Evidence map›Paper›PMID 26610587›Full record

ArticleBiomolecules2015

In Vivo Acute on Chronic Ethanol Effects in Liver: A Mouse Model Exhibiting Exacerbated Injury, Altered Metabolic and Epigenetic Responses.

Shivendra D Shukla, Annayya R Aroor, Ricardo Restrepo, Kusum K Kharbanda, Jamal A Ibdah

Open access · goldAbstract read
In one paragraph

Article in Biomolecules, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.0field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 21 citations in OpenAlex.

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  13. Physiological processes underlying organ injury in alcohol abuse.American journal of physiology. Endocrinology and metabolism · 2016
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Shivendra D ShuklaDepartment of Medical Pharmacology and Physiology, School of Medicine, University of Missouri, Columbia, MI 65212, USA. shuklaSD@missouri.edu.
Annayya R AroorDepartment of Medical Pharmacology and Physiology, School of Medicine, University of Missouri, Columbia, MI 65212, USA. aroora@health.missouri.edu.
Ricardo RestrepoDepartment of Medical Pharmacology and Physiology, School of Medicine, University of Missouri, Columbia, MI 65212, USA. restreporj@health.missouri.edu.
Kusum K KharbandaVeterans Affairs Nebraska-Western Iowa Health Care System, Omaha, NE 68105, USA. Kusum.Kharbanda@va.gov.
Jamal A IbdahDepartment of Internal Medicine, School of Medicine, University of Missouri, Columbia, MI 65212, USA. ibdahj@health.missouri.edu.
University of Missouri · USVA Nebraska Western Iowa Health Care System · US

Funding

Effect of Alcohol on Hepatic Creatine Biosynthesis: Role of Defective MethylationI01BX001155 · VA · OMAHA VA MEDICAL CENTER · PI KHARBANDA, KUSUM K. · 2012 to 2015
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BLRD VA I01 BX001155
6 · The paper itself

Abstract

Chronic alcoholics who also binge drink (i.e., acute on chronic) are prone to an exacerbated liver injury but its mechanism is not understood. We therefore investigated the in vivo effects of chronic and binge ethanol ingestion and compared to chronic ethanol followed by three repeat binge ethanol on the liver of male C57/BL6 mice fed ethanol in liquid diet (4%) for four weeks followed by binge ethanol (intragastric administration, 3.5 g/kg body weight, three doses, 12h apart). Chronic followed by binge ethanol exacerbated fat accumulation, necrosis, decrease in hepatic SAM and SAM:SAH ratio, increase in adenosine levels, and elevated CYP2E1 levels. Histone H3 lysine acetylation (H3AcK9), dually modified phosphoacetylated histone H3 (H3AcK9/PS10), and phosphorylated H2AX increased after binge whereas phosphorylation of histone H3 ser 10 (H3S10) and H3 ser 28 (H3S28) increased after chronic ethanol-binge. Histone H3 lysine 4 and 9 dimethylation increased with a marked dimethylation in H3K9 in chronic ethanol binge group. Trimethylated histone H3 levels did not change. Nuclear levels of histone acetyl transferase GCN5 and histone deacetylase HDAC3 were elevated whereas phospho-CREB decreased in a distinctive manner. Taken together, acute on chronic ethanol ingestion caused amplification of liver injury and elicited characteristic profiles of histone modifications, metabolic alterations, and changes in nuclear protein levels. These findings demonstrate that chronic ethanol exposure renders liver more susceptible to repeat acute/binge ethanol induced acceleration of alcoholic liver disease.

Indexed as

Epigenesis, GeneticProtein Processing, Post-TranslationalAcetylationAnimalsBinge DrinkingCyclic AMP Response Element-Binding ProteinEthanolHistone Deacetylase 3Histone DeacetylasesHistonesLipid MetabolismLiverLiver Diseases, AlcoholicMaleMethylationMiceCyclic AMP Response Element-Binding ProteinEthanolHistone Deacetylase 3Histone DeacetylasesHistonesacute ethanolacute on chronic ethanolalcoholic liver diseasebinge alcoholchronic-binge alcoholepigeneticshistone modificationsmouse liver

Identifiers

PMID26610587
PMCPMC4693278
OpenAlexW2179235830

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.