promoter in a BAC containing the Pdyn backbone. Trangenic mice were made with FvB embryos via pro-nuclear injection. Transgene-positive progenies were bred to C57BL/6J for more than five generations before being used in the current experiment. Triplicates of 6-8 hypothalami were collected per sample from wild-type and ob/ob adult mice. Polysomal IP RNA and total Input RNA were purified from each sample. Affymetrix GeneChip Mouse 430 2.0 arrays (900495) were used to identify transcripts that are specifically expressed in Pdyn neurons with a fold change (IP vs. Input) of >=2 in wild-type mice. The same microarrays were also used to identify Pdyn-specific transcripts that are differentially regulated transcriptionally by leptin deficiency with a fold change (ob IP vs. wt IP) of >=1.5.
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