Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1056905 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To elucidate the molecular mechanism behind the anti-NAFLD effect of HDCA, we screened for potential HDCA binding proteins using biotin-labeled HDCA and HuProt human proteome microarray.
2023-08-17 | GSE241065 | GEO
Project description:HDCA supplementation ameliorated diet-induced NAFLD in C57 wild type mice. In attempt to comprehensively understand the molecular mechanism occurring during the protective effect of HDCA, transcriptomic and proteomic profiles of mouse liver were first analyzed utilizing RNA-Sequencing and Tandem Mass Tag-based quantitative proteomic approach, respectively. Then, we screened for potential HDCA binding proteins by using biotin-labeled HDCA and human proteome microarray.
2023-08-18 | PXD044613 |
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.
2021-07-31 | GSE181077 | GEO
Project description:We aim to establish NAFLD model of Zebrafish. Zebrafish larvae fed with high cholesterol diet，high fructose diet and overfeed diet to induce liver steatosis. RNA-seq was employed to analyze the effects of different diets on NAFLD development.
2018-12-01 | E-MTAB-6636 | biostudies-arrayexpress
Project description:To understand the therapeutic mechanisms of QHD, we examined the effects of QHD treatment on the liver transcriptomes of NAFLD rats and identified multiple therapeutic targets of QHD. We used microarrays to examine the effects of QHD and GC treatment on the liver transcriptomes of NAFLD rats induced by high fat diet and identified multiple therapeutic targets of QHD.
2016-10-01 | GSE87432 | GEO
Project description:Dysregulated glucose homeostasis and lipid accumulation characterize non-alcoholic fatty liver disease (NAFLD), but underlying mechanisms are obscure. We report here that Krüppel-like factor 6 (KLF6), a ubiquitous transcription factor that promotes adipocyte differentiation, also provokes the metabolic abnormalities of NAFLD. Mice with either hepatocyte-specific knockdown of KLF6 (DeltaHepKlf6) or global KLF6 heterozygosity (Klf6 +/-) have reduced body fat content and improved glucose and insulin tolerance. Mice with KLF6 depletion, compared to wild type mice, are protected from high fat diet-induced steatosis. Three mice with a hepatocyte-specific knockdown of KLF6 (DeltaHepKlf6) on high fat diet and 3 littermate controls on the same diet were sacrificed after 8 weeks of diet. Liver tissue was preserved in RNAlater® (Ambion, Austin, TX). RNA was isolated from liver tissue and homogenized in TRIzol® reagent (Invitrogen, Carlsbad, CA). In order to identify potential KLF6 targets that contributed to changes in glucose- and lipid-metabolism, we performed an Affymetrix Exon1 S.T. Genearray® (Affymetrix, Santa Clara, CA).
2012-03-23 | E-GEOD-36724 | biostudies-arrayexpress
Project description:Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease.MicroRNAs play roles in the onset and progression of the disease. This study aimed to screen microRNA profiles and potential RNA networks for the diagnosis and treatment of NAFLD. Mice were high-fructose diet (HFrD) fed to induce NAFLD. MicroRNA expression profiles of the livers in HFrD mice and chow-diet fed mice were analyzed by RNA-seq. We successfully constructed high fructose induced NAFLD. There are 13 differentially expressed (DE) miRNAs in the livers of NAFLD mice. In summary, this study furthered our understanding of the genome mechanisms and the development of potential biomarkers for the treatment of fructose-induced NAFLD.
2024-11-15 | GSE263701 | GEO
Project description:Protein post-translational modifications (PTMs) participate in important bioactive regulatory processes and therefore can help elucidate the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Here, we investigate the involvement of PTMs in ketogenic diet (KD)-improved fatty liver by multi-omics and reveal a core target of lysine malonylation, acetyl-CoA carboxylase 1 (ACC1). ACC1 protein levels and Lys1523 malonylation are significantly decreased by KD. It is discovered that a malonylation-mimic mutant in ACC1 increases its enzyme activity and stability to promote hepatic steatosis, whereas the malonylation-null mutant upregulates the ubiquitination degradation of ACC1. A customized Lys1523ACC1 malonylation antibody confirms the increased malonylation of ACC1 in the NAFLD samples. Overall, the lysine malonylation of ACC1 is attenuated by KD in NAFLD and plays an important role in promoting hepatic steatosis. Malonylation is critical for ACC1 activity and stability, highlighting the anti-malonylation effect of ACC1 as a potential strategy for treating NAFLD.
2023-07-21 | PXD040481 | Pride
Project description:Multi-omics study identifies unique metabolic responses to high glycemic diet in liver and retina
| PRJNA1020144 | ENA
Project description:Protein post-translational modifications (PTMs) participate in important bioactive regulatory processes and therefore can help elucidate the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Here, we investigate the involvement of PTMs in ketogenic diet (KD)-improved fatty liver by multi-omics and reveal a core target of lysine malonylation, acetyl-CoA carboxylase 1 (ACC1). ACC1 protein levels and Lys1523 malonylation are significantly decreased by KD. It is discovered that a malonylation-mimic mutant in ACC1 increases its enzyme activity and stability to promote hepatic steatosis, whereas the malonylation-null mutant upregulates the ubiquitination degradation of ACC1. A customized Lys1523ACC1 malonylation antibody confirms the increased malonylation of ACC1 in the NAFLD samples. Overall, the lysine malonylation of ACC1 is attenuated by KD in NAFLD and plays an important role in promoting hepatic steatosis. Malonylation is critical for ACC1 activity and stability, highlighting the anti-malonylation effect of ACC1 as a potential strategy for treating NAFLD.
2023-03-05 | GSE226139 | GEO