Gene expression changes in liver tissues from alcohol treated mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE44237 | GEO | 2013/02/12
SECONDARY ACCESSION(S): PRJNA189233
REPOSITORIES: GEO
Similar Datasets
Project description:transcriptomic changes in the early stages of ALD in mice fed the Lieber-Decarli liquid diet with or without alcohol for four months to identify biomarkers for the early stage of alcohol induced liver damage. Mice were sampled after 1, 2 and 4 months treatment. Two-condition experiment, control vs. alcohol treated at specified time point. Sample pooled from six biological replicates in each group. Reverse-fluorescence replicates.
2013-02-12 | E-GEOD-44237 | biostudies-arrayexpress
Project description:transcriptomic changes in wild typw and PPARa-null mice fed the Lieber-Decarli liquid diet with or without alcohol for up to four months to identify biomarkers for the early stage of alcohol induced liver damage. Mice were sampled after 1, 2 and 4 months treatment.
2014-01-14 | GSE54034 | GEO
Project description:transcriptomic changes in wild typw and PPARa-null mice fed the Lieber-Decarli liquid diet with or without alcohol for up to four months to identify biomarkers for the early stage of alcohol induced liver damage. Mice were sampled after 1, 2 and 4 months treatment. single-color experiment using Agilent Mouse GE 8x60K Microarray Cat.# G4858A-028005
2014-01-14 | E-GEOD-54034 | biostudies-arrayexpress
Project description:Alcoholic liver disease, which varies in severity from mild steatosis to cirrhosis and hepatitis, is one of the most prevalent chronic liver diseases worldwide. Excessive alcohol consumption remains the leading cause of ALD and alcohol-related complications and deaths. However, no medications have been developed to treat this disease and its pathogenesis remains elusive. Here, to understand alcohol-induced AhR activation in more detail, transcriptomic data was conducted using livers from mice subjected to either control or Lieber-DeCarli alcohol diets.
2022-09-06 | GSE179398 | GEO
Project description:The mice were fed with Lieber-Decarli alcohol liquid diet and intraperitoneal injection of carbon tetrachloride to induce alcoholic liver fibrosis in mice. The drug group was treated with kinsenoside at the same time to study the protective effect and mechanism of kinsenoside on alcoholic liver injury in mice.
2022-01-13 | PXD027621 | Pride
Project description:Alcohol’s impairment of both hepatic lipid metabolism and insulin resistance (IR) are key drivers of alcoholic steatosis, the initial stage of alcoholic liver disease (ALD). Pharmacologic reduction of lipotoxic ceramide prevents alcoholic steatosis and glucose intolerance in mice, but potential off-target effects limit its strategic utility. Here, we employed a hepatic-specific acid-ceramidase (ASAH) overexpression model to reduce hepatic ceramides in a Lieber-DeCarli model of experimental alcoholic steatosis. We examined effects of alcohol on hepatic lipid metabolism, body composition, energy homeostasis and insulin sensitivity as measured by hyperinsulinemic-euglycemic clamp. Our results demonstrate that hepatic ceramide reduction ameliorates the effects of alcohol on hepatic lipid droplet accumulation by promoting VLDL secretion and lipophagy, the latter of which involves ceramide cross-talk between the lysosomal and lipid droplet compartments. We additionally demonstrate that hepatic ceramide reduction prevents alcohol’s inhibition of hepatic insulin signaling. These effects on the liver are associated with a reduction in oxidative stress markers and are relevant to humans, as we observe peri-lipid droplet ASAH expression in human ALD. Together, our results suggest a potential role for hepatic ceramide inhibition in preventing ALD.
2020-07-08 | GSE139015 | GEO
Project description:Background & Aims: Alcohol-associated liver disease (ALD) is associated with loss of vitamin A (retinoids), increased steatosis, and greater oxidative stress. Although a strong correlation has been observed between loss of retinoids and ALD, if retinoid loss plays a causal role in the pathophysiology of ALD is not clear. Approach & Results: Based on our prior published data indicating that a selective retinoic acid receptor beta (RARβ) agonist limits nonalcohol-related liver disease (NAFLD) pathology, we generated AlbCre;RARβ knockout (BKO) mice and fed these mice a Lieber DeCarli ethanol diet (ETOH). We also generated cultured human hepatocytes (HepG2) that lack RARβ (RARβ-KO) and treated them with ETOH. Here we show that the livers of BKO mice develop greater steatosis, oxidative stress (assessed by 4-HNE), cell proliferation, and hypertrophy on the ETOH diet when compared to wild type (WT). Compared to ETOH-WT mice, the ETOH-BKO mice also exhibit higher hepatic transcript levels of ATF4, MYC, a subset of integrated stress response (ISR) genes (Trib3, Asns, Nqo1, and Hmox1), and the common ATF4 and MYC target, 4EBP1(EIF4EBP1). In RARβ-KO HepG2 cells, ETOH treatments (24 and 72h) resulted in more rapid and greater development of reactive oxygen species compared to parental HepG2. Notably, even without ETOH, ATF4 protein was higher in the RARβ-KO than in parental HepG2. Conclusions: Our research identifies hepatocyte RARβ as a crucial negative regulator of oxidative stress, MYC, ATF4, and proliferation in ALD.
2023-11-28 | GSE221713 | GEO
Project description:Alcohol induced fatty liver cause a dangerous health problem and is the major cause of morbidity and mortality worldwide. Garlic (Allium sativum) is documented to possess anti-fatty liver properties. However the exact molecular mechanisms are unknown. The main aim of this experiment is to elucidate the underlying pathways through which garlic ameliorates alcohol induced fatty liver. Dially disulfide and garlic oil were the garlic compounds used in this study. Leiber DeCarli ethanol liquid diet was to induce fatty liver in C57BL/6 mice model. Also the expression impaired by alcohol induced fatty liver is another aim of this study. Leiber-Decarli ethanol diet was used to induce fatty liver in male C57BL/6 mice (n=12). For control, Lieber-DeCarli liquid control diet was fed to mice (n=4). The control mice were pair-fed to the ethanol mice. After adaptation, the ethanol fed mice were divided into three groups viz. alcohol (n=4), dially disulfide [DADS] (n=4) and garlic oil [GO] (n=4). The study started with the administration of DADS (15 mg/kg bw) or GO (50 mg/kg bw) mixed in 0.1 ml olive oil through gavage. For the control and alcohol groups, same amount of olive oil (0.1 ml) was gavaged. The mice were gavaged daily for 4 weeks. The mice were euthanized by CO2 and blood was collected by cardiac puncture. Liver, kidney, spleen, lungs and hearts were collected and their weights recorded. A portion of liver was snap frozen in liquid nitrogen (200 mg) for RNA extraction.
2012-10-01 | E-GEOD-40334 | biostudies-arrayexpress
Project description:Alcohol-associated liver disease (ALD) is a major cause of alcohol related mortality. The specific mechanisms responsible for ALD development and progression are not fully understood, and there is limited therapy for any stage of ALD. Sex differences are often disregarded in in genetic and mechanistic studies. We aimed to take an unbiased approach to define sex specific pathways in livers exposed to alcohol. METHODS: Mice were fed LieberDeCarli alcohol liquid diet for 3 weeks. To identify the role of Kdm5b and Kdm5c we injected mice with AAV-shControl at 2x10^11 gc per mouse or AAV-shKdm5b and AAV-Kdm5c vectors at 10^11 gc per mouse. To assess the role of AhR we injected mice with AAV-shControl or AAV-shAhR vectors at 10^11 gc per mouse. RESULTS: We found several pathways affected by alcohol in sex specific way and identified KDM5 demethylases as contributors to that specificity.
2022-02-08 | GSE195889 | GEO
Project description:Heavy alcohol drinking dysregulates lung immunity and host defense, which makes individuals with AUD more susceptible to develop inflammatory condition in lungs with poor prognosis. Current study, we focused on exploring the effects of chronic alcohol consumption on lungs using NIAAA alcohol feeding model in mice with 10 days of a Lieber-DeCarli liquid diet containing 5% ethanol followed by a single ethanol binge (5 g/kg) and population based human lung transcriptome data from Genotype-Tissue Expression (GTEx) project consist of 328 alcohol drinkers and 110 non-drinkers. Flow cytometry and transcriptomics analysis in mice lungs revealed that alcohol consumption dysregulates cellularity of immune cell levels and lung immunity. Transcriptomics analysis both in lungs and liver at 9-, 24- hours and 14 days post ethanol binge in mice uncovered that the lungs were more sensitive to alcohol effect to down-regulate pathways of immune system regulations than liver. Comparative data analysis of lung transcriptomes between mice and human subjects not only confirmed similar dysregulation on lung immunity but also provided evidence that immunometabolic changes are the central driver of alterations in lung transcriptome with down regulating immune pathways and upregulating metabolic pathways. Since the NIAAA model recapitulates multiple changes in the lung transcriptome that had been observed in human subjects with chronic alcohol drinking, this makes the mouse model suitable for experimental studies exploring role of alcohol drinking in lung health. Chronic alcohol drinking reduced mTOR signaling and cellularity of immune cells, which can be further attenuated by selective inhibition of mTOR. BCAA-mTOR signaling axis can be an upstream regulator of alcohol induced dysregulation in lung immunity
2024-07-22 | GSE248233 | GEO