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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Gene expression changes in liver tissues from alcohol treated mice

ABSTRACT: 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.

ORGANISM(S): Mus musculus

SUBMITTER: Henghong Li

PROVIDER: E-GEOD-44237 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression changes in liver tissues from alcohol treated mice

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.

2013-02-12 | GSE44237 | GEO

Gene expression changes in liver tissues from alcohol treated PPARa-null mice

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

Gene expression changes in liver tissues from alcohol treated PPARa-null mice

2014-01-14 | GSE54034 | GEO

Transcriptomic data from the liver of Ahr knockout mice

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

Liver-specific ceramide reduction alleviates steatosis and insulin resistance in alcohol-fed mice

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

Protective effect and mechanism of kinsenoside on alcoholic liver injury

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

Alcohol Consumption Effects During the Inflammatory Stage of Fracture Healing in Rat Bones

Project description:Sprague-Dawley rats were placed on an ethanol-containing or pair-fed Lieber and DeCarli diets for 4 wks prior to surgical fracture. Following insertion of a medullary pin, a closed mid-diaphyseal fracture was induced using a Bonnarens and Einhorn fracture device. At 3 days post-fracture, the region of the fracture calluses were harvested from the right hind-limb. RNA was extracted and microarray analysis was conducted against the entire rat genome to study the effects of alcohol-consumption on the fracture healing. The experiments were on four rat subjects, i.e., pair-fed rats with subsequent surgical fracture or no surgical fracture, and alcohol-fed rats with subsequent surgical fracture or no surgical fracture. Each rat subject described above has three replicates so 6 kinds of pairing can be made and each pairing has a dye-swap replicate (thus, a total 12 array experiments). The focus of this study is on the pair-fed fracture subject vs. alcohol-fed fracture subject.

2011-05-01 | E-GEOD-16003 | biostudies-arrayexpress

Retinoic Acid Receptor β Loss in Hepatocytes Increases Steatosis and Elevates the Integrated Stress Response in Alcohol-Associated Liver Disease

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

Transcriptome analysis of garlic induced hepatoprotection against alcoholic fatty liver

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

Alcohol Consumption Effects During the Inflammatory Stage of Fracture Healing in Rat Bones

2011-05-01 | GSE16003 | GEO

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