Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1084780 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28242700_1.fastq.gz | Fastqsanger.gz | |||
| SRR28242700_2.fastq.gz | Fastqsanger.gz | |||
| SRR28242701_1.fastq.gz | Fastqsanger.gz | |||
| SRR28242701_2.fastq.gz | Fastqsanger.gz | |||
| SRR28242702_1.fastq.gz | Fastqsanger.gz |
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Project description:Diet-induced obesity is the central cause of diabetes, cardiovascular disease as well as metabolic syndrome. Here, we have studied the efficacy of cycles of a 4-5 day fasting mimicking diet (FMD) in inhibiting high-fat, high calorie diet (HFCD) -induced obesity in mature female C57BL/6 mice. We show that a monthly 5-day cycle of FMD inhibit HFCD-mediated obesity by causing a reduction in calorie intake and accumulation of visceral and subcutaneous fat depots without lean body mass loss. FMD cycles also increase cardiac vascularity, function and stress resistance, and reverse the hypercholesterolemia caused by the HFCD. The sustained activation of adipocyte genes associated with mitochondrial metabolism and biogenesis and the sustained ketogenesis in the HFCD-fed mice subjected to monthly cycles of FMD indicate a reprogramming of fat cell metabolism that is likely to be at the center of obesity reversal. All these improvements could explain the protection from early mortality elicited by the high-fat, high calorie diet.
2021-08-19 | GSE163060 | GEO
Project description:Because of the epidemic rise of obesity worldwide, the identification of novel target genes for pharmacological treatment of obesity and related disorders is becoming of high importance. IFRD1 and IFRD2 are members of a novel transcriptional regulators family. Intestinal over-expression of mouse homologue of IFRD1 promoted intestinal triglyceride uptake and induced whole body adiposity in mice. To further elucidate the role of IFRD1 and IFRD2 in vivo, we generated mice lacking both mouse homologues of IFRD1 (TIS7) and IFRD2 (SKMc15) genes. Here, we report that mice deficient in TIS7 and SKMc15 genes, despite normal calorie intake had severely reduced amount of adipose tissue, were resistant to diet-induced obesity and displayed high glucose tolerance. Lower dietary fat entry into the circulation suggested that this phenotype resulted from impaired intestinal lipid transport. We identified down-regulation of CD36, a fatty acid transporter, both on RNA and protein levels. Reporter assays indicated that TIS7 and SKMc15 transcriptionally regulated CD36 expression and CD36 overexpression partially restored fatty acid uptake in vitro. Hence, our study suggested that TIS7 and SKMc15 play an important role in the regulation of the lipid metabolism and might represent a novel strategy for treatment of disorders caused by excess fat intake. To determine whether decreased intestinal lipid absorption might be caused by changes in expression of lipid processing and transport molecules, we performed Affymetrix microarray analyses of total RNA samples isolated from the jejunum of HFD-fed WT type and dKO animals. The moderated t-test was used to calculate p-values for significance of differential gene expression between 3 dKO and 3 wild type mice. These raw p-values were adjusted for multiple hypothesis testing using the method from Benjamini and Hochberg for a strong control of the false discovery rate (FDR) and genes with thus adjusted p-values < 0.05 were considered significant. Age-matched (7-10 week old) male wild type and TIS7 (Ifrd1) SKMc15 (Ifrd2) double knock out mice (C57Bl6 background) were caged individually and maintained from 3 weeks up to 8 weeks on a synthetic high saturated fat (HFD) diet (Ssniff). Small intestines (jejunum) were harvested for total RNA isolation. RNAs from 3 WT and 3 dKO mice were subjected to Affymetrix based whole genome gene expression analysis (Mouse 430.2 GeneChip).
2012-07-31 | E-GEOD-27019 | biostudies-arrayexpress
Project description:Nonalcoholic fatty liver disease (NAFLD) is one of the most common chronic diseases globally and nonalcoholic steatohepatitis is its progressive stage with limited therapeutic options. Here a role for intestinal peroxisome proliferator-activated receptor α (PPARα)-fatty acid binding protein 1 (FABP1) in obesity-associated metabolic syndrome, fatty liver and nonalcoholic steatohepatitis via modulating dietary fat absorption was uncovered. Intestinal PPARα is highly activated accompanied by marked upregulation of FABP1 by high-fat diet (HFD) in mice and obese humans. Intestine-specific PPARα or FABP1 disruption in mice decreases HFD-induced obesity, fatty liver and nonalcoholic steatohepatitis and intestinal PPARα disruption fails to further decrease obesity and NASH. Chemical PPARα antagonism improves metabolic disorders depending on the presence of intestinal PPARα or FABP1. Translationally, GW6471 decreases human PPARα-driven intestinal fatty acid uptake and therapeutically improves obesity in PPARA-humanized, but not Ppara-null, mice. These results suggest that intestinal PPARα-FABP1 axis could be a therapeutic target for NASH.
2022-09-01 | GSE190140 | GEO
Project description:Obesity is a global health concern affecting over 650 million adults with a major contributor being an increased consumption of a high-fat diet. Maternal obesity often results in an increased risk of offspring developing obesity. In this study, we examined the effect of diet on visceral adipose in a pre-clinical model of generational diet-induced obesity that included maternal cohorts of C57BL/6 mice fed either a control diet (10% fat) or a high-fat diet (45% fat) and the resulting female offspring fed either diet. Using bottom-up proteomics on omental adipose tissue, differential protein expression was determined with the greatest difference resulting from the generational obese cohort. Differentially expressed proteins were involved in pathways related to cancer, inflammatory disease and immune response. Taken together, the results of this study provide molecular-level insight that will enable the development of more targeted, modifiable interventions that could be implemented pre-, during and post-pregnancy.
2024-10-17 | PXD042092 | Pride
Project description:Drosophila melanogaster was used to investigate the influence of microbiota-derived intestinal flora and its metabolites on host transcriptional regulation by adding sodium butyrate to a sterile diet for constructing a sterile Drosophila model. In order to further investigate the effects of sodium butyrate on Drosophila melanogaster at the molecular mechanism level, we detected the abundance and composition of midgut microbial colonies based on 16S rRNA gene sequences, and analyzed the overall structure and metabolic activities of host transcriptional networks by combining transcriptome and non-target metabolomics data.
2021-05-24 | GSE169135 | GEO
Project description:Core diet-induced obesity networks were constructed using Ingenuity pathway analysis (IPA) based on 332 high-fat diet responsive genes identified in liver by time-course microarray analysis (8 time-points over 24 weeks) of high-fat diet fed mice compared to normal diet fed mice. IPA identified five core diet-induced obesity networks with time-dependent gene expression changes in liver. When we merged core diet-induced obesity networks, Tlr2, Cd14 and Ccnd1 emerged as hub genes associated with both liver steatosis and inflammation and were altered in a time-dependent manner. Further protein-protein interaction network analysis revealed Tlr2, Cd14 and Ccnd1 were inter-related through the ErbB/insulin signaling pathway. Dynamic changes occur in molecular networks underlying diet-induced obesity. Tlr2, Cd14 and Ccnd1 appear to be hub genes integrating molecular interactions associated with the development of NASH. Therapeutics targeting hub genes and core diet-induced obesity networks may help ameliorate diet-induced obesity and NASH. Total RNA obtained from isolated liver of C57BL/6J mice fed normal diet or high fat diet for 0, 2, 4, 6, 8, 12, 16, 20 and 24 weeks.
2014-03-01 | E-GEOD-40481 | biostudies-arrayexpress
Project description:Objective: To investigate the effects of metformin on intestinal carbohydrate metabolism in vivo.
Method: Male mice preconditioned with a high-fat, high-sucrose diet were treated orally with metformin or a control solution for two weeks. Fructose metabolism, glucose production from fructose, and production of other fructose-derived metabolites were assessed using stably labeled fructose as a tracer.
Results: Metformin treatment decreased intestinal glucose levels and reduced incorporation of fructose-derived metabolites into glucose. This was associated with decreased intestinal fructose metabolism as indicated by decreased enterocyte F1P levels and diminished labeling of fructose-derived metabolites. Metformin also reduced fructose delivery to the liver. Proteomic analysis revealed that metformin coordinately down-regulated proteins involved carbohydrate metabolism including those involved in fructolysis and glucose production within intestinal tissue.
Conclusion: Metformin reduces intestinal fructose metabolism, and this is associated with broad-based changes in intestinal enzyme and protein levels involved in sugar metabolism indicating that metformin's effects on sugar metabolism are pleiotropic.
2024-04-27 | PXD041833 | JPOST Repository
Project description:Little is known about how pro-obesity diets regulate tissue stem and progenitor cell function. Here we find that high fat diet (HFD)-induced obesity augments the numbers and function of Lgr5+ intestinal stem cells (ISCs) of the mammalian intestine. Like HFD, ex vivo treatment of intestinal organoid cultures with palmitic acid (PA), a constituent of the HFD, enhances the self-renewal potential of these organoid bodies. Mechanistically, HFD induces a robust peroxisome proliferator-activated receptor delta (PPAR-delta signature in intestinal stem and progenitor cells and pharmacologic activation of PPAR-delta recapitulates the effects that HFD has on these cells. Interestingly, HFD- and agonist-activated PPAR-delta signaling endows organoid-initiating capacity to non-stem cells and enforced PPAR-delta signaling permits these non-stem cells to form in vivo tumors upon loss of the tumor suppressor Apc. These findings highlight how diet-modulated PPAR-delta activation alters not only the function of intestinal stem and progenitor cells but also their capacity to initiate tumors. mRNA profiles of intestinal stem cells (GFP-Hi) and progenitors (GFP-Low) from WT or HFD fed mice were generated by deep sequencing using HiSeq 2000.
2016-02-16 | E-GEOD-67324 | biostudies-arrayexpress
Project description:We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. Goal and objectives: To study the requirement of HCV viral proteins and/or environmental factors (such as alcohol or obesity) in synergistic liver caner development in HCV Core or NS5A Tg mice given alcohol or high-cholesterol high-fat diet, mice were fed alcohol or high-cholesterol high-fat diet and liver tissues from these mice were examined for gene profiles. Alcohol or obesity contributes to synergistic tumor incidence and HCV Core or Ns5a-induced effects. Thus, analysis of gene profiling of these transgenic mice will identify the critical pathways to induce synergistic tumor formation caused by alcohol or obesity. Liver samples for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain gene profiling data in order to increase understanding the pathways. To perform gene array and proteomic analyses, mice were fed alcohol or high-cholesterol high-fat for 12 months and euthanized after 12 months feeding. Livers were collected at the time of euthanasia.
2014-09-16 | E-GEOD-61435 | biostudies-arrayexpress