The storage conditions of high fat diet are the key factors for diet induced obesity and liver damage [HFDfre vs. HFDfri]
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ABSTRACT:
PROVIDER: PRJNA838224 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19214087_1.fastq.gz | Fastqsanger.gz | |||
| SRR19214087_2.fastq.gz | Fastqsanger.gz | |||
| SRR19214088_1.fastq.gz | Fastqsanger.gz | |||
| SRR19214088_2.fastq.gz | Fastqsanger.gz | |||
| SRR19214089_1.fastq.gz | Fastqsanger.gz |
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Project description:The diet induced obesity (DIO) mouse model has been widely used for obesity studies. Comparing to the composition of nutrients in the diet, the effects of storage conditions for high fat diet (HFD) on metabolic homeostasis have not been systemically investigated. In the current study, we tested the effects of HFD stored in different conditions and found the mice fed by HFD stored in the fridge (HFDfri) gained less weight than freezer (HFDfre). Further analysis revealed the changes of the relative abundance of medium chain triglyceride (MCT) in the HFDfri, which has much lower intestinal absorption rates, contributed to the body weight differences. In contrast, advanced liver damages and elevation of unfolded protein responses (UPR) was observed in the mice fed by the HFDfri. Depletion of UPR regulated gene Nnmt alleviated liver damages via inhibition of integrated stress response (ISR). Our study provided the initial evidence that HFD storage conditions have great impacts on both body weight changes and liver damages in the DIO model.
2022-12-31 | GSE203039 | GEO
Project description:The diet induced obesity (DIO) mouse model has been widely used for obesity studies. Comparing to the composition of nutrients in the diet, the effects of storage conditions for high fat diet (HFD) on metabolic homeostasis have not been systemically investigated. In the current study, we tested the effects of HFD stored in different conditions and found the mice fed by HFD stored in the fridge (HFDfri) gained less weight than freezer (HFDfre). Further analysis revealed the changes of the relative abundance of medium chain triglyceride (MCT) in the HFDfri, which has much lower intestinal absorption rates, contributed to the body weight differences. In contrast, advanced liver damages and elevation of unfolded protein responses (UPR) was observed in the mice fed by the HFDfri. Depletion of UPR regulated gene Nnmt alleviated liver damages via inhibition of integrated stress response (ISR). Our study provided the initial evidence that HFD storage conditions have great impacts on both body weight changes and liver damages in the DIO model.
2022-12-31 | GSE203038 | GEO
Project description:The storage conditions of high fat diet are the key factors for diet induced obesity and liver damage.
| PRJNA838220 | ENA
Project description:The storage conditions of high fat diet are the key factors for diet induced obesity and liver damage [WT vs. Nnmt KO]
| PRJNA838225 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2022-12-31 | GSE203040 | 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: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:This dataset contains proteomic data from mice with high or low weight gain in response to a high fat diet. Both host and microbial proteins are present. In the supplemental, there are also tables and supplementary files that can be used for replicating the bioinformatic analysis.
Abstract:
Consumption of refined high-fat, low-fiber diets promotes development of obesity and its associated consequences. While genetics play an important role in dictating susceptibility to such obesogenic diets, mice with nearly uniform genetics exhibit marked heterogeneity in their extent of obesity in response to such diets. This suggests non-genetic determinants play a role in diet-induced obesity. Hence, we sought to identify parameters that predict, and/or correlate with, development of obesity in response to an obesogenic diet. We assayed behavior, metabolic parameters, inflammatory markers/cytokines, microbiota composition, and the fecal metaproteome, in a cohort of mice (n=50) prior to, and the 8 weeks following, administration of an obesogenic high-fat low-fiber diet. Neither behavioral testing nor quantitation of inflammatory markers broadly predicted severity of diet-induced obesity. Although, the small subset of mice that exhibited basal elevations in serum IL-6 (n=5) were among the more obese mice in the cohort. While fecal microbiota composition changed markedly in response to the obesogenic diet, it lacked the ability to predict which mice were relative prone or resistant to obesity. In contrast, fecal metaproteome analysis revealed functional and taxonomic differences among the proteins associated with proneness to obesity. Targeted interrogation of microbiota composition data successfully validated the taxonomic differences seen in the metaproteome. While future work will be needed to determine the breadth of applicability of these associations to other cohorts of animals and humans, this study nonetheless highlights the potential power of gut microbial proteins to predict and perhaps impact development of obesity.
2019-06-04 | MSV000083891 | MassIVE
Project description:Younger age and obesity increase the incidence and rates of metastasis of triple-negative breast cancer (TNBC), an aggressive subtype of breast cancer. The tissue microenvironment, specifically the extracellular matrix (ECM), is known to promote tumor invasion and metastasis. We sought to characterize the effect of both age and obesity on the ECM of mammary fat pads. We used a diet-induced obesity (DIO) model where 10-week-old female mice were fed a high-fat diet (HFD) for 16 weeks or a control chow diet (CD) where time points were every 4 weeks to monitor age and obesity HFD progression. We isolated the mammary fat pads to characterize the ECM at each time point. Utilizing proteomics, we found that the early stages of obesity were sufficient to induce distinct differences in the ECM composition of mammary fat pads that promote TNBC cell invasion. ECM proteins previously implicated in driving TNBC invasion Collagen IV and Collagen VI, were enriched with weight gain. Together these data implicate ECM changes in the primary tumor microenvironment as mechanisms by which age and obesity contribute to breast cancer progression.
2024-06-06 | PXD050250 | 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