Schisandrin C Regulates Obesity through CD36, CYP7A1 and CYP7B1 in High Fat Diet induced Obese Mice
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PROVIDER: PRJNA944981 | ENA |
REPOSITORIES: ENA
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Project description:Using the Illumina high-throughput sequencing platform, we conducted transcriptional profiling on liver tissues of C57BL/6 mice that were treated with a high-fat diet and administered Schisandrin C, simvastatin, or both. We analyzed the resulting transcript data to determine differential gene expression at the transcript level.
2024-12-31 | GSE227401 | GEO
Project description:Analysis of gene expression profiles of epididymal fat from DIO rats We applied a comparative functional genomics approach to evaluate diet-induced obese (DIO) rats as an obesity model Keywords: single time point, comparison control animal vs. diet induced obese animal
2007-08-07 | GSE8700 | 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. 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:Although there are studies on obesity and sarcopenia, our understanding of obesity-mediated sarcopenia is insufficient. Additionally, no studies have investigated the application of luteolin in sarcopenia. We attempted to determine the effect of luteolin on obese sarcopenia in mice with high-fat diet (HFD)-induced obesity. Luteolin exerted suppressive effects on obesity, inflammation, and protein degradation in HFD-fed obese mice. Luteolin inhibited lipid infiltration into the muscle and decreased p38 and JNK activity and mRNA expression of inflammatory factors, such as TNFα, Tlr2, Tlr4, MCP1, and MMP2, in the muscle. Suppression of muscle inflammation by luteolin led to the inhibition of myostatin, FoxO, atrogin, and MuRF expression, which reduced protein degradation and improved muscle function. This is the first study to demonstrate that luteolin exerts a protective effect against obese sarcopenia, as its anti-obesity and anti-inflammatory activities inhibited protein degradation. Therefore, luteolin may be a useful supplement for prevention of obese sarcopenia.
2022-07-27 | GSE209778 | 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:At present, the global obesity problem is becoming more and more serious, placing a huge burden on individuals and society. Obesity causes obesity-associated kidney disease, which poses great challenges to patients' lives and economies. We designed a set of experiments to study the effects of low-fat diet and adenosine interventions on kidney complications in obese mice, and found target proteins to protect obesity-associated kidney disease.
2025-01-14 | PXD059759 |
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:It has been found that fat oxidation is reduced in the skeletal muscle of obese humans. This study aims to identify the mRNA of proteins involved in fat oxidation that may be reduced in obese and morbidly obese individuals. Information gathered will help in understanding how obesity contributes to cardiovascular disease via insulin resistance. Samples were obtained from patients undergoing elective abdominal surgery.
2007-09-28 | E-GEOD-474 | biostudies-arrayexpress
Project description:We investigated anti-obesity mechanism of Chrysanthemum morifolium Ramat leaves extracts on high-fat diet induced obese mice using lipid profiling and RNA-seq transcriptomic profling.
2020-11-16 | GSE124777 | 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