Evidence map›Paper›PMID 29323242›Full record

ArticleScientific reports2018

Adipose-specific lipin1 overexpression in mice protects against alcohol-induced liver injury.

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

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. 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
1.6field-weighted citation impact, top 19% 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, 25 citations in OpenAlex.

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  15. Sex differences in mitochondrial respiratory function in human skeletal muscle.American journal of physiology. Regulatory, integrative and comparative physiology · 2018
    Article
  16. Lipin deactivation after acetaminophen overdose causes phosphatidic acid accumulation in liver and plasma in mice and humans and enhances liver regeneration.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2018
    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

5 authors at 1 institution in 1 country.

Wenliang ZhangCenter for Translational Biomedical Research, University of North Carolina at Greensboro, North Carolina Research Campus, Kannapolis, NC, 28081, USA.
Wei ZhongCenter for Translational Biomedical Research, University of North Carolina at Greensboro, North Carolina Research Campus, Kannapolis, NC, 28081, USA.
Qian SunCenter for Translational Biomedical Research, University of North Carolina at Greensboro, North Carolina Research Campus, Kannapolis, NC, 28081, USA.
Xinguo SunCenter for Translational Biomedical Research, University of North Carolina at Greensboro, North Carolina Research Campus, Kannapolis, NC, 28081, USA.
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

UNIV OF NORTH CAROLINA CLINICAL NUTRITION RESEARCH UNITP30DK056350 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SUSAN M. SMITH · 1999 to 2026
$31.6M
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
NIAAA NIH HHS R01 AA018844NIAAA NIH HHS R01 AA020212NIDDK NIH HHS P30 DK056350
6 · The paper itself

Abstract

Excessive fatty acid release from the white adipose tissue (WAT) contributes to the development of alcoholic liver disease (ALD). Lipin1 (LPIN1), as a co-regulator of DNA-bound transcription factors and a phosphatidic acid (PA) phosphatase (PAP) enzyme that dephosphorylates PA to form diacylglycerol (DAG), is dramatically reduced by alcohol in the WAT. This study aimed at determining the role of adipose LPIN1 in alcohol-induced lipodystrophy and the development of ALD. Transgenic mice overexpressing LPIN1 in adipose tissue (LPIN1-Tg) and wild type (WT) mice were fed a Lieber-DeCarli alcohol or isocaloric maltose dextrin control liquid diet for 8 weeks. Alcohol feeding to WT mice resulted in significant liver damage, which was significantly alleviated in the LPIN1-Tg mice. Alcohol feeding significantly reduced epididymal WAT (EWAT) mass, inhibited lipogenesis, and increased lipolysis in WT mice, which were attenuated in the LPIN1-Tg mice. LPIN1 overexpression also partially reversed alcohol-reduced plasma leptin levels. In WT mice, alcohol feeding induced hepatic lipid accumulation and down-regulation of beta-oxidation genes, which were dramatically alleviated in the LPIN1-Tg mice. LPIN1 overexpression also significantly attenuated alcohol-induced hepatic ER stress. These results suggest that overexpression of LPIN1 in adipose tissue restores WAT lipid storage function and secretive function to alleviate alcohol-induced liver injury.

Indexed as

Adipose Tissue, WhiteAnimalsCell LineDisease Models, AnimalEndoplasmic Reticulum StressFatty Liver, AlcoholicLeptinLipodystrophyLipogenesisLipolysisMaleMiceMice, TransgenicNuclear ProteinsPhosphatidate PhosphatasePhosphatidic AcidsLeptinLpin1 protein, mouseNuclear ProteinsPhosphatidate PhosphatasePhosphatidic Acids

Identifiers

PMID29323242
PMCPMC5765113
OpenAlexW2781692652

What OpenQuestion holds

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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.