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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data of bone marrow and peripheral adipocytes from leptin deficient mice and obese mice fed with a high fat diet

ABSTRACT: The aim of this study was to characterize the obesity-related gene expression profiles between bone marrow adipocytes and peripheral white adipocytes from obese mice fed with high fat diet and leptin deficient mice Alterations of gene expression with high fat diet and in mice lacking leptin were analyzed in bone marrow and peripheral white adipocytes isolated from C57BL/6J male mice using Affymetrix Mouse Gene 1.0 ST arrays. Bone marrow adipocytes and peripheral white adipocytes (n=6-10 animals per group) were isolated from male C57BL/6J mice (6-months, 14-months ) fed with either standard chow or a high fat diet containg 60% calories from fat. Samples were grouped into diet (standard chow vs. high fat diet) and age (6-month (6M), 14-month (14M) and 18-month (18M)).

ORGANISM(S): Mus musculus

SUBMITTER: Li Fen Liu

PROVIDER: E-GEOD-27017 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from mouse bone marrow adipocytes with age

Project description:The aim of this study was to characterize the age-related gene expression profiles between bone marrow adipocytes and peripheral white adipocytes. Alterations of gene expression with aging were analyzed in bone marrow and peripheral white adipocytes isolated from C57BL/6J male mice using Affymetrix Mouse Gene 1.0 ST arrays. Bone marrow adipocytes and peripheral white adipocytes (n=6-10 animals per group) were isolated from male C57BL/6J mice (6-months, 14-months and 18-months of age). Samples were grouped into cell type (bone marrow adipocytes vs. peripheral adipocytes) and age (6-month (6M), 14-month (14M) and 18-month (18M)).

2011-11-29 | E-GEOD-25905 | biostudies-arrayexpress

Expression Data from Bone Marrow Progenitor-Derived Adipocytes, White Adipocytes and Brown Adipocytes.

Project description:We have identified a population of adipocytes in fat tissue that arise from bone marrow-derived progenitor cells. We used microarrays to compare the global gene expression patterns of the bone marrow progenitor-derived adipocytes as well as conventional white and brown adipocytes to evaluate the relationship between these adipocyte subpopulations. Gonadal fat tissue (for white adipocytes) and intrascapular fat tissue (for brown adipocytes) was digested with collagenase and adipocytes were recovered by centrifugation/flotation. Bone marrow derived adipocytes were isolated from the adipocyte fraction of gonadal fat tissue from mice receiving bone marrow tranplants from donors expressing either green fluorescent protein (GFP) or beta-galactosidase (LacZ) by flow cytometry.

2010-01-08 | E-GEOD-19757 | biostudies-arrayexpress

Expression data of bone marrow and peripheral adipocytes from leptin deficient mice and obese mice fed with a high fat diet

Project description:The aim of this study was to characterize the obesity-related gene expression profiles between bone marrow adipocytes and peripheral white adipocytes from obese mice fed with high fat diet and leptin deficient mice Alterations of gene expression with high fat diet and in mice lacking leptin were analyzed in bone marrow and peripheral white adipocytes isolated from C57BL/6J male mice using Affymetrix Mouse Gene 1.0 ST arrays.

2011-11-29 | GSE27017 | GEO

Transcriptional co-factor TBLR1 controls lipid mobilization in white adipose tissue

Project description:Lipid mobilization (lipolysis) in white adipose tissue (WAT) critically controls lipid turnover and adiposity in humans. While the acute regulation of lipolysis has been studied in detail, the transcriptional determinants of WAT lipolytic activity remain still largely unexplored. Here we show that the genetic inactivation of transcriptional co-factor transducin beta-like-related (TBLR) 1 blunts the lipolytic response of white adipocytes through the impairment of cAMP-dependent signal transduction. Indeed, mice lacking TBLR1 in adipocytes are defective in fasting-induced lipid mobilization and when placed on a high fat diet show aggravated adiposity, glucose intolerance and insulin resistance. TBLR1 levels are found to increase under lipolytic conditions in WAT of both human patients and mice, correlating with serum free fatty acids (FFA). As a critical regulator of WAT cAMP signaling and lipid mobilization, proper activity of TBLR1 in adipocytes may thus represent a critical molecular checkpoint for the prevention of metabolic dysfunction in subjects with obesity-related disorders. We used microarrays to identify global gene expression in 3T3-L1 adipocytes lacking TBLR1 and compared gene expression to control shRNA treated cells in both basal and isoproterenol stimulated states. We analyzed 12 RNA samples extracted from 3T3-L1 adipocytes that were treated with either control or TBLR1 specific shRNAs and with or without 10 ÂµM isoproterenol for 3 hrs. Three replicates of each condition.

2013-04-01 | E-GEOD-43658 | biostudies-arrayexpress

C/EBP? and PPAR?-specific transcriptional programs in mature adipocytes in vivo

Project description:We took a systematic approach to determine the transcriptional programs that are specifically regulated by C/EBP? in mature white adipocytes of mice on chow diet or high fat diet. The hypothesis tested in the present study was that C/EBP?, as a lipogenic transcription factor, has unique direct targets compared to PPAR?. Our inducible adipocyte specific knockout system allows us to test the direct targets of C/EBP? and PPAR? in adipocytes by short-term C/EBP? or PPAR? elimination in mature adipocytes in vivo. Results indicate that although it has been shown that C/EBP? and PPAR? cross-regulate each other, they have distinct direct responsive targets. Moreover, there are very few C/EBP? specific targets in mice on a chow diet, most of the C/EBP? targets in mature adipocytes are genes modulated by HFD feeding. Total RNA obtained from subcutaneous adipose tissue of Adn-C/EBP?-/- mice on doxycycline chow diet for 3 days, doxycycline high fat diet for 3 days or 1 month and Adn-PPAR?-/- mice on doxycycline chow diet for 3 days, compared to control littermates.

2014-11-04 | E-GEOD-62937 | biostudies-arrayexpress

Effect of sesaminol on C2C12 cells on myogenesis pathway

Project description:Adipocytes are key players in maintaining energy homeostasis and are classified into two different categories: white and brown adipocyte. While white adipocytes store energy as triacylglycerols in lipid droplets, brown adipocytes combust excess chemical energy and release in the form of heat through uncoupled respiration. This characteristic phenomenon of brown fat attracts researchers and pharmacological industries to view brown fat as one of the potential therapeutic targets for obesity and associated metabolic disease. In the current study, we investigated the effect of a small molecule, sesaminol (SML) on brown fat activity and found that SML induces thermogenic program in primary white adipocytes as well as chow diet fed mice. In particular, SML treatment to mice elevated mitochondrial complex proteins and the rate oxygen consumption in brown and white fat. Administration of SML to high fat diet (HFD) challenged mice decreased weight gain, adiposity and cholesterol levels along with an increase of brown fat gene program in brown and white fat. Mechanistically, SML repressed the myogenic gene program in C2C12 myoblasts and increased all mitochondrial marker genes as appeared in brown adipose cells. Together, our results demonstrate that SML stimulates brown adipose function and protects mice against diet induced weight gain.

2020-03-27 | GSE147599 | GEO

Adipocyte long noncoding RNA transcriptome analysis of obese mice identified Lnc-leptin which regulates Leptin

Project description:Obesity induces profound transcriptome changes in adipocytes; recent evidence suggests that lncRNAs play key roles in this process. Here, we performed a comprehensive transcriptome study by RNA-Seq in adipocytes isolated from interscapular brown, inguinal and epididymal white adipose tissues in diet-induced obese mice. Our analysis reveals a set of obesity-dysregulated lncRNAs, many of which exhibit dynamic changes in fed vs. fasted state, potentially serving as novel molecular markers reflecting adipose energy status. Among the most prominent ones is Lnc-leptin, an lncRNA transcribed from an enhancer region upstream of Leptin. Expression of Lnc-leptin is sensitive to insulin and closely correlates to Leptin expression across diverse pathophysiological conditions. Functionally, induction of Lnc-leptin is essential for adipogenesis, and its presence is required for a loop formation between exon2 of Lnc-leptin and promoter of Leptin in mature adipocytes and the maintenance of Leptin expression in vitro and in vivo. Our study establishes Lnc-leptin as a new regulator of Leptin.

2018-04-19 | GSE113315 | GEO

Transcription profiling of mouse adipocytes and white adipose tissue of mice maintained on normal chow or high fat diet

Project description:We studied the role of the cAMP responsive factor CREB in promoting insulin resistance following its activation in adipose under obese conditions; We identified genes that were upregulated in primary cultures of mouse adipocytes following exposure to forskolin; and we characterized genes that are also induced in white adipose tissue in mice maintained on a high fat diet. Experiment Overall Design: Primary cultures of mouse adipocytes,harvested from visceral adipose tissue, were exposed to forskolin (10uM) or vehicle control (DMSO) for 2 hours. White adipose tissue (epididymal fat pads) were collected from mice maintained on a 60% high fat diet for 12 weeks and from control mice on normal chow.

2009-03-07 | E-GEOD-14363 | biostudies-arrayexpress

Phosphoprotein network analysis of white adipose tissues unveils deregulated pathways in response to high-fat diet

Project description:Despite wide efforts in the last decade, signaling aberrations associated with obesity remain enigmatic. Here, we carried out phosphoproteomic analysis of mouse white adipose tissues (WAT) upon low-fat diet (LFD) and high-fat diet (HFD) to dissect underlying molecular mechanisms of obesity. Of the 7696 phosphopeptides quantified, 191 proteins including various insulin-responsive proteins and metabolic enzymes functioning in lipid homeostasis, exhibited differential phosphorylation with high-fat feeding. Kinase predictions and integrated network analysis identified several deregulated kinase signaling pathways, and suggested possibilities of HFD-induced transcriptional rewiring. Further, functional validation of a novel HFD-responsive site on cytoplasmic acetyl-coA forming ACSS2 (S263) suggested that the phosphorylation is important in regulating insulin signaling and maintaining triglyceride levels. This study represents one of the first comprehensive phosphoproteome data in mouse obesity models, and describes a systems-level approach for identifying deregulated molecular events and potential therapeutic targets in the context of high-fat feeding and adipocyte perturbation.

2016-05-20 | PXD002927 | Pride

Gene expression data from adipocytes of insulin resistant mice

Project description:We developed a novel network inference approach, Biologically Anchored Knowledge Expansion (BAKE), to analyze large volume gene expression data obtained from a mouse model of insulin resistance progression. Both genetic aspects and dietary factors, specifically high caloric high-fat high-sugar diets, contribute to the progression of insulin resistance. To mimic genetic predisposition, we used a mouse model with double heterozygous deletion of early insulin signaling pathway intermediates, insulin receptor (IR) and insulin receptor substrate 1 (IRS1) genes. These mice were fed with high-fat (Western) or low-fat (Chow) diet for 8 and 16 weeks starting at 8 weeks of age. Gene expression data was collected from adipocytes isolated from these mice. Applying BAKE analysis to the adipocyte gene expression data, we demonstrate that we can accurately discover a novel regulatory gene in the insulin signaling pathway. The mouse model of double heterozygous deletion of insulin receptor (IR) and insulin receptor substrate 1 (IRS1) was originally introduced as a polygenic model to study the development of type 2 diabetes. This mouse model, on an atherosclerosis-prone ApoE null background (IR+/- IRS1+/- ApoE-/-), also shows increased atherosclerotic lesions due to impaired insulin signaling. For our study we used female double heterozygous mice (IR+/- IRS1+/-, 'Dhet' mice or 'Dâ mice) on an ApoE null background (ApoE-/-, âEâ) fed with a Western (high-fat) diet for 8 (DW8, n=5) and 16 (DW16, n=9) weeks starting at 8 weeks of age or with a Chow (low-fat) diet (DC8, n=7; DC16, n=5). There were also ApoE null mice (ApoE-/-, 'Eâ) fed either Western diet for 8 (EW8, n=6) and 16 (EW16, n=8) weeks or Chow diet for 16 weeks (EC16, n=5) starting at 8 weeks of age.

2015-12-31 | E-GEOD-76428 | biostudies-arrayexpress

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