Evidence map›Paper›PMID 24113770›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2013

Increased plasma corticosterone contributes to the development of alcoholic fatty liver in mice.

Xiuhua Sun, Weijun Luo, Xiaobing Tan, Qiong Li, Yantao Zhao, Wei Zhong, Xinguo Sun, Cory Brouwer, Zhanxiang Zhou

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

17 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
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  4. The Role of NOxidative medicine and cellular longevity · 2022
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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

9 authors at 4 institutions in 2 countries.

Xiuhua SunCtr. for Translational & Biomedical Research, The Univ. of North Carolina at Greensboro, North Carolina Research Campus, Kannapolis, NC 28081. z_zhou@uncg.edu.
Weijun Luo
Xiaobing Tan
Qiong Li
Yantao Zhao
Wei Zhong
Xinguo Sun
Cory Brouwer
Zhanxiang Zhou
Center for Translational Molecular Medicine · NLUniversity of North Carolina at Charlotte · USNorth Carolina Agricultural and Technical State University · USUniversity 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 R01 AA014623NIAAA NIH HHS R01 AA016013NIAAA NIH HHS R01AA018844NIAAA NIH HHS R01AA020212
6 · The paper itself

Abstract

Ethanol ingestion increases endogenous glucocorticoid levels in both humans and rodents. The present study aimed to define a mechanistic link between the increased glucocorticoids and alcoholic fatty liver in mice. Plasma corticosterone levels were not affected in mice on a 2-wk ethanol diet regimen but significantly increased upon 4 wk of ethanol ingestion. Accordingly, hepatic triglyceride levels were not altered after 2 wk of ethanol ingestion but were elevated at 4 wk. Based on the observation that 2 wk of ethanol ingestion did not significantly increase endogenous corticosterone levels, we administered exogenous glucocorticoids along with the 2-wk ethanol treatment to determine whether the elevated glucocorticoid contributes to the development of alcoholic fatty liver. Mice were subjected to ethanol feeding for 2 wk with or without dexamethasone administration. Hepatic triglyceride contents were not affected by either ethanol or dexamethasone alone but were significantly increased by administration of both. Microarray and protein level analyses revealed two distinct changes in hepatic lipid metabolism in mice administered with both ethanol and dexamethasone: accelerated triglyceride synthesis by diacylglycerol O-acyltransferase 2 and suppressed fatty acid β-oxidation by long-chain acyl-CoA synthetase 1, carnitine palmitoyltransferase 1a, and acyl-CoA oxidase 1. A reduction of hepatic peroxisome proliferation activator receptor-α (PPAR-α) was associated with coadministration of ethanol and dexamethasone. These findings suggest that increased glucocorticoid levels may contribute to the development of alcoholic fatty liver, at least partially, through hepatic PPAR-α inactivation.

Indexed as

AnimalsCarnitine O-PalmitoyltransferaseCorticosteroneDexamethasoneDiacylglycerol O-AcyltransferaseEthanolFatty Liver, AlcoholicLipid MetabolismMiceMice, Inbred C57BLPPAR alphaTranscription, GeneticCarnitine O-PalmitoyltransferaseCorticosteroneDexamethasoneDGAT2 protein, mouseDiacylglycerol O-AcyltransferaseEthanolPPAR alphaalcoholic fatty liverglucocorticoidslipid metabolism

Identifiers

PMID24113770
PMCPMC3882437
OpenAlexW2116050617

What OpenQuestion holds

Textmetadata
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.