Periprostatic fat gene expression in male mouse diet induced obesity study
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PROVIDER: PRJNA508410 | ENA |
REPOSITORIES: ENA
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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: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: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
Project description:Adult PPARg floxed male and female mice were fed a high fat diet (HFD) for 16 weeks to induce obesity. Half of these mice were then injected with AAV8-TBG-Cre to knockout PPARg in hepatocytes. The remaining half were injected with AAV8-TBG-Null to generate control mice. After two weeks, mice fed the HFD were either maintained on this diet or switched to a high fat, high cholestrol, high fructose (HFCF) diet for an additional 16 weeks. This study was designed to examine whether the loss of hepatocyte PPARg in mice with established obesity would alter the liver transcriptomics in a PPARg dependent manner when the mice are fed a HFD or a HFCF diet.
2023-01-11 | GSE200352 | GEO
Project description:The prevalence of obesity has steadily increased since decades. In the meantime, in line with the exposition of populations of from industrialized countries have been exposed to fat-rich diet with high exaggerated ù6/ù3 ratio of ù6- over ù3-polyunsaturated fatty acids. To assess the contribution of dietary fatty acids, male and female mice fed a human-like fat diet were mated randomly and maintained after breeding on the same diet for successive generations. Offspring showed over 4 generations a gradual enhancement in fat mass due to combined hyperplasia and hypertrophy with no change in energy intake. Transgenerational alterations in adipokine levels were accompanied by hyperinsulinemia. When switched to a standard diet, the obese phenotype (termed revHF4) reversed partially. Offspring of revHF4 mice exhibited higher birth weight and faster gain weight compared to control mice. Gene expression analyses of the stromal vascular fraction of adipose tissue over generations revealed i) underexpression of genes favoring angiogenesis and controlling oxidative stress and ii) overexpression of genes involved in inflammation, and in adipogenesis .and in insulin resistance. Thus, under conditions of genome stability, our results show that metabolic imprinting induced by a human-like fat diet is accompanied by a gradual fat mass enhancement, in accordance with the increasing prevalence of obesity observed in humans over generations.
2010-06-01 | GSE16636 | GEO
Project description:The experimental goals of this study were to determine differences in adipose tissue gene expression in genetically identical mice that have variability in their susceptibility towards diet-induced obesity following 4 weeks feeding a high saturated fat diet. Keywords: comparative gene expression analysis
2006-04-28 | GSE4692 | GEO
Project description:High-fat diet (HFD) induced obesity (DIO) has been shown impacts on metabolism, hormonal profile, male fertility, and spermatogenesis. We employed genome-wide transcriptional analysis on the testis of diet induced obesity (DIO) and normal chow (NC) C57BL/6 J male mice to search genes regulated by obesity in testis. Both blood glucose and lipids contents significantly increased in DIO mice after 8 weeks fat-rich feeding. RNA-seq analysis revealed 371 down-regulated and 460 up-regulated transcripts in DIO group comparing to NC group. Chromosome 3, 4, 9, 16, and 18 were significantly more active, while chromosome 5, 10, and 19 were significantly more inactive after 8-week fat-diet feeding. Wilcoxon enrichment analysis discovered that the thermogenesis pathway (KEGG) was significantly enriched in the testis of DIO group (with 8 enriched up-regulated genes: Smarca2, Adcy3, Atp5pb, Creb1, Gnas, Rps6kb2, Upcrc1 and Dpf1). Real-time PCR further confirmed that Smarca2 and Atp5pb were upregulated in the testis of DIO mice. These finding implied that diet-induced thermogenesis pathways could be altered in the testis of DIO mice.
2023-02-04 | GSE196119 | GEO