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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

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

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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.

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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

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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2016-05-20 | PXD002927 | Pride

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