DIO
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB58786 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR10752500_1.fastq.gz | Fastqsanger.gz | |||
| ERR10752500_2.fastq.gz | Fastqsanger.gz | |||
| ERR10752600_1.fastq.gz | Fastqsanger.gz | |||
| ERR10752600_2.fastq.gz | Fastqsanger.gz | |||
| ERR10772800_1.fastq.gz | Fastqsanger.gz |
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Project description:Inbred C57BL/6J mice differ in their susceptibility to diet-induced obesity. Comparison of the liver transcriptomes leads to genes that are involved in the development as well as the maintenance of fatty liver during the onset of obesity upon high fat diet feeding. Genes being upregulated in DIO responder can be seen as drivers of fatty liver development, while genes upregulated in DIO non-responder are most likely involved in the protection against fatty liver diseases.
2018-10-30 | GSE74542 | GEO
Project description:Soybean oil consumption is increasing worldwide and parallels the obesity epidemic in the U.S. Rich in unsaturated fats, especially linoleic acid, soybean oil is assumed to be healthy, and yet it induces obesity, diabetes, insulin resistance and fatty liver in mice. The genetically modified soybean oil Plenish came on the U.S. market in 2014: it is low in linoleic acid and similar to olive oil in fatty acid composition. Here we show that Plenish induces less obesity than conventional soybean oil: metabolomics, proteomics and a transgenic mouse model implicate oxylipin metabolites of omega-6 and omega-3 fatty acids (linoleic and α-linolenic acid, respectively), which are generated by target genes of nuclear receptor HNF4α. While Plenish induces less insulin resistance than conventional soybean oil, it results in hepatomegaly and liver dysfunction as does olive oil. Altering the fatty acid profile of soybeans could help reduce obesity but may also cause liver complications.
2017-03-20 | GSE79408 | GEO
Project description:A recent study showed that 54% of type 2 diabetes (T2D) patients have nonalcoholic fatty liver disease, which is a risk factor for aggravation diabetic symptoms. Previous studies suggested components in maple syrup alleviated liver injury and found polyphenols as food components to improve the symptoms and complications of diabetes. Therefore, we hypothesized that a polyphenol fraction in maple syrup improves the symptoms and complications of diabetes. To address the hypothesis, we investigated the effects of a polyphenol-rich maple syrup extract (MSE) on a T2D model mice. KK-Ay mice were fed a normal or 0.1% MSE-supplemented diet for 43 days. The results showed that the levels of serum alanine aminotransferase and aspartate aminotransferase were significantly reduced in mice that ingested MSE. Hepatic genes related to lipogenesis and lipolysis were down- and upregulated, respectively, in mice that ingested MSE. These results suggest that MSE intake alleviates liver injury and suppresses lipid accumulation in the livers of T2D mice.
2020-01-13 | GSE134185 | GEO
Project description:An excessive high-fat/energy diet is a major cause of obesity and associated complications, such as non-alcoholic fatty liver disease (NAFLD). Betaine has been shown to effectively improve hepatic lipid metabolism. However, the mechanistic basis for this improvement is largely unknown. Herein, integration of transcriptomics sequencing (RNA-seq) and ribosome footprints profiling (Ribo-seq) was used to investigate the means by which betaine alleviates hepatic lipid metabolic disorders induced by a high-fat diet. For the transcriptome, gene set enrichment analysis demonstrated betaine to reduce liver steatosis by up-regulation of fatty acid beta oxidation, lipid oxidation, and fatty acid catabolic processes. For the translatome, 574 differentially expressed genes were identified, 17 of which were associated with the NAFLD pathway. By combined analysis of RNA-seq and Ribo-seq, we found that betaine had the greatest effect on NAFLD at the translational level. Further, betaine decreased translational efficiency (TE) for IDI1, CYP5A1, TM7SF2, and APOA4, which are related to lipid biosynthesis. In summary, this study demonstrates betaine to alleviate lipid metabolic dysfunction at the translational level. The powerful multi-omics data integration approach used herein provides for a new understanding of the means by which to treat NAFLD.
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Project description:Pancreatic beta-cell dysfunction and death are central in the pathogenesis of type 2 diabetes. Saturated fatty acids cause beta-cell failure and contribute to diabetes development in genetically predisposed individuals. Here we used RNA-sequencing to map transcripts expressed in five palmitate-treated human islet preparations, observing 1,325 modified genes. Palmitate induced fatty acid metabolism and endoplasmic reticulum (ER) stress. Functional studies identified novel mediators of adaptive ER stress signaling. Palmitate modified genes regulating ubiquitin and proteasome function, autophagy and apoptosis. Inhibition of autophagic flux and lysosome function contributed to lipotoxicity. Palmitate inhibited transcription factors controlling beta-cell phenotype including PAX4 and GATA6. 59 type 2 diabetes candidate genes were expressed in human islets, and 11 were modified by palmitate. Palmitate modified expression of 17 splicing factors and shifted alternative splicing of 3,525 transcripts. Ingenuity Pathway Analysis of modified transcripts and genes confirmed that top changed functions related to cell death. DAVID analysis of transcription binding sites in palmitate-modified transcripts revealed a role for PAX4, GATA and the ER stress response regulators XBP1 and ATF6. This human islet transcriptome study identified novel mechanisms of palmitate-induced beta-cell dysfunction and death. The data point to crosstalk between metabolic stress and candidate genes at the beta-cell level. 5 human islet of Langerhans preparations examined under 2 conditions (control and palmitate treatment)
2014-01-09 | E-GEOD-53949 | biostudies-arrayexpress
Project description:Objective: Obesity contributes to the dysfunction of salivary gland. To explore the specific underlying mechanism for obesity-induced hyposalivation, a model for high-fat diet-induced obese (DIO) mice were constructed to analyze long non-coding RNAs (lncRNAs) and messenger RNAs (mRNAs) expression profiles. Methods: The DIO group and control group were fed a diet containing 60 kcal% fat and a normal chow diet for 16 weeks respectively. Microarray analyses were performed to detect the expression profiles of lncRNA and mRNA in submandibular gland tissues from control group mice and DIO mice. Gene ontology, kyoto encyclopedia of genes and genomes, protein-protein interaction, coding-non-coding gene co-expression, transcription factors and competing endogenous RNA analyses were performed to examine the function of differential expressed genes. Results: The microarray identified that 624 lncRNAs, along with 297 mRNAs were differentially expressed. Bioinformatic analyses revealed that “complement and coagulation cascades”, “glutathione metabolism”, “cysteine and methionine metabolism”, and “estrogen signaling pathway” were significantly associated with candidate lncRNAs, transcription factors analysis on candidate lncRNAs reveled several genes such as tribbles pseudokinase 3 may play regulatory roles. Conclusions: Our results revealed the expression profiles of lncRNAs and mRNAs and provided new insights into the mechanism of obesity-induced hyposalivation using bioinformatic analyses.
2020-12-31 | GSE162953 | GEO
Project description:Soybean oil consumption is increasing worldwide and parallels the rise in obesity. Rich in unsaturated fats, especially linoleic acid, soybean oil is assumed to be healthy, and yet it induces obesity, diabetes, insulin resistance and fatty liver in mice. Here, we show that the genetically modified soybean oil Plenish, which came on the U.S. market in 2014 and is low in linoleic acid, induces less obesity than conventional soybean oil in C57BL/6male mice.
2017-06-08 | MSV000081149 | MassIVE
Project description:Pancreatic beta-cell dysfunction and death are central in the pathogenesis of type 2 diabetes. Saturated fatty acids cause beta-cell failure and contribute to diabetes development in genetically predisposed individuals. Here we used RNA-sequencing to map transcripts expressed in five palmitate-treated human islet preparations, observing 1,325 modified genes. Palmitate induced fatty acid metabolism and endoplasmic reticulum (ER) stress. Functional studies identified novel mediators of adaptive ER stress signaling. Palmitate modified genes regulating ubiquitin and proteasome function, autophagy and apoptosis. Inhibition of autophagic flux and lysosome function contributed to lipotoxicity. Palmitate inhibited transcription factors controlling beta-cell phenotype including PAX4 and GATA6. 59 type 2 diabetes candidate genes were expressed in human islets, and 11 were modified by palmitate. Palmitate modified expression of 17 splicing factors and shifted alternative splicing of 3,525 transcripts. Ingenuity Pathway Analysis of modified transcripts and genes confirmed that top changed functions related to cell death. DAVID analysis of transcription binding sites in palmitate-modified transcripts revealed a role for PAX4, GATA and the ER stress response regulators XBP1 and ATF6. This human islet transcriptome study identified novel mechanisms of palmitate-induced beta-cell dysfunction and death. The data point to crosstalk between metabolic stress and candidate genes at the beta-cell level.
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Project description:To identify mediators of obesity-linked reductions in PGC-1, we tested the effects of cellular nutrients in C2C12 myotubes. While overnight exposure to high insulin, glucose, glucosamine, or amino acids had no effect, saturated fatty acids (FA) potently reduced PGC-1a and b mRNA expression. Experiment Overall Design: Cell culture - Mouse C2C12 myoblasts (ATCC, Manassas, VA) were maintained in Dulbecco's modified Eagle's medium (DMEM) supplemented with 20% fetal bovine serum (Invitrogen), at a confluency of 60-70%. To initiate differentiation, cells were allowed to reach 100% confluency and medium was changed to DMEM containing 2% horse serum (Invitrogen) and changed every 2 days. Full differentiation, with myotube fusion and spontaneous twitching, was observed at 5 days. Fatty acid stock preparation - Fatty acids were dissolved in 0.1 N sodium hydroxide (final concentration 100 mM) at 65 degrees C for 2 hours and then complexed with 10% fatty acid-free BSA, yielding a final stock of 5 mM. Three replicates for each fatty-acid. Microarray analysis - RNA was isolated as described from C2C12 myotubes treated overnight with 500 uM palmitate or 1% BSA, and cRNA was synthesized. 10 mg of cRNA were hybridized to Affymetrix mouse 430A 2.0 arrays. Intensity values were quantified using MAS 5.0 software. MAPPFinder (www.genmapp.org) was used to integrate expression data with known pathways. Transcription profiling of mouse C2C12 myotubes treated overnight with 500 uM palmitate or 1% BSA to identify mediators of obesity-linked reductions in PGC-1.
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