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Transcriptomic analysis of liver mRNA from TSP-1 KO and WT mice fed with normal diet or choline deficient amino acid defined diet (CDAHFD, human NASH model)

ABSTRACT: Transcriptomic profiles of wild type and TSP1 knockout mice that were fed control (normal) diet or CDAHFD (choline deficient amino acid defiend high fat diet) chow for 12 weeks to model Non-alcoholic Steatohepatitis (NASH) disease in humans.

ORGANISM(S): Mus musculus

PROVIDER: GSE120977 | GEO | 2019/05/31

REPOSITORIES: GEO

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Role of Cyp2b in diet-induced nonalcoholic steatohepatitis (NASH)

Project description:To investigate the role of hepatic CYP2B in diet-induced nonalcoholic steatohepatitis (NASH), a Cyp2b triple knockout mouse lacking Cyp2b9, Cyp2b10, and Cyp2b13 was developed using CRISPER/Cas9. Wildtype (WT) and Cyp2b-null mice were fed a normal diet (ND) or a choline-deficient, L-amino acid-defined high-fat diet (CDAHFD), containing 0.1% methionine and 62% fat for 8 weeks. RNA was extracted from the livers of female and male mice from all treatment groups and used for RNA seqencing. RNAseq data demonstrated that a lack of Cyp2b was protective in female but more harmful in male mice. Hepatic gene expression revealed a higher number of phase I-III xenobiotic metabolism and inflammatory response genes were down-regulated in CDAHFD-fed WT female and Cyp2b-null male mice.

2019-12-31 | GSE137449 | GEO

Transcriptomic analysis of liver mRNA from TSP-1 KO and WT mice fed with normal diet or choline deficient amino acid defined diet (CDAHFD, human NASH model)

Project description:Transcriptomic analysis of liver mRNA from TSP-1 KO and WT mice fed with normal diet or choline deficient amino acid defined diet (CDAHFD, human NASH model)

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CDAHFD induced NASH mouse model

Project description:Non-alcoholic steatohepatitis (NASH) is the most significant cause of chronic liver disease worldwide, with limited therapeutic options. In this experiment, a choline-deficient amino acid-defined high fat diet (CDAHFD) were used to construct a mouse NASH model. After 16 weeks of CDAHFD diets, liver samples were collected. We want to further confirm that the elevated EFHD2 is specifically expressed in infiltrated macrophages/monocytes in NASH.

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Microarray analysis of choline-deficient L-amino acid-defined (CDAA) diet-induced NAFLD animal model.

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Gene expression profiles of mouse liver tissues in response to choline deficient diet

Project description:The objective of this study is to explore gene expression profiles of liver tissues in response to choline defficient diet by DNA microarray data analysis. Male CD-1mice (5 weeks) were fed either a choline-deficient diet (F2CDD, Oriental Yeast) or F2CDD plus 0.2% choline bitartrate for 3 weeks. Liver tissue from control versus choline-deficient samples were analyzed for gene expression on an Agilent Whole Mouse Genome Microarray.

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Proteomic Analysis of Mouse Liver in Response to a Choline-Deficient, L-Amino Acid-Defined, High-Fat Diet (CDAHFD)

Project description:We investigated proteomic changes in the livers of mice subjected to various dietary and genetic interventions. Three comparisons were made: (1) Mice fed CDAHFD (n = 6) vs. mice fed regular chow (RC) (n = 6); (2) Mice treated with Coasy ASO under CDAHFD conditions (n = 6) vs. mice treated with control ASO under CDAHFD conditions (n = 6); (3) Mice treated with Coasy ASO and 2% cholesterol under CDAHFD conditions (n = 6) vs. mice treated with Coasy ASO under CDAHFD conditions (n =6).

2025-04-17 | PXD063049 | JPOST Repository

Maternal Dietary Choline Levels Cause Transcriptome Shift due to Genotype-by-Diet Interaction in Rainbow Trout (Oncorhynchus mykiss)

Project description:The objective of this study was to identify metabolic regulatory mechanisms affected by choline availability in rainbow trout (Oncorhynchus mykiss) broodstock diets associated with increased offspring growth performance. Three customized diets were formulated to have different levels of choline: (a) 0% choline supplementation (Low Choline: 2065 ppm choline), (b) 0.6% choline supplementation (Medium Choline: 5657 ppm choline), and (c) 1.2% choline supplementation (High Choline: 9248 ppm choline). Six all-female rainbow trout families were fed experimental diets beginning 18 months post-hatch until spawning; their offspring were fed a commercial diet. Experimental broodstock diet did not affect overall choline, fatty acid, or amino acid content in the oocytes (p > 0.05), apart from tyrosine (p ≤ 0.05). Offspring body weights from the High and Low Choline diets did not differ from those in the Medium Choline diet (p > 0.05); however, family-by-diet and sire-by-diet interactions on offspring growth were detected (p ≤ 0.05). The High Choline diet did not improve growth performance in the six broodstock families at final harvest (520-days post-hatch, or dph). Numerous genes associated with muscle development and lipid metabolism were identified, including myosin, troponin C, and fatty acid binding proteins, which were associated with key signaling pathways of lipid metabolism, muscle cell development, muscle cell proliferation, and muscle cell differentiation. These findings indicate that supplementing broodstock diets with choline does regulate expression of genes related to growth and nutrient partitioning but does not lead to growth benefits in rainbow trout families selected for disease resistance.

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Microarray analysis of choline-deficient L-amino acid-defined (CDAA) diet-induced NAFLD animal model.

Project description:Microarray analysis of choline-deficient L-amino acid-defined (CDAA) diet-induced NAFLD animal model.

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Gene expression profiles of mouse liver tissues in response to choline deficient diet

Project description:The objective of this study is to explore gene expression profiles of liver tissues in response to choline defficient diet by DNA microarray data analysis.

2016-02-25 | GSE78053 | GEO

PPARα agonist and metformin co-treatment ameliorates NASH in mice induced by a choline-deficient, amino acid-defined diet with 45% fat.

Project description:We explored the beneficial effects of GW7647, a peroxisome proliferator activated receptor α (PPARα) agonist, and metformin, an anti-diabetic drug on an advanced nonalcoholic steatohepatitis (NASH) model in rodents and investigated the possible mechanisms involved. Mice were fed control chow or a choline-deficient L-amino acid-defined diet containing 45% fat (HF-CDAA). The mice fed HF-CDAA diets for 16 weeks were divided into four groups: the no treatment (HF-CDAA), HF-CDAA containing 1000 mg/kg metformin, HF-CDAA containing 10 mg/kg GW7647, and HF-CDAA with both metformin and GW7647 groups. Metformin alone slightly deteriorated the aspartate and alanine aminotransferase (AST/ALT) values, whereas co-treatment with GW7647 and metformin greatly suppressed liver injury and fibrosis via activation of the AMP-activated protein kinase (AMPK) pathway. Further study revealed that co-treatment decreased the expression of inflammatory-, fibrogenesis-, and endoplasmic reticulum (ER) stress-related genes and increased the oxidized nicotinamide adenine dinucleotide (NAD)/reduced nicotinamide adenine dinucleotide (NADH) ratio, suggesting the superiority of co-treatment due to restoration of mitochondrial function. The additive benefits of a PPARα agonist and metformin in a HF-CDAA diet-induced advanced NASH model was firstly demonstrated, possibly through restoration of mitochondrial function and AMPK activation, which finally resulted in suppression of hepatic inflammation, ER stress, then, fibrosis.

| S-EPMC7658250 | biostudies-literature

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