Periprostatic fat gene expression in male mouse diet induced obesity study
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA508410 | ENA |
REPOSITORIES: ENA
Similar Datasets
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: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. We found that supplemental 17β-estradiol (E2) could decrease periprostatic WAT inflammation in obese male mice in association with reduction in weight and calorie consumption. Here, we tested the hypothesis that calorie restriction alone would have similar effects on periprostatic WAT inflammation in obese male mice. To test this hypothesis, male mice were fed high fat diet to induce obesity and then switched to a 30% caloric restriction diet for an addition 7 weeks until sacrifice. LFD fed mice and mice fed HFD ad libitum serve as controls.
2019-07-22 | GSE123348 | GEO
Project description:Periprostatic fat gene expression in male mouse diet induced obesity and calorie restriction study
| PRJNA508408 | ENA
Project description:This project includes proteomic data of brown adipose tissue from high-fat diet-induced obese mice versus wild-type mice. WTB reprents the brown adipose tissue from wild-type mice.DIOB reprents the brown adipose tissue from diet-induced obesity mice.
2026-05-22 | PXD067866 | Pride
Project description:The experimental goals of this study were to determine the differences in hypothalamus gene expression in genetically identical mice that have variability in their susceptibility towards diet-induced obesity following 6 weeks feeding a high fat diet, 2 weeks low fat diet and 6 weeks high fat diet. Keywords: Comparative gene expression analysis
2006-04-28 | GSE4697 | GEO
Project description:This project includes proteomic data of inguinal white adipose tissue from high-fat diet-induced obese mice versus wild-type mice. WTi reprents the inguinal white adipose tissue from wild-type mice.DIOi reprents the inguinal white adipose tissue from diet-induced obesity mice.
2026-05-22 | PXD067877 | Pride
Project description:We systematically observed the effects of PA by constructing an obesity model in mice. Preliminary results indicate that a high-fat diet (HFD) containing PA can reverse the obesity process in mice. In mice fed with HFD, the addition of PA can prevent the elevation of lipoprotein a [LP(a)] levels, which is a risk factor for atherosclerosis. These results suggest that PA may have the potential to prevent obesity as well as cardiovascular and heart-related diseases.To further explore the mechanism of action of PA, we continued RNA-seq experiments on mice fed with a normal diet (ND), HFD, and HFD supplemented with different concentrations of PA (HFD + PA). The results indicate that hundreds of HFD-regulated genes are functionally enriched in fat metabolism and defense systems. The high-fat diet containing PA reverses a significant portion of the upregulated and downregulated genes induced by HFD, with the reversed genes significantly enriched in metabolism and defense Gene Ontology (GO) terms. This suggests that PA may prevent obesity and inflammatory infections in mice by interfering with lipid synthesis and improving defense systems.
2025-09-21 | GSE279177 | GEO
Project description:Obesity affects the progress of lung cancer. To understand this more, we performed single-cell RNA sequencing of dissociated tumors of four mouse lung cancer cell-lines grown subcutaneously in adult male C57BL/6 mice with and without high-fat diet-induced obesity.
2025-03-31 | GSE280717 | GEO
Project description:Rodents respond to chronic high fat diet in at least two ways: some of them may readily gain body weight and become obese (termed obesity-prone), and others may not (termed obesity-resistant). An integrated approach of transcript and metabolic profiling of obesity-prone and obesity-resistant rats has been conducted, showing significantly different transcript and metabolic profiles in the two phenotypes. The major transcriptional differences involved hepatic fatty acid metabolism and ketogenesis in response to 16 weeks of high fat diet. At the same time, the different metabolic profiles (in liver tissue extracts, serum, and urine) between the two phenotypes could be ascribed to the corresponding pathways identified with multivariate statistical analysis, including fatty acid metabolism, Krebs cycle, and amino acid metabolism. The integration of results from both transcript and metabolic profiling revealed the different responses to dietary intervention of the two phenotypes and the physiological basis of susceptibility to metabolic disease in obesity-prone rats from a systematic view.
2008-05-20 | GSE11492 | GEO
Project description:Objective Recent evidence indicates that the adult hematopoietic system is susceptible to diet-induced lineage skewing. It is not known whether the developing hematopoietic system is subject to metabolic programming via in utero high fat diet (HFD) exposure, an established mechanism of adult disease in several organ systems. We previously reported substantial losses in offspring liver size with prenatal HFD. As the liver is the main hematopoietic organ in the fetus, we asked whether the developmental expansion of the hematopoietic stem and progenitor cell (HSPC) pool is compromised by prenatal HFD and/or maternal obesity. Methods We used quantitative assays, progenitor colony formation, flow cytometry, transplantation, and gene expression assays with a series of dietary manipulations to test the effects of gestational high fat diet and maternal obesity on the day 14.5 fetal liver hematopoietic system. Results Maternal obesity, particularly when paired with gestational HFD, restricts physiological expansion of fetal HSPCs while promoting the opposing cell fate of differentiation. Importantly, these effects are only partially ameliorated by gestational dietary adjustments for obese dams. Competitive transplantation reveals compromised repopulation and myeloid-biased differentiation of HFD-programmed HSPCs to be a niche-dependent defect, apparent in HFD-conditioned male recipients. Fetal HSPC deficiencies coincide with perturbations in genes regulating metabolism, immune and inflammatory processes, and stress response, along with downregulation of genes critical for hematopoietic stem cell self-renewal and activation of pathways regulating cell migration. Conclusions Our data reveal a previously unrecognized susceptibility to nutritional and metabolic developmental programming in the fetal HSPC compartment, which is a partially reversible and microenvironment-dependent defect perturbing stem and progenitor cell expansion and hematopoietic lineage commitment. Examination of differentially expressed genes between gestational day 15 (+/- 0.5 days) C57BL/6 mouse fetal livers from diet-induced (60% fat diet) obese or control female mice.
2014-10-25 | E-GEOD-62715 | biostudies-arrayexpress