Mus musculus
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ABSTRACT:
PROVIDER: PRJNA274366 | ENA |
REPOSITORIES: ENA
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Project description:We are exploring pathways influenced by short-term dietary methionine restriction (MR) in thoracic aorta and associated perivascular adipose tissue (PVAT) from obese C57BL/6J male mice around 26 weeks of age. Mice were fed 60% high fat diet (HFD) until they were obese, experimental mice were given 60% HFD with 0.12% methionine for 3, 5, and 10 days while the control group maintained a 60% HFD with 0.86% methionine. All mice were euthanized on the same day, then thoracic aorta was harvested, the PVAT was removed, and both sample types were prepared and analyzed separately. Three mice per group were assessed with LC-MS/MS. MR diet induced lean phenotype in PVAT, which was observed histologically, and we hypothesized that changes in lipid metabolism and mitochondrial bioenergetics mediated this response.
2025-04-07 | PXD051504 | Pride
Project description:We identified differentially expressed genes in epididymal white adipose tissue of high fat diet(HFD)-fed mice compared to low fat diet-fed mice using microarray analysis. Microarray analysis revealed that genes related to lipolysis, fatty acid metabolism, mitochondrial energy transduction, oxidation-reduction, insulin sensitivity, and skeletal system development were downregulated in HFD-fed mice, and genes associated with extracellular matrix (ECM) components, ECM remodeling, and inflammation were upregulated. The top 10 up- or downregulated genes include Acsm3, mt-Nd6, Fam13a, Cyp2e1, Rgs1, and Gpnmb, whose roles in obesity-associated adipose tissue deterioration are poorly understood.
2015-07-01 | GSE63198 | GEO
Project description:Using standardized, semipurified diets is a crucial factor for reproducibility of experimental nutritional studies. For the purpose of comparability and integration of research, two European consortia, Mitofood and BIOCLAIMS, proposed an AIN-93-based standard reference diet, the standardized BIOCLAIMS low-fat diet (LFD) as well as a high-fat diet (HFD). In order to evaluate the BIOCLAIMS LFD and HFD, we performed short-term (5 days) and long-term (12 weeks) feeding experiments using male C57BL/6 mice. The HFD has the same composition as the LFD except the fat content is increased to 40% energy in exchange for carbohydrates. Both diets were accepted by the animals and proof of principle was given that the BIOCLAIMS HFD increases body weight and body fat and affects glucose homeostasis. Short-term feeding trials (5 days) were performed in order to identify metabolic and molecular parameters which can serve as acute predictors for metabolic disorders due to high-fat diet-induced obesity. We analyzed gene expression in gonadal white adipose tissue of short- and long-term fed animals with whole genome microarrays. The BIOCLAIMS HFD strongly influenced gene expression in white adipose tissue after short- and long-term intervention. A total number of 973 and 4678 transcripts were significantly different between both diets after 5 days feeding and 12 weeks feeding, respectively. A total number of 764 transcripts encoding 549 genes were significantly differentially regulated between LF and HF animals after 12 weeks feeding as well as after 5 days feeding. Of these 549 overlapping genes, a substantial number (434 genes) were expressed at a lower level and 115 genes were expressed at a higher level in the HF mice compared to the LF mice. Without exception, all genes were regulated equally. Pathway analysis revealed a prominent role for genes involved in lipid metabolism, carbohydrate metabolism and oxidative phosphorylation. This was confirmed by quantitative real-time reverse transcription PCR. The high predictive value of gene expression changes in our short-term study compared to long-term high fat feeding is a promising step to get well-defined, early biomarkers that could shorten animal trials considerably and allow a more rapid and efficient screening of different compounds. C57BL/6J wildtype male mice, aged 12 weeks, received a low-fat diet or a high-fat diet for 5 days or 12 weeks. After sacrification, white adipose tissue depots were dissected, and immediately snap frozen in liquid nitrogen. Total RNA was isolated, quantified and qualified, and subsequently used for global gene expression profiling using Agilent 4x44K microarrays.
2013-08-27 | E-GEOD-38337 | biostudies-arrayexpress
Project description:We identified differentially expressed genes in epididymal white adipose tissue of high fat diet(HFD)-fed mice compared to low fat diet-fed mice using microarray analysis. Microarray analysis revealed that genes related to lipolysis, fatty acid metabolism, mitochondrial energy transduction, oxidation-reduction, insulin sensitivity, and skeletal system development were downregulated in HFD-fed mice, and genes associated with extracellular matrix (ECM) components, ECM remodeling, and inflammation were upregulated. The top 10 up- or downregulated genes include Acsm3, mt-Nd6, Fam13a, Cyp2e1, Rgs1, and Gpnmb, whose roles in obesity-associated adipose tissue deterioration are poorly understood. Total RNA of epididymal white adipose tissue was obtained from low fat diet (10 kcal% fat)- and high fat diet(45 kcal% fat)-fed mice and mRNA expression was measured using microarray analysis.
2015-07-01 | E-GEOD-63198 | biostudies-arrayexpress
Project description:Macrophages are primary immune cells involved in obesity-triggered chronic low-grade inflammation in adipose tissues. Prostaglandin (PG) E2, mainly generated from macrophages, can regulate adipose tissue remodeling. Here, we observed that PGE2 receptor subtype 3 (EP3) was remarkably downregulated in adipose tissue macrophages from high-fat diet (HFD)-fed mice and patients with obesity. Notably, macrophage-specific deletion of EP3 exacerbated HFD-induced obesity in mice, whereas EP3α isoform overexpression in macrophages alleviated obesity phenotype in HFD-fed mice. EP3 deficiency suppressed anti-adipogenic secreted protein acidic and rich in cysteine (SPARC) secretion in macrophages. SPARC deletion in macrophages abrogated the protection of EP3α-overexpression against HFD-induced obesity in mice. Mechanistically, EP3 activation promoted SPARC expression by suppressing DNA methylation in macrophages through the PKA/Sp1/Dnmt1/3a signaling cascade. EP3 agonist treatment ameliorates HFD-induced obesity in mice. Thus, EP3 inhibits adipogenesis through promoting macrophage releasing SPARC and may serve as a therapeutic target for managing diet-induced obesity.
2025-05-25 | PXD063443 | Pride
Project description:Adipose tissue dysfunction is closely associated with the development and progression of nonalcoholic fatty liver disease (NAFLD). Recent studies have implied an important role of prohibitin-1 (PHB1) in adipose tissue function. In the current study, we aimed to explore the function of adipocyte PHB1 in the development and progression of NAFLD. The PHB1 protein levels in adipose tissues were markedly decreased in mice fed a high-fat diet (HFD) compared to those fed a chow diet. To explore the function of adipocyte PHB1 in the progression of NAFLD, mice with adipocyte-specific (adipo) deletion of Phb1 (Phb1adipo-/- mice) were generated. Notably, Phb1adipo-/- mice did not develop obesity but displayed severe liver steatosis under HFD feeding. Compared to HFD-fed wild-type (WT) mice, HFD-fed Phb1adipo-/- mice displayed dramatically lower fat mass with significantly decreased levels of total adipose tissue inflammation, including macrophage and neutrophil number as well as the expression of inflammatory mediators. To our surprise, although liver steatosis in Phb1adipo-/- mice was much more severe, liver inflammation and fibrosis were similar to WT mice after HFD feeding. RNA sequencing analyses revealed that the interferon pathway was markedly suppressed while the bone morphogenetic protein 2 pathway was significantly up-regulated in the liver of HFD-fed Phb1adipo-/- mice compared with HFD-fed WT mice. Conclusion: HFD-fed Phb1adipo-/- mice display a subtype of the lean NAFLD phenotype with severe hepatic steatosis despite low adipose mass. This subtype of the lean NAFLD phenotype has similar inflammation and fibrosis as obese NAFLD in HFD-fed WT mice; this is partially due to reduced total adipose tissue inflammation and the hepatic interferon pathway.
2022-09-17 | GSE213355 | GEO
Project description:Abstract Background In obesity, adipose tissue undergoes a remodeling process characterized by increased adipocyte size (hypertrophia) and number (hyperplasia). The individual ability to tip the balance toward the hyperplastic growth, with recruitment of new fat cells through adipogenesis, seems to be critical for a healthy adipose tissue expansion, as opposed to the development of inflammation and detrimental metabolic consequences. However, the molecular mechanisms underlying this fine-tuned regulation are far from being understood. Methods We analyzed by mass spectrometry-based proteomics visceral white adipose tissue (vWAT) samples collected from C57BL6 mice fed with a HFD for 8 weeks. A subset of these mice, called low responders (LowR HFD), showed a low susceptibility to the onset of adipose tissue inflammation, as opposed to their HFD counterpart. We identified the discriminants between LowR HFD and HFD vWAT samples and explored their function in Adipose Derived human Mesenchymal Stem Cells (AD-hMSCs) differentiated to adipocytes. Results We quantified 6051 proteins. Among the candidates that most differentiate LowR HFD from HFD vWAT, we found proteins involved in adipocyte function, including adiponectin and hormone sensitive lipase, suggesting that adipocyte differentiation is enhanced in LowR HFD, as compared to HFD. The chromatin modifier SET and MYND Domain Containing 3 (SMYD3), whose function in adipose tissue was totally unknown, was another top-scored hit. SMYD3 expression was significantly higher in LowR HFD vWAT, as confirmed by western blot analysis. In vitro, we found that SMYD3 mRNA and protein levels decrease rapidly along the differentiation process of AD-hMSCs. Moreover, SMYD3 knock-down at the beginning of adipocyte differentiation resulted in reduced cell proliferation and, at longer term, reduced lipid accumulation in adipocytes. Conclusions Our study describes for the first time the role of SMYD3 as a regulator of adipocyte proliferation during the early steps of adipogenesis.
2024-01-03 | PXD043165 | Pride
Project description:Cytokines of the IL-1 family are important modulators of obesity-induced inflammation and the development of systemic insulin resistance. Here, we report that IL-37, a newly-described antiinflammatory member of the IL-1 family, affects obesity-induced inflammation and insulin resistance. IL-37 transgenic mice (IL-37tg) did not develop an obese phenotype in response to a high-fat diet (HFD). Unlike WT mice, IL-37tg mice exhibited reduced numbers of adipose tissue macrophages and preserved glucose tolerance and insulin sensitivity after 16 weeks of HFD. A short-term HFD intervention revealed that the IL-37-mediated improvement in glucose tolerance is independent of bodyweight. IL-37tg mice manifested a beneficial metabolic profile with higher circulating levels of the anti-inflammatory adipokine adiponectin. In vitro treatment of differentiating adipocytes with recombinant IL-37 reduced adipogenesis. The beneficial effects of recombinant IL-37 involved activation of AMPK signaling. In humans, steady-state IL-37 adipose tissue mRNA levels were positively correlated with insulin sensitivity, lower adipose tissue levels of leptin and a lower inflammatory status of the adipose tissue. These findings reveal IL-37 as an important anti-inflammatory modulator during obesity-induced inflammation and insulin resistance in both mice and humans and suggest that IL-37 is a potential target for the treatment of obesity-induced insulin resistance and type 2 diabetes. Gene arrays were performed on epidydimal white adipose tissue samples from wild type and human IL37-overexpressing transgenic mice fed a high fat diet for 16 weeks.
2015-05-18 | E-GEOD-58952 | biostudies-arrayexpress
Project description:Administration of inulin modulates gut microbiota of mice fed HFD short- and long-term in a different way
| PRJNA892501 | ENA
Project description:Analysis of gene expression in adipose tissue of female mice after continuous high fat diet (HFD) feeding for three generations. The hypothesis in this study is that continuous HFD feeding has transgenerational amplification effects to the offspring. Results provide important information on the impacts of over-nutrition over one generation on the offspring, such as transgenerational up-regulated or down-regulated genes. Total RNA was obtained from adipose tissue of the HFD fed mice, including F0, F1 and F2 generations. Normal chow fed mice were used as controls.
2013-05-10 | E-GEOD-37238 | biostudies-arrayexpress