Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Ethanol and its nonoxidative metabolites promote acute liver injury by inducing ER stress, adipocyte death and lipolysis

ABSTRACT: We gave mice either a 5g/kg ethanol (EtOH) gavage, a 7g/kg EtOH gavage, or an isocaloric maltose gavage (equivalent to 5g/kg EtOH) in the morning and sacrificed mice 9h later. Microarray analyses were performed on liver tissue from these mice to determine genes and pathways contributing to acute ethanol-induced liver injury. Lipid metabolism-associated genes were found to be dysregulated in both the 5g/kg and 7g/kg groups, with the majority of changes occuring in the 7g/kg group. Genes related to fatty acid metabolism were most changed in the 7g/kg group compared to control and 5g/kg groups.

ORGANISM(S): Mus musculus

PROVIDER: GSE214778 | GEO | 2022/10/07

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Ethanol induced hepatic gene expression changes during gestation

2006-12-03 | GSE3740 | GEO

Transcription profiling of rat liver to investigate ethanol induced hepatic gene expression changes during gestation

Project description:The specific role of nutritional status during gestation in exacerbating or mitigating fetal toxicity of ethanol (EtOH) remains unclear. We used an intragastric infusion model (Total enteral nutrition, TEN) to appropriately control for dietary EtOH consumption and caloric intake. Time impregnated female Sprague Dawley rats (250-300 g) were surgically cannulated with intragastric cannulae (on gestation day 4) and infused either control or EtOH-containing diets. Rats were fed 220 kcal/ kg3/4/d (NRC recommended caloric intake for gestation) or 160 kcal/ kg3/4/d (undernourished to 72% of control) diets containing either 12 g/kg/d EtOH or an isocaloric amount of carbohydrates from gestation days 6-15. Maternal hepatic gene expression profiles were assessed on GD15. The present data dissect specific effects of nutritional status during gestation and EtOH intake and the interaction thereof. The data reveal a highly significant interaction between undernutrition and EtOH consumption. Experiment Overall Design: Four groups of time impregnated female Sprague Dawley rats were utilized. Experiment Overall Design: Group 1: Control, TEN-220, control group fed normal (non-EtOH containing) diets at 220 kcal/ kg3/4/d. Experiment Overall Design: Group 2: Ethanol-220, EtOH-220 (EtOH group fed EtOH containing diets) at 12 g EtOH/kg/d diets at 220 kcal/ kg3/4/d. Experiment Overall Design: Group 3: Control-160, TEN-160, (undernourished control group fed normal (non-EtOH containing) diets at 160 kcal/ kg3/4/d. Experiment Overall Design: Group 4: Ethanol-160, EtOH-160, (undernourished rats fed EtOH containing diets) at 12 g EtOH/kg/d diets at 160 kcal/ kg3/4/d

2008-06-12 | E-GEOD-3740 | biostudies-arrayexpress

Molecular consequences of fetal alcohol exposure on amniotic exosomal miRNAs with functional implications for stem cell potency and differentiation

Project description:Alcohol (ethanol, EtOH) consumption during pregnancy can result in fetal alcohol spectrum disorders (FASDs), which are characterized by prenatal and postnatal growth restriction and craniofacial dysmorphology. The specific mechanisms by which alcohol mediates these injuries have yet to be determined. Cell-derived extracellular vesicles, including exosomes and microvesicles containing several species of RNAs (exRNAs), have recently emerged as a mechanism of cell-to-cell communication. However, EtOH’s effects on the biogenesis and function of non-coding exRNAs during fetal development have not been explored. Therefore, we studied the effects of maternal EtOH exposure on the composition of exRNAs in the amniotic fluid (AF) using a rat fetal alcohol exposure (FAE) model. Timed pregnant Sprague Dawley rats received 0 or 2.5 g/kg of 20% EtOH by oral gavage on embryonic days 5, 8, 10, 12 and 15. Through RNA-Seq analysis we identified and verified AF exosomal miRNAs with differential expression levels specifically associated with maternal EtOH exposure.

2019-06-11 | GSE132437 | GEO

Alcohol potentiates the psychostimulant and reinforcing effects of mephedrone in adolescent mice: role of D3 receptors and associated changes in gene expression

Project description:Mephedrone (Meph) is a novel psychostimulant whose recreational consumption is often associated to other drugs, especially alcohol (EtOH). This kind of drug consumption during adolescence is a matter of concern. We studied, in adolescent CD-1 mice, whether low-moderate doses of EtOH could enhance the psychostimulant (locomotor acivity) and reinforcing (conditioned place preference, CPP) effects of mephedrone. Simultaneously we also determined the most relevant transcriptional changes associated to a reinforcing treatment. A single dose of Meph (10 mg/kg, sc) induced an increase of about 100% in locomotor activity, which was a further enhanced by 40% when associated with a dose of EtOH (1 g/kg). The hyperlocomotion was partially antagonized by ketanserin and haloperidol, but only haloperidol blocked the potentiation induced by EtOH. Furthermore, Meph (25 mg/kg) induced significant positive conditioning, which increased by 70% when administered with 0.75 mg/kg EtOH. Microarray analysis of mRNA extracted from anterior striata of the mice used in CPP experiments reported significant modifications in genes related with neurotransmission and synaptic plasticity, which were further validated by Real-time PCR for all three drug-treated groups. Four groups were compared in the study: adolescent Swiss CD-1 mice treated with saline, ethanol, mephedrone or mephedrone + ethanol during the conditioned place preference (CPP) ten-day procedure, aimed at evaluating reward. Twelve samples are provided, which correspond to triplicates of each treatment group. The samples provided were subsequently normalized and analyzed using the GeneSpring GX 7.3.1 software.

2016-08-01 | E-GEOD-58279 | biostudies-arrayexpress

Binge Alcohol Disrupts Skeletal Muscle Core Molecular Clock Independent of Glucocorticoids

Project description:Circadian rhythms are central to optimal physiological functioning and their interruption contributes to the development of several chronic diseases. Alcohol (EtOH) intoxication disrupts circadian rhythms within liver, brain, and intestines, but it is unknown whether alcohol also disrupts components of the core clock in skeletal muscle. Female C57BL/6Hsd mice were randomized to receive either saline (control) or alcohol (EtOH) (5g/kg) via intraperitoneal injection at the start of the dark cycle (ZT12), and gastrocnemius was collected every 4hr from Control and EtOH treated mice for the next 48hr following isoflurane anesthetization. In addition, metyrapone was administered prior to alcohol intoxication in separate mice to determine whether the alcohol-induced increase in serum corticosterone contributed to circadian gene regulation. Finally, synchronized C2C12 myotubes were treated with alcohol (100mM) to assess the influence of centrally or peripherally mediated effects of alcohol on the muscle clock. Alcohol significantly disrupted the mRNA expression of Bmal1, Per1/2, and Cry1/2 in addition to perturbing the clock-controlled genes, Myod1, Dbp, Tef, and Bhlhe40 (p<0.05). Alcohol increased serum corticosterone levels and glucocorticoid target genes, Redd1 and Klf15, in muscle. Metyrapone decreased serum corticosterone in EtOH mice but did not normalize the mRNA expression of Per1, Cry1 and Cry2 and Myod1 which were altered by EtOH. Alcohol did not alter core clock gene expression (Bmal, Per1/2, Cry1/2) at 4, 8, and 12hrs post treatment in synchronized C2C12 myotubes. Therefore, binge alcohol disrupted genes of the core molecular clock independently of elevated serum corticosterone.

2021-09-10 | GSE183665 | GEO

Wistar rat, lung, NanoLC-MS/MS

Project description:Wistar rats, male, treated with 500 mg/Kg/day of diacetyl by gavage, during 4 weeks

2018-04-18 | PXD004504 | Pride

Genomic Microarray of Rat Alveolar Type 2 cells Following Chronic Ethanol Ingestion

Project description:Chronic alcohol ingestion changes the alveolar landscape. We used microarrays to characterize the change in mRNA expression following chronic alcohol ingestion in male Sprague Dawley rates (EtOH 36% of calories) We used microarrays to characterize the change in mRNA expression following chronic alcohol ingestion in male Sprague Dawley rats (EtOH 36% of calories for 6 weeks). Control animals were given an isocaloric substitution for EtOH for 6 weeks. Alveolar type 2 cells were isolated using an immuno-absorption /technique and RNA was extracted by Trizol. Four control animals and three EtOH treated animals were used for this study.

2014-07-02 | E-GEOD-55243 | biostudies-arrayexpress

Alcohol potentiates the psychostimulant and reinforcing effects of mephedrone in adolescent mice: role of D3 receptors and associated changes in gene expression

2016-08-01 | GSE58279 | GEO

Pregnane X receptor promotes ehtanol-induced hepatosteatosis in female mice

Project description:The pregane X receptor (PXR), a xenobiotioc-sensing nuclear receptor has been implicated in alcohol-associated liver disease (ALD). The role of PXR signaling in potentiating ethanol (EtOH)-induced hepatotoxicty in male wild-type (WT) mice was reported previously, however, how PXR signaling modulated EtOH-induced hepatotoxicty in female is still unknown. Several mRNAs that are involved in retinol and steroid hormone biosynthesis, chemical carcinogeneiss, and arachidonic acid metabolism were increased by EtOH in a PXR-dependent manner. Overall, female PXR-null mice are resistant against chronic EtOH-induced hepatotoxicity than their WT counterparts.

2023-08-09 | GSE239714 | GEO

Uropathogenic E. coli UTI89 cells in the presence of dimethyl sulfoxide or ethanol

Project description:The expression levels of uropathogenic E. coli (UPEC) UTI89 cells in YESCA broth with and without 4% dimehtyl sulfoxide (DMSO) and 2% ethanol (EtOH) were studied.

2012-02-15 | GSE35797 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data