Evidence map›Paper›PMID 23951308›Full record

ArticlePloS one2013

The g0/g1 switch gene 2 is an important regulator of hepatic triglyceride metabolism.

Yinfang Wang, Yahui Zhang, Hang Qian, Juan Lu, Zhifeng Zhang, Xinwen Min, Mingjian Lang, Handong Yang, Nanping Wang, Peng Zhang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

38 citing papers in PubMed, 55 citations in OpenAlex.

  1. Trial
  2. Review
  3. Recent advances on the role of G0S2.Discover oncology · 2025
    Review
  4. Article
  5. Article
  6. Article
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  12. Review
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  16. Genetically modified mouse models to study hepatic neutral lipid mobilization.Biochimica et biophysica acta. Molecular basis of disease · 2019
    Review
  17. Article
  18. Hepatocyte-specific Sirt6 deficiency impairs ketogenesis.The Journal of biological chemistry · 2019
    Article
  19. Article
  20. 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

10 authors at 2 institutions in 1 country.

Yinfang WangCardiovascular Research Center, Hubei University of Medicine, Hubei, China.
Yahui Zhang
Hang Qian
Juan Lu
Zhifeng Zhang
Xinwen Min
Mingjian Lang
Handong Yang
Nanping Wang
Peng Zhang
Hubei University of Medicine · CNXi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nonalcoholic fatty liver disease is associated with obesity and insulin resistance. Factors that regulate the disposal of hepatic triglycerides contribute to the development of hepatic steatosis. G0/G1 switch gene 2 (G0S2) is a target of peroxisome proliferator-activated receptors and plays an important role in regulating lipolysis in adipocytes. Therefore, we investigated whether G0S2 plays a role in hepatic lipid metabolism. Adenovirus-mediated expression of G0S2 (Ad-G0S2) potently induced fatty liver in mice. The liver mass of Ad-G0S2-infected mice was markedly increased with excess triglyceride content compared to the control mice. G0S2 did not change cellular cholesterol levels in hepatocytes. G0S2 was found to be co-localized with adipose triglyceride lipase at the surface of lipid droplets. Hepatic G0S2 overexpression resulted in an increase in plasma Low-density lipoprotein (LDL)/Very-Low-density (VLDL) lipoprotein cholesterol level. Plasma High-density lipoprotein (HDL) cholesterol and ketone body levels were slightly decreased in Ad-G0S2 injected mice. G0S2 also increased the accumulation of neutral lipids in cultured HepG2 and L02 cells. However, G0S2 overexpression in the liver significantly improved glucose tolerance in mice. Livers expressing G0S2 exhibited increased 6-(N-(7-nitrobenz-2-oxa-1-3-diazol-4-yl) amino)-6-deoxyglucose uptake compared with livers transfected with control adenovirus. Taken together, our results provide evidence supporting an important role for G0S2 as a regulator of triglyceride content in the liver and suggest that G0S2 may be a molecular target for the treatment of insulin resistance and other obesity-related metabolic disorders.

Indexed as

AnimalsCell Cycle ProteinsCell LineCholesterol, HDLCholesterol, LDLCholesterol, VLDLFatty LiverGene ExpressionGlucoseHepatocytesHumansKetone BodiesLipid MetabolismLiverMaleMiceCell Cycle ProteinsCholesterol, HDLCholesterol, LDLCholesterol, VLDLG0S2 protein, humanGlucoseKetone BodiesPeroxisome Proliferator-Activated ReceptorsRNA, MessengerTriglycerides

Identifiers

PMID23951308
PMCPMC3741160
OpenAlexW1984989897

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.