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Analysis of liver gene expression profile in male mice fed alcoholic (Lieber-Decarli's) diet and calorie-matched control diet for 6 weeks

ABSTRACT: Microarray analysis showed dysregulation of genes involved in lipid, xenobiotic and glutathione metabolism as well as those involved in mitochondrial function and cell proliferation in the livers of C57BL6 mice fed alcoholic liquid diet for 6 weeks.

ORGANISM(S): Mus musculus

PROVIDER: GSE30829 | GEO | 2012/12/19

SECONDARY ACCESSION(S): PRJNA144181

REPOSITORIES: GEO

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Analysis of liver gene expression profile in male mice fed alcoholic (Lieber-Decarli's) diet and calorie-matched control diet for 6 weeks

Project description:Microarray analysis showed dysregulation of genes involved in lipid, xenobiotic and glutathione metabolism as well as those involved in mitochondrial function and cell proliferation in the livers of C57BL6 mice fed alcoholic liquid diet for 6 weeks. We analyzed liver RNA from 4 mice fed alcoholic diet and 4 mice fed control diet using the Affymetrix Mouse Exon 1.0 ST platform. Array data was processed by Affymetrix Exon Array Computational Tool.

2012-12-19 | E-GEOD-30829 | biostudies-arrayexpress

Hepatic gene expression in C56BL/6J mice fed a quercetin diet for 20 weeks

Project description:Both the 0.05% and 1% querceitn diets did not significantly affect the body weight, fat accumulation, and blood components. However, 0.05% quercetin significantly increased the glutathione/oxidized glutathione ratio in the liver. Moreover, the 1% quercetin diet reduced the lipid peroxidation markers 8-isoprostane in plasma and malondialdehyde in the liver, epididymal adipose tissues, and small intestine. Although comprehensive gene expression analysis dot not detect the genes with significantly different expression levels among the groups of mice, RT-PCR analysis showed that the 1% quercetin diet significantly induced the expression of the antioxidant enzymes Gpx1, Cat, and Sod1 in the liver and Gpx1 and Cat in the epididymal adipose tissues. The transcription factor nuclear factor E2-related factor 2 (Nrf2) was slightly induced in the nuclear fraction of the livers of mice fed the 1% quercetin diet. Quercetin may induce antioxidant enzymes by directly or indirectly activating the Nrf2 pathway in the liver.

2015-07-24 | GSE62805 | GEO

Hepatic gene expression in C56BL/6J mice fed a quercetin diet for 20 weeks

2015-07-24 | E-GEOD-62805 | biostudies-arrayexpress

Effect of sarsasapogenin (SAR) on non-alcoholic fatty liver disease in mice fed with methionine choline deficiency (MCD) diet

Project description:This study aimed to investigate the effects and underlying mechanisms of sarsasapogenin (SAR) on dietary methionine choline deficiency induced non-alcoholic fatty liver disease in mice, The differentially expressed genes in liver tissue in “Normal VS model ”and “Model VS SAR” were identified by RNA-seq.

2023-01-20 | GSE222935 | GEO

Transcriptomic analysis of primary hepatocytes and total livers from WT mice fed with CSAA or CDAA-HSHC diet during 2 weeks.

Project description:Mouse primary hepatocytes (PH) and total livers (TL) prepared from C57Bl6 male adult mice which were fed either a CDAA supplemented cholesterol with glucose and fructose or a CSAA diet during 2 weeks.

2024-04-01 | GSE212617 | GEO

Combined Metabolic Activators Decrease Liver Steatosis by Activating Mitochondrial Metabolism in Hamsters Fed with a High-Fat Diet

Project description:Purpose: Although the prevalence of non-alcoholic fatty liver disease (NAFLD) continues to increase, there is no effective treatment approved for this condition. We previously showed, in high-fat diet (HFD)-fed mice, that the supplementation of combined metabolic activators (CMA), including nicotinamide riboside (NAD+ precursor) and the potent glutathione precursors serine and N-acetyl-l-cysteine (NAC), significantly decreased fatty liver by promoting fat oxidation in mitochondria. Afterwards, in a one-day proof-of-concept human supplementation study, we observed that this CMA, including also L-carnitine tartrate (LCT), resulted in increased fatty acid oxidation and de novo glutathione synthesis. However, the underlying molecular mechanisms associated with supplementation of CMA have not been fully elucidated. Conclusions: Our study demonstrated in hamsters that the chronic supplementation of this CMA (changing serine for betaine) at two doses significantly decreased hepatic steatosis. We further generated liver transcriptomics data and integrated these data using a liver-specific genome-scale metabolic model of liver tissue. We systemically determined the molecular changes after the supplementation of CMA and found that it activates mitochondria in the liver tissue by modulating global lipid, amino acid, antioxidant and folate metabolism. Our findings provide extra evidence about the beneficial effects of a treatment based on this CMA against NAFLD.

2021-10-22 | GSE186165 | GEO

Risk of symptomatic gallstones and cholecystectomy after a very-low-calorie diet or low-calorie diet in a commercial weight loss program: 1-year matched cohort study.

Project description:BackgroundConcern exists regarding gallstones as an adverse event of very-low-calorie diets (VLCDs; <800?kcal per day).ObjectiveTo assess the risk of symptomatic gallstones requiring hospital care and/or cholecystectomy in a commercial weight loss program using VLCD or low-calorie diet (LCD).DesignA 1-year matched cohort study of consecutively enrolled adults in a commercial weight loss program conducted at 28 Swedish centers between 2006 and 2009. A 3-month weight loss phase of VLCD (500?kcal per day) or LCD (1200-1500?kcal per day) was followed by a 9-month weight maintenance phase. Matching (1:1) was performed by age, sex, body mass index, waist circumference and gallstone history (n=3320:3320). Gallstone and cholecystectomy data were retrieved from the Swedish National Patient Register.ResultsOne-year weight loss was greater in the VLCD than in the LCD group (-11.1 versus -8.1?kg; adjusted difference, -2.8?kg, 95% CI -3.1 to -2.4; P<0.001). During 6361 person-years, 48 and 14 gallstones requiring hospital care occurred in the VLCD and LCD groups, respectively, (152 versus 44/10?000 person-years; hazard ratio, 3.4, 95% CI 1.8-6.3; P<0.001; number-needed-to-harm, 92, 95% CI 63-168; P<0.001). Of the 62 gallstone events, 38 (61%) resulted in cholecystectomy (29 versus 9; hazard ratio, 3.2, 95% CI 1.5-6.8; P=0.003; number-needed-to-harm, 151, 95% CI 94-377; P<0.001). Adjusting for 3-month weight loss attenuated the hazard ratios, but the risk remained higher with VLCD than LCD for gallstones (2.5, 95% CI 1.3-5.1; P=0.009) and became borderline for cholecystectomy (2.2, 95% CI 0.9-5.2; P=0.08).ConclusionThe risk of symptomatic gallstones requiring hospitalization or cholecystectomy, albeit low, was 3-fold greater with VLCD than LCD during the 1-year commercial weight loss program.

| S-EPMC3921672 | biostudies-literature

Changes of hepatic gene expression in C57BL/6N male mice fed high-fat high-calorie fructose (HFHC) diet for 8 weeks

Project description:In murine NAFL/NASH models, high-fat high-calorie fructose (HFHC) diet fed for 16 weeks induces hepatic steatosis, inflammatory cells infilatration and early stage fibrosis. In addition, HFHC diet 16 weeks but not 8 weeks is accompanied with weight gain and insulin resistance. The aim of this study is to determine the gene expression changes in mouse liver by HFHC diet for 8weeks.

2021-12-08 | GSE154426 | GEO

Expression data from human non-alcoholic fatty liver disease stages

Project description:Global gene expression patterns of 2 human steatosis and 9 human non-alcoholic steatohepatitis (NASH) together with their respective control patterns were analyzed to define the non-alcoholic fatty liver disease (NAFLD) progression molecular characteristics and to define NASH early markers from steatosis. Human liver samples of steatosis and non-alcoholic steatohepatitis were selected for RNA extraction and hybridization on Affymetrix microarrays. This dataset is part of the TransQST collection.

2014-11-07 | E-GEOD-63067 | biostudies-arrayexpress

Microarray analysis among non-alcoholic fatty liver, non-alcoholic steatohepatitis, and type 2 diabetes mellitus rats

Project description:Non-alcoholic fatty liver (NAFL) has the potential to progress to non-alcoholic steatohepatitis (NASH) or to promote type 2 diabetes mellitus (T2DM). However, NASH and T2DM do not always develop coordinately. We established rat models of NAFL, NASH, and NAFL + T2DM to recapitulate different phenotypes associated with NAFLD and its progression. Microarrays were used to identify hepatic gene expression changes in each of these models. The goal is to identify a predictor of different NAFLD progressions. Non-alcoholic fatty liver disease (NAFLD) is recognized as a low-grade systemic inflammatory state with both hepatic and extra-hepatic manifestations. We aimed to identify common key regulators and adaptive pathways in different NAFLD phenotypes. NAFL, NASH and NAFL+T2DM rat models were used to represent simple fatty liver, fatty liver with severe hepatic manifestations, and fatty liver with severe metabolic manifestations, respectively. We applied microarray analysis to characterize the key regulators and adaptive pathways in different NAFLD phenotypes. There are 12 samples in our study which belonged to 4 groups, and each group contains 3 different samples.

2015-01-23 | E-GEOD-65220 | biostudies-arrayexpress

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