Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA137695 | ENA |
REPOSITORIES: ENA
Similar Datasets
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. 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)).
2011-11-29 | E-GEOD-27017 | biostudies-arrayexpress
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
Project description:Adipogenin (Adig) is an adipocyte-enriched transmembrane protein. Its expression is induced during adipogenesis in rodent cells and a recent genome wide association study associated BMI-adjusted leptin levels with the ADIG locus. In order to begin to understand the biological function of adipogenin, we studied adipogenesis in Adig deficient cultured adipocytes and phenotyped Adig null (Adig-/-) mice. Data from Adig deficient cells showed that Adig is required for adipogenesis. In vivo, Adig-/- mice were leaner than wildtype mice when fed a high-fat diet and when crossed with Ob/Ob hyperphagic mice. In addition to the impact on adipogenesis and fat mass accrual, Adig deficiency also reduced fat mass adjusted plasma leptin levels and impaired leptin secretion from adipose explants, suggesting an additional direct impact on the regulation of leptin secretion.
2020-11-11 | GSE158005 | GEO
Project description:To investigate the transcriptional profiles of adipocytes and stromal vascular cells from mouse visceral adipose tissue(vWAT) in lean (Low fat diet, LFD fed), obese (high fat diet, HFD fed) and formerly obese (diet switch (SW) from 9 weeks HFD, to 3 weeks LFD) to induce weight loss.
2022-08-04 | GSE210014 | GEO
Project description:Compare miRNA expression profiles in epididymal adipocytes from normal and leptin deficient obese mice
2009-02-21 | E-MEXP-1789 | biostudies-arrayexpress
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
Project description:Purpose: RNAseq analyses were conducted to screen for the genes undergoing transcriptional changes either in the liver of high-fat-diet (HFD)-induced obese mice or in the liver of Lepr-deficient db/db mice compared to the livers of the respective control mice Methods: C57BL/6 wild-type male mice were fed on high-fat diet (HFD) or a low-fat diet (NCD) for 18 weeks starting from 6 weeks of age, and the livers were collected at 24 weeks of age at ad libitum-fed condition.Misty/misty or db/db were sacrificed at ad libitum-fed condition at 10weeks and the liver was collected. Results: 2079 genes and 1085 genes were identified in high-fat-diet fed mice and db/db mice, respectively.
2022-01-06 | GSE188344 | GEO
Project description:The experiment measures liver-tissue gene expression in Aquaporin-9 wildtype and knockout mice, in the leptin receptor deficient, obese C57Bl/6 mice. The knockout strategy has been published here PMID:17360690. Mice were 17-19 weeks old at tissue harvesting and provided a standardized control diet (Altromin #20000033; 22,0% protein und 5% fat) during the final 2 weeks of the experiment. Furthermore, the mice were removed from food for the final 4 hours before tissue harvesting.
2015-11-02 | E-MTAB-3526 | biostudies-arrayexpress
Project description:Obesity is associated with an increased incidence of high grade prostate cancer (PC) and worse prognosis for PC patients. Recently, we showed in men that obesity-related periprostatic white adipose tissue (WAT) inflammation, characterized by macrophages surrounding dead or dying adipocytes forming crown-like structures, was associated with high grade PC. Possibly, interventions that suppress periprostatic WAT inflammation will improve outcomes for men with PC. Prior to testing interventions we conducted this study to identify transcriptomic differences in periprostatic fat from lean and obese mice. We hypothesized that periprostatic fat from obese mice would have a proinflammatory signature in gene expression pattern. To test our hypothesis that obese mice would develop molecular signatures of inflammation in periprostatic fat, we fed mice low fat diet or high fat diet for 12 weeks and then harvested periprostatic fat at sacrifice. RNA was isolated and analyzed from 5 lean and 5 obese mice and analyzed by microarray.
2019-07-22 | GSE123355 | GEO
Project description:Maternal obesity is linked with increased adverse outcomes for mother and fetus. However, the metabolic impact of excessive fat accumulation within the altered hormonal context of pregnancy is not well understood. We used a murine model of obesity, the high fat diet-fed C57BL/6J mouse to determine adipose tissue-mediated molecular mechanisms driving metabolic dysfunction throughout pregnancy. Remarkably, obese mice exhibited a normalization of visceral fat accumulation at late-stage pregnancy (-53%, P<0.001 E18.5) to achieve levels comparable in mass (per gram of body weight) to that of non pregnant, control diet fed mice. Moreover, whilst obese pregnant mice showed a marked glucose intolerance and apparent insulin resistance at mid-stage pregnancy (E14.5), glucose homeostasis converged with that of lean pregnant mice at late-stage pregnancy, suggesting an unexpected amelioration of the worsening metabolic dysfunction in obese pregnant mice. Transcriptomic analysis of the late-stage visceral fat indicated reduced de novo lipogenic drive (Me1, Fasn, Scd1, Dgat2), retinol metabolism (Rdh11, Rbp4) and inflammation (Mcp1, Tnfα) in obese pregnant mice that was confirmed functionally by their lower adipose proinflammatory macrophage density. Elevated expression of estrogen receptor a (ERα) in visceral adipose tissue was identified as potential unifying mechanism for the transcriptional changes and reduced adiposity of late stage obese pregnancy. Support for a role for ERα was provided by experiments showing that the ERα selective agonist PPT suppressed lipogenesis in primary mouse adipocytes and suppressed Me1, Fasn, SCD1 and Dgat2 mRNA levels in mature female human ChubS7 clonal fat cells. Our data reveal a novel role for elevated visceral adipocyte estrogen signaling as a protective mechanism against visceral fat hypertrophy and inflammation in late pregnancy. Pregnant high fat, pregnant control fat, non pregnant high fat, non pregnant control fat. Five biologial replictes each (20 samples).
2013-12-31 | E-GEOD-48811 | biostudies-arrayexpress