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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE78053 | GEO | 2016/02/25

SECONDARY ACCESSION(S): PRJNA312453

REPOSITORIES: GEO

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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.

2016-02-25 | E-GEOD-78053 | biostudies-arrayexpress

Transcriptional profiling of mouse liver tissue following control, choline and methonine/choline deficient diet intervention

Project description:Choline and methionine/choline deficient diets are widely used to generate severe rodent hepatic steatosis and steatohepatitis in an attempt to reflect stages of human non-alcoholic fatty liver disease (NAFLD). The underlying mechanism of hepatic injury in these models, and how this reflects human disease remains incompletely understood. We used detailed transcriptional analysis to interrogate the molecular mechanisms of this intervention and its similarity to human disease. Adult C57Bl/6J mice were maintained on control, choline deficient (CDD) or methionine/choline deficient (MCDD) diets for 4 weeks. Isolated liver RNA was used for transcriptional profiling by micro array analysis.

2016-06-01 | E-MTAB-3943 | biostudies-arrayexpress

Effect of methionine/choline deficient diet on liver and suprachiasmatic nucleus circadian transcriptome.

Project description:The feeding/fasting cycles controlled by our circadian clock impose great daily metabolic and physiological changes, and yet investigations into the consequences of metabolic deficiencies, either dietary or genetic, have often ignored the time of day or the circadian time of the animals or subjects. In addition, these deficiencies may themselves disrupt our circadian clock, causing secondary metabolic, physiological and behavioural disorders. Dietary methionine/choline deficiency in rodents is a common model for human non-alcoholic steatohepatitis, but methionine and choline are nutrients essential for many other processes beyond fatty acid synthesis in the liver, including biological methylations and 1-carbon metabolism, regulation of translation notably via the mTOR pathway, phospholipid synthesis, polyamine pathway and glutathione synthesis. We have previously shown that circadian rhythms in many organisms are highly sensitive to deficiency or excesses of 1-carbon metabolites. Using a methionine/choline deficient diet in mice, we illustrate the nutrigenomic crosstalk between circadian rhythms and 1-carbon metabolism. We show not only that circadian locomotor activity behaviour is profoundly, rapidly and reversibly affected by methionine/choline deficiency, but also that the effects of methionine/choline deficiency on gene expression and 1-carbon metabolites are dependent on circadian time, illustrating the importance of considering circadian rhythms in metabolic studies. This study also highlights the impact of what we eat, or don't, on our behaviour and biological rhythms.

2024-01-05 | GSE252364 | GEO

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.

2024-02-09 | GSE243186 | 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 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.

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Transcriptomic profile of replicating NAFLD hepatocytes (from High-Fat High-Sucrose Diet - HFHS and Choline-Deficient High-Fat Diet - CDHFD).

Project description:C57Bl6/J male mice were put on different diets at 5 weeks of age, with a standard diet (SD) or a High-Fat High-Sucrose Diet (HFHS) or a Choline-Deficient High-Fat Diet (CDHFD) during 6 months. Primary hepatocytes cultures from 3 different models were synchronized in the cell cycle. Transcriptomic analysis was perfomed at 48hours of culture when HFHS and CDHFD hepatocytes harbor replication stress.

2020-07-11 | GSE154194 | GEO

Differential gene expression of embryonic brains in maternal choline deficiency

Project description:Choline plays an important role during pregnancy. The study focuses on gene expression profile of whole brain tissues of embryos in mouse female treated with choline deficient diet or chow diet.

2024-03-13 | GSE239589 | GEO

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

Project description:Nonalcoholic Fatty Liver Disease (NAFLD) is a broad spectrum of liver disorders ranging from simple steatosis to nonalcoholic steatohepatitis, cirrhosis and hepatocellular carcinoma. The choline-deficient L-amino acid-defined (CDAA) diet-induced NAFLD animal model has traditionally been used to understand the molecular mechanisms of disease development and progression. Although this animal model shows a similar course of disease progression to human NAFLD, it does not develop comorbidities such as obesity and type 2 diabetes. Therefore, its relevance to human NAFLD (what aspects of the disease etiology are recapitulated in this model?) is not fully understood. We applied microarray analysis to characterize its pathophysiology, and evaluate the similarity across species.

2023-03-25 | GSE227714 | GEO

Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for the histone modifications H3K27ac and H3K9me3 in liver tissues from MCD and regular chow diet mice

Project description:Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for the histone modifications H3K27ac and H3K9me3 in liver tissues from Methionine- and choline-deficient diet (MCD) and regular chow diet mice.

2024-05-02 | GSE266077 | GEO

Interstrain differences in the severity of liver injury induced by a choline- and folate-deficient diet in mice are associated with dysregulation of genes involved in lipid metabolism.

Project description:Nonalcoholic fatty liver disease (NAFLD) is a major health problem and a leading cause of chronic liver disease in the United States and developed countries. In humans, genetic factors greatly influence individual susceptibility to NAFLD. The goals of this study were to compare the magnitude of interindividual differences in the severity of liver injury induced by methyl-donor deficiency among individual inbred strains of mice and to investigate the underlying mechanisms associated with the variability. Feeding mice a choline- and folate-deficient diet for 12 wk caused liver injury similar to NAFLD. The magnitude of liver injury varied among the strains, with the order of sensitivity being A/J M-bM-^IM-^H C57BL/6J M-bM-^IM-^H C3H/HeJ < 129S1/SvImJ M-bM-^IM-^H CAST/EiJ < PWK/PhJ < WSB/EiJ. The interstrain variability in severity of NAFLD liver damage was associated with dysregulation of genes involved in lipid metabolism, primarily with a down-regulation of the peroxisome proliferator receptor M-NM-1 (PPARM-NM-1)-regulated lipid catabolic pathway genes. Markers of oxidative stress and oxidative stress-induced DNA damage were also elevated in the livers but were not correlated with severity of liver damage. These findings suggest that the PPARM-NM-1-regulated metabolism network is one of the key mechanisms determining interstrain susceptibility and severity of NAFLD in mice. Male A/J, C3H/HeJ and WSB/EiJ inbred mice were maintained on either control or choline- and folate-deficient (CFD) diets for 12 weeks. Gene expression profiles in the livers from control mice and mice fed a CFD-diet were investigated.

2014-10-16 | E-GEOD-62362 | biostudies-arrayexpress

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