Evidence map›Paper›PMID 26501337›Full record

ArticleBiomolecules2015

Modulation of Intestinal Barrier and Bacterial Endotoxin Production Contributes to the Beneficial Effect of Nicotinic Acid on Alcohol-Induced Endotoxemia and Hepatic Inflammation in Rats.

Wei Zhong, Qiong Li, Wenliang Zhang, Qian Sun, Xinguo Sun, Zhanxiang Zhou

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 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 30 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Wei ZhongCenter for Translational Biomedical Research, University of North Carolina at Greensboro, North Carolina Research Campus, Kannapolis, NC 28081, USA. w_zhong@uncg.edu.
Qiong LiCenter for Translational Biomedical Research, University of North Carolina at Greensboro, North Carolina Research Campus, Kannapolis, NC 28081, USA. liqiongbmu@gmail.com.
Wenliang ZhangCenter for Translational Biomedical Research, University of North Carolina at Greensboro, North Carolina Research Campus, Kannapolis, NC 28081, USA. w_zhang2@uncg.edu.
Qian SunCenter for Translational Biomedical Research, University of North Carolina at Greensboro, North Carolina Research Campus, Kannapolis, NC 28081, USA. q_sun@uncg.edu.
Xinguo SunCenter for Translational Biomedical Research, University of North Carolina at Greensboro, North Carolina Research Campus, Kannapolis, NC 28081, USA. x_sun4@uncg.edu.
Zhanxiang ZhouCenter for Translational Biomedical Research, University of North Carolina at Greensboro, North Carolina Research Campus, Kannapolis, NC 28081, USA. z_zhou@uncg.edu.
University of North Carolina at Greensboro · US

Funding

Aldehydes in Alcohol-Induced Organ InjuryR01AA020212 · NIAAA · UNIVERSITY OF NORTH CAROLINA GREENSBORO · PI ZHANXIANG ZHOU · 2010 to 2026
$6.4M
Lipotoxicity in Alcoholic Liver DiseaseR01AA018844 · NIAAA · UNIVERSITY OF NORTH CAROLINA GREENSBORO · PI ZHANXIANG ZHOU · 2009 to 2026
$6.0M
Zinc and Alcohol-Induced Oxidative Liver InjuryR01AA014623 · NIAAA · UNIVERSITY OF LOUISVILLE · PI ZHOU, ZHANXIANG · 2005 to 2009
$1.4M
Zinc inhibition of endotoxemia in alcoholic liver injuryR01AA016013 · NIAAA · UNIVERSITY OF NORTH CAROLINA GREENSBORO · PI ZHOU, ZHANXIANG · 2009 to 2010
$739k
NIAAA NIH HHS 2R01AA018844NIAAA NIH HHS R01 AA014623NIAAA NIH HHS R01 AA016013NIAAA NIH HHS R01 AA018844NIAAA NIH HHS R01 AA020212NIAAA NIH HHS R01AA020212
6 · The paper itself

Abstract

Alcohol consumption causes nicotinic acid deficiency. The present study was undertaken to determine whether dietary nicotinic acid supplementation provides beneficial effects on alcohol-induced endotoxin signaling and the possible mechanisms at the gut-liver axis. Male Sprague-Dawley rats were pair-fed the Lieber-DeCarli liquid diets containing ethanol or isocaloric maltose dextrin for eight weeks, with or without dietary supplementation with 750 mg/liter nicotinic acid. Chronic alcohol feeding elevated the plasma endotoxin level and activated hepatic endotoxin signaling cascade, which were attenuated by nicotinic acid supplementation. Alcohol consumption remarkably decreased the mRNA levels of claudin-1, claudin-5, and ZO-1 in the distal intestine, whereas nicotinic acid significantly up-regulated these genes. The concentrations of endotoxin, ethanol, and acetaldehyde in the intestinal contents were increased by alcohol exposure, and niacin supplementation reduced the intestinal endotoxin and acetaldehyde levels. Nicotinic acid supplementation upregulated the intestinal genes involved in aldehyde detoxification via transcriptional regulation. These results demonstrate that modulation of the intestinal barrier function and bacterial endotoxin production accounts for the inhibitory effects of nicotinic acid on alcohol-induced endotoxemia and hepatic inflammation.

Indexed as

AnimalsEndotoxemiaEthanolIntestinal MucosaIntestinesLiver Diseases, AlcoholicMaleNiacinRatsRats, Sprague-DawleyEthanolNiacinalcoholendotoxemiagut permeabilityinflammationnicotinic acid

Identifiers

PMID26501337
PMCPMC4693251
OpenAlexW2160259090

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.