Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA381164 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:A history of obesity leaves an inflammatory fingerprint in liver and adipose tissue [Liver]
| PRJNA381160 | ENA
Project description:A history of obesity leaves an inflammatory fingerprint in liver and adipose tissue
| PRJNA381159 | ENA
Project description:To analyze the gene expression profile of BAT and gWAT from Pgam1 depletion mice, we performed whole genome microarray expression profiling using brown adipose tissue (BAT) and gonadal white adipose tissue (gWAT) from adipose tissue-specific Pgam1 knockout (KO) mice.
2022-04-11 | GSE186030 | GEO
Project description:In addition to total body fat, the regional distribution and inflammatory status of enlarged adipose tissue are strongly linked to metabolic and cardiovascular complications of obesity. We recently showed that the severity of liver non-alcoholic histopathology in obese subjects increased with the amounts of macrophages in visceral adipose tissue (VAT), while no relation was found with the subcutaneous adipose tissue (SAT). In the abdominal region, SAT is anatomically divided into superficial (sSAT) and deep (dSAT) layers. The aim of the present study was to test the hypothesis that these distinct compartments differentially contribute to hepatic alteration in obesity. Total RNA was isolated from two different strata of human adipose tissue of 8 subjects.
2011-08-31 | E-GEOD-30133 | biostudies-arrayexpress
Project description:Background: Obesity is associated with infiltration of macrophages into adipose tissue. Adipose macrophages may contribute to an elevated inflammatory status by secreting a variety of pro-inflammatory mediators, including TNFalpha and IL-6. Recent data suggest that during diet-induced obesity the phenotype of adipose-resident macrophages changes from alternatively activated macrophages towards a more classical and pro-inflammatory phenotype. Here, we explore the effect of PPARγ-activation on obesity-induced inflammation in 129SV mice fed a high fat diet for 20 weeks. High fat feeding increased bodyweight gain, adipose tissue mass and liver triglycerides. Rosiglitazone treatment further increased adipose mass, reduced liver triglycerides and changed adipose tissue morphology towards smaller adipocytes. Surprisingly, rosiglitazone markedly increased the number of macrophages in adipose tissue, as shown by immunohistochemical analysis and quantification of macrophage marker genes CD68 and F4/80+. In adipose tissue, markers for classically activated macrophages including IL-18 were down regulated whereas markers characteristic for alternatively activated macrophages (Arginase 1, IL-10) were up regulated by rosiglitazone. Importantly, conditioned media from rosiglitazone-treated alternatively activated macrophages neutralized the inhibitory effect of macrophages on 3T3-L1 adipocyte differentiation, suggesting that alternatively activated macrophages may be involved in mediating the effects of rosiglitazone on adipose tissue morphology and mass. Our results suggest that short term rosiglitazone treatment increases infiltration of alternatively activated macrophages in adipose tissue. The alternatively activated macrophages might play a role in PPARγ-dependent expansion and remodeling of adipose tissue. Keywords: metabolic state analysis
2008-04-29 | GSE11295 | GEO
Project description:Liver and adipose tissue undergo dynamic inflammatory changes during the progression of obesity. This study was designed to evaluate the changes in gene expression profile and function of subpecific macophage subsets.
2020-12-11 | GSE163003 | GEO
Project description:We report the gene expression changes in the gWAT tissue of adipose-specific Med19 knockout mice
2020-08-01 | GSE150250 | GEO
Project description:Metabolic plasticity is the ability of a biological system to adapt its metabolic phenotype to different environmental stressors. We used a whole-body and tissue- specific phenotypic, functional, metabolomic and transcriptomic approach to systematically assess metabolic plasticity in diet-induced obese mice after a combined nutritional and exercise intervention. Although most pathological features were successfully reverted, we observed a high degree of metabolic dysfunction irreversibility in visceral white adipose tissue, characterised by abnormal mitochondrial morphology and functionality. Despite two sequential therapeutic interventions and apparent global phenotypic recovery, obesity specifically triggered in visceral adipose tissue a cascade of events progressing from mitochondrial metabolic and proteostatic defects to widespread cellular stress, which compromises its biosynthetic and recycling capacity. Our data indicate that obesity prompts a lasting metabolic fingerprint that leads to an aging-like progressive breakdown of metabolic plasticity in white adipose tissue. A similar phenomenon was observed in an obese human cohort following weight loss. Further human studies should help dissect patients’ stratification of this significant milestone in obesity progression.
2022-07-04 | PXD025503 | Pride
Project description:Specific metabolic activation of adipose tissue macrophages during obesity promotes inflammatory responses
| PRJNA327794 | ENA
Project description:In addition to total body fat, the regional distribution and inflammatory status of enlarged adipose tissue are strongly linked to metabolic and cardiovascular complications of obesity. We recently showed that the severity of liver non-alcoholic histopathology in obese subjects increased with the amounts of macrophages in visceral adipose tissue (VAT), while no relation was found with the subcutaneous adipose tissue (SAT). In the abdominal region, SAT is anatomically divided into superficial (sSAT) and deep (dSAT) layers. The aim of the present study was to test the hypothesis that these distinct compartments differentially contribute to hepatic alteration in obesity.
2011-09-01 | GSE30133 | GEO