Evidence map›Paper›PMID 25758202›Full record

ReviewExperimental and molecular pathology2015

How to prevent alcoholic liver disease.

S W French

Open access · greenAbstract readReview
In one paragraph

Review in Experimental and molecular pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

7 citing papers in PubMed, 16 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
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

1 author at 1 institution in 1 country.

S W FrenchHarbor-UCLA Medical Center, Torrance, CA 90509, United States. Electronic address: french7@ucla.edu.
UCLA Medical Center · US

Funding

ALCOHOLIC HEPATITIS PATHOGENESIS AS DETERMINED FROM HUMAN LIVER TISSUE ANALYSISU01AA021898 · NIAAA · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI FRENCH, SAMUEL WILLIAM · 2013 to 2017
$1.0M
NIAAA NIH HHS U01 AA021898PHS HHS UOS021898-02
6 · The paper itself

Abstract

Betaine supplements of alcoholic beverages are proposed to prevent the development of alcoholic liver disease in patients that abuse alcohol. This recommendation is based on the observation of studies where it has been shown in binge drinking and chronic ethanol feeding animal models that betaine prevents liver injury resulting from high blood alcohol levels. The basic observation is that betaine added to ethanol being ingested increases the elimination rate of blood alcohol, which prevents the blood alcohol levels (BALs) from reaching high levels. The mechanism of how betaine does this is postulated to be that betaine causes the increase in the elimination rate by increasing the metabolic rate which generates NAD the rate limiting cofactor of alcohol oxidation by ADH. Betaine does this most likely by supporting the methylation of norepinephrine to form epinephrine by phenylethanolamine N-methyltransferase. Epinephrine is 5 to 10-fold more active than norepinephrine in increasing the metabolic rate.

Indexed as

AlcoholismAnimalsBetaineEnergy MetabolismEpinephrineEthanolHumansLiverLiver Diseases, AlcoholicMethylationModels, AnimalNorepinephrineOxidation-ReductionPhenylethanolamine N-MethyltransferaseRatsBetaineEpinephrineEthanolNorepinephrinePhenylethanolamine N-MethyltransferaseBetaineBlood alcoholBlood alcohol elimination rateEpinephrineGenerates NAD(+)Metabolic rate

Identifiers

PMID25758202
PMCPMC4388812
OpenAlexW1980461163

What OpenQuestion holds

Textmetadata
LicenceTDM
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.