Evidence map›Paper›PMID 27566282›Full record

ArticleRedox biology2016

The methyl donor S-adenosylmethionine prevents liver hypoxia and dysregulation of mitochondrial bioenergetic function in a rat model of alcohol-induced fatty liver disease.

Adrienne L King, Sudheer K Mantena, Kelly K Andringa, Telisha Millender-Swain, Kimberly J Dunham-Snary, Claudia R Oliva, Corinne E Griguer, Shannon M Bailey

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

21 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
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  4. Amino acid metabolism in health and disease.Signal transduction and targeted therapy · 2023
    Review
  5. Review
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  7. Liver PP2A-Cα Protects From Parenteral Nutrition-associated Hepatic Steatosis.Cellular and molecular gastroenterology and hepatology · 2022
    Article
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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

8 authors at 1 institution in 1 country.

Adrienne L KingDepartments of Environmental Health Sciences, University of Alabama at Birmingham, Birmingham, AL 35294, United States. Electronic address: aking125@kennesaw.edu.
Sudheer K MantenaDepartments of Environmental Health Sciences, University of Alabama at Birmingham, Birmingham, AL 35294, United States. Electronic address: sushdheer@yahoo.com.
Kelly K AndringaDepartments of Environmental Health Sciences, University of Alabama at Birmingham, Birmingham, AL 35294, United States. Electronic address: kellyandringa@uabmc.edu.
Telisha Millender-SwainDepartments of Environmental Health Sciences, University of Alabama at Birmingham, Birmingham, AL 35294, United States; Departments of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, United States. Electronic address: telishaswain@uabmc.edu.
Kimberly J Dunham-SnaryDepartments of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, United States. Electronic address: Kimberly.dunhamsnary@queensu.ca.
Claudia R OlivaDepartments of Neurosurgery, University of Alabama at Birmingham, Birmingham, AL 35294, United States. Electronic address: coliva@uabmc.edu.
Corinne E GriguerDepartments of Neurosurgery, University of Alabama at Birmingham, Birmingham, AL 35294, United States. Electronic address: cegriguer@uabmc.edu.
Shannon M BaileyDepartments of Environmental Health Sciences, University of Alabama at Birmingham, Birmingham, AL 35294, United States; Departments of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, United States. Electronic address: shannonbailey@uabmc.edu.
University of Alabama at Birmingham · US

Funding

University of Alabama at Birmingham's Diabetes Research CenterP30DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Kirk Michael Habegger · 2013 to 2026
$19.5M
Alcoholic Liver Dysfunction Potentiation by Hyperlipidemia and Cigarette SmokeR01AA018841 · NIAAA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BAILEY, SHANNON MARIE · 2009 to 2013
$1.5M
Cytochrome C Oxidase in Malignant GliomasR01CA160821 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GRIGUER, CORINNE E. · 2012 to 2016
$1.5M
Redox Modification of Thiols in Alcohol HepatotoxicityR01AA015172 · NIAAA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BAILEY, SHANNON MARIE · 2004 to 2008
$1.4M
NCI NIH HHS R01 CA160821NIAAA NIH HHS R01 AA015172NIAAA NIH HHS R01 AA018841NIDDK NIH HHS P30 DK079626
6 · The paper itself

Abstract

backgroundMitochondrial dysfunction and bioenergetic stress play an important role in the etiology of alcoholic liver disease. Previous studies from our laboratory show that the primary methyl donor S-Adenosylmethionine (SAM) minimizes alcohol-induced disruptions in several mitochondrial functions in the liver. Herein, we expand on these earlier observations to determine whether the beneficial actions of SAM against alcohol toxicity extend to changes in the responsiveness of mitochondrial respiration to inhibition by nitric oxide (NO), induction of the mitochondrial permeability transition (MPT) pore, and the hypoxic state of the liver.

methodsFor this, male Sprague-Dawley rats were pair-fed control and alcohol-containing liquid diets with and without SAM for 5 weeks and liver hypoxia, mitochondrial respiration, MPT pore induction, and NO-dependent control of respiration were examined.

resultsChronic alcohol feeding significantly enhanced liver hypoxia, whereas SAM supplementation attenuated hypoxia in livers of alcohol-fed rats. SAM supplementation prevented alcohol-mediated decreases in mitochondrial state 3 respiration and cytochrome c oxidase activity. Mitochondria isolated from livers of alcohol-fed rats were more sensitive to calcium-mediated MPT pore induction (i.e., mitochondrial swelling) than mitochondria from pair-fed controls, whereas SAM treatment normalized sensitivity for calcium-induced swelling in mitochondria from alcohol-fed rats. Liver mitochondria from alcohol-fed rats showed increased sensitivity to NO-dependent inhibition of respiration compared with pair-fed controls. In contrast, mitochondria isolated from the livers of SAM treated alcohol-fed rats showed no change in the sensitivity to NO-mediated inhibition of respiration.

conclusionCollectively, these findings indicate that the hepato-protective effects of SAM against alcohol toxicity are mediated, in part, through a mitochondrial mechanism involving preservation of key mitochondrial bioenergetic parameters and the attenuation of hypoxic stress.

Indexed as

Organelle BiogenesisAnimalsBiomarkersCell RespirationDisease Models, AnimalElectron Transport Complex IElectron Transport Complex IVEthanolFatty Liver, AlcoholicHypoxiaLiverMitochondria, LiverMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreNitric OxideRatsBiomarkersElectron Transport Complex IElectron Transport Complex IVEthanolMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreNitric OxideReactive Oxygen SpeciesS-AdenosylmethionineAlcoholHypoxiaLiverMitochondriaNitric oxideS-Adenosylmethionine

Identifiers

PMID27566282
PMCPMC5007436
OpenAlexW2515115215

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.