Transcriptomic Analysis of High Fat Diet Fed Mouse Brain Cortex
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PROVIDER: PRJNA744745 | ENA |
REPOSITORIES: ENA
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Project description:High fat diet can lead to metabolic diseases such as obesity and diabetes known to be chronic inflammatory diseases with high prevalence worldwide. Recent studies have reported cognitive dysfunction in obese patients is caused by a high fat diet. Accordingly, such dysfunction is called “type 3 diabetes” or “diabetic dementia.” Although dysregulation of protein-coding genes has been extensively studied, profiling of non-coding RNAs including long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) has not been reported yet. Therefore, the objective of this study was to obtain profiles of diverse RNAs and determine their patterns of alteration in high fat fed brain cortex compared to normal brain cortex. To investigate regulatory roles of both coding and non-coding RNAs in high fat diet brain, we performed RNA sequencing of ribosomal RNA-depleted RNAs and identified genome-wide lncRNAs and circRNAs expression and co-expression patterns of mRNAs in high fat diet mouse brain cortex. Our results showed expression levels of mRNAs related to neurogenesis, synapse, and calcium signaling were highly changed in high fat diet fed cortex. In addition, numerous differentially expressed lncRNAs and circRNAs were identified. Our study provides valuable expression profiles and potential function of both coding and non-coding RNAs in high fat diet fed brain cortex.
2021-07-11 | GSE179711 | GEO
Project description:The composition of the diet affects many processes in the body, including body weight and endocrine system. We have previously shown that dietary fat also affects the immune system. Mice fed high fat diet rich in polyunsaturated fatty acids survive S. aureus infection to a much greater extent than mice fed high fat diet rich in saturated fatty acids. Here we present data regarding the dietary effects on protein expression in spleen from mice fed three different diets, I) low fat/chow diet (LFD, n=4), II) high fat diet rich in saturated fatty acids (HFD-S, n=4) and III) high fat diet rich in polyunsaturated fatty acids (HFD-P, n=4). We performed mass spectrophotometry based quantitative proteomics analysis of isolated spleen by implementing the isobaric tags for relative and absolute quantification (iTRAQ) approach. Mass spectrometry data were analysed using Proteome Discoverer 2.4 software using the search engine mascot against Mus musculus in SwissProt. 924 proteins are identified in all sets (n=4) for different dietary effects taken for statistical analysis using Qlucore Omics Explorer software. Only 20 proteins were found to be differentially expressed with a cut-off value of false discovery rate < 0.1 (q-value) when comparing HFD-S and HFD-P but no differentially expressed proteins were found when LFD was compared with HFD-P or HFD-S. We identified a subset of proteins that showed an inverse expression pattern between two high fat diets. These differentially expressed proteins were further classified by gene ontology for their role in biological processes and molecular functions.
2020-08-06 | PXD020365 | Pride
Project description:Proteomics of liver tissue from mice fed a high fat diet (HFD) or regular chow diet. Data accompany our paper entitled “Dynamic Regulation of N6,2′-O-dimethyladenosine (m6Am) in Obesity” scheduled for publication in Nature Communications, 2021
2021-10-27 | PXD029280 | Pride
Project description:High Fat Diet Experiment SD rats fed either an AIN93G-based low fat diet or an AIN93G-based high fat diet. Keywords: ordered
2006-01-01 | GSE2226 | GEO
Project description:The popularity of high fat foods in modern society has been associated with epidemic of various metabolic diseases characterized by insulin resistance, the pathology of which involves complex interactions between multiple tissues such as liver, skeletal muscle and white adipose tissue (WAT). To uncover the mechanism by which excessive fat impairs insulin sensitivity, we conducted a multi- tissue study by using TMT-based quantitative proteomics. 3-week-old ICR mice were fed with high fat diet (HFD) for 19 weeks to induce insulin resistance. Liver, skeletal muscle and epididymal fat were collected for proteomics screening. Additionally, PRM was used for validating adipose differential proteins. By comparing tissue-specific protein profiles of HFD mice, multi-tissue regulation of glucose and lipid homeostasis and corresponding underlying mechanisms was systematically investigated and characterized. NC: normal birth weight + chow diet; NH: normal birth weight + high fat diet; LC: low birth weight + chow diet; LH: low birth weight + high fat diet.
2022-01-26 | PXD021046 | Pride
Project description:To gain insight into the role of testosterone in modulating hepatic fat accumulation, we collected liver tissues from high fat diet-fed intact male pigs, castrated male pigs, and castrated male pigs with testosterone replacement. RNA-Seq was employed to profile hepatic gene expression in pigs with different testosterone levels. Liver mRNA profiles of intact male pigs fed a HFC diet, castrated male pigs fed a HFC diet, and castrated male pigs treated with testosterone fed a HFC diet were generated by deep sequencing, using Illumina HiSeq 2000.
2015-01-08 | E-GEOD-62696 | biostudies-arrayexpress
Project description:Type 2 diabetic cardiomyopathy (DCM) has been linked to Ca2+ signaling alterations, notably a decreased mitochondrial Ca2+ uptake. Uncovering of Ca2+ microdomains between cardiac mitochondria and reticulum launched a new investigation avenue for cardiometabolic diseases. We here aimed to study if the impairment of mitochondrial Ca2+ handling could be due to a dysregulation of the reticulum-mitochondria interactions or of the mitochondrial Ca2+ uniporter in the diabetic mice heart. Phenotypic alterations of the type 2 diabetic mouse heart, was done using an in vivo obesogenic high fat high sucrose diet fed mouse model (HFHSD: 20% proteins, 36% lipids). The composition of the cardiac MAM fractions between standard diet-fed (SD) mice and HFHSD (HF) mice at 16 weeks was analysed by MS-based quantitative proteomics.
2020-12-02 | PXD015280 | Pride
Project description:Background: Epidemiological studies suggest an association between maternal obesity and adverse neurodevelopmental outcomes in offspring. Objective: To compare the global proteomic portrait in the cerebral cortex between mice born to mothers on a high-fat or control diet who themselves were fed a high-fat or control diet. Methods: Male mice born to dams fed a control (C) or high fat (H) diet four weeks before conception and during gestation and lactation were assigned to either C or H diet at weaning. Mice (n=24) were sacrificed at 19-weeks and their cerebral cortices were pooled into 8 samples and analysed using an iTRAQ based 2D LC-MS methodology. Results: A total of 6,695 proteins were identified and fully quantified (q<0.01). Approximately 10% of these proteins demonstrated a minimum of one Standard Deviation of regulation across all biological replicates in at least one of the experimental groups (CH, HC, HH) relative to the control (CC). Principal component analysis and hierarchical clustering analysis showed that mice clustered based on the diet of the mother and not their current diet. In silico bioinformatics analysis revealed that maternal high-fat diet was significantly associated with response to hypoxia/oxidative stress and apoptosis in the cerebral cortex of the adult offspring. Conclusion: Maternal high-fat diet was associated with distinct endophenotypic changes of the adult mouse cerebral cortex independent of the diet of the offspring. The identified modulated proteins could represent novel therapeutic targets for the prevention of neuropathological features resulting from maternal obesity.
2018-01-29 | PXD001540 | Pride
Project description:Chronic high-fat/high-sugar (HFS) feeding is linked to the development of insulin resistance as well as arterial wall and adipose tissue inflammation in nonhuman primates. These changes are significantly reduced when the animals are fed a HFS diet supplemented with resveratrol (RSV) for two years. Herein, we evaluated the occurrence of cerebral cortex injury in these HFS-fed middle-aged male rhesus monkeys and investigated the possibility of brain protection by RSV treatment. HFS caused a reduction in capillary density in the cerebral cortex that was preempted by RSV supplementation. The patterns of cDNA microarray analysis revealed upregulation of markers of oxidative stress, inflammation and apoptosis in the cortical cortex of HFS-fed monkeys, which was reversed by RSV. The underlying mechanism of RSV action included its ability to prevent the HFS-mediated NF-kappa-B activation and loss in mitochondrial aldehyde dehydrogenase 2 expression. We conclude that RSV may confer neuroprotection against HFS-mediated cerebral vascular dysfunction and activation of inflammatory pathways.
2017-02-14 | GSE70255 | GEO
Project description:The serum samples from wild type mice fed high-fat diet for 12 weeks (WT_Serum) and Mdm2 adipocyte-specific knock-in mice fed high-fat diet for 12 weeks (KI_Serum) were mixed separately, and subjected to proteomic study by Label-free quantitative techniques and mass spectrometry-based proteomics techniques in Jingjie PTM BioLab (Hangzhou) Co. Ltd (www.ptm-biolab.com.cn). The difference was determined by 1.5-fold-change criterion, FDR < 0.01.
2022-08-11 | PXD034069 | Pride