Evidence map›Paper›PMID 29713145›Full record

ArticleDrug design, development and therapy2018

Inhibition of ghrelin

Shaoren Zhang, Yuqing Mao, Xiaoming Fan

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.6field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Ghrelin regulating liver activity and its potential effects on liver fibrosis andFrontiers in cellular and infection microbiology · 2023
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. mTOR: A Potential New Target in Nonalcoholic Fatty Liver Disease.International journal of molecular sciences · 2022
    Review
  13. [Dihydromyricetin reduces lipid accumulation in LO2 cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022
    Article
  14. Review
  15. Article
  16. Ghrelin Based Therapy of Metabolic Diseases.Current medicinal chemistry · 2021
    Review
  17. Recent progress in the discovery of ghrelinRSC medicinal chemistry · 2020
    Review
  18. Ghrelin and liver disease.Reviews in endocrine & metabolic disorders · 2020
    Review
  19. Ghrelin Signaling: GOAT and GHS-R1a Take a LEAP in Complexity.Trends in endocrinology and metabolism: TEM · 2020
    Review
  20. Frontiers in pharmacology · 2020
    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

3 authors at 1 institution in 1 country.

Shaoren ZhangDepartment of Gastroenterology and Hepatology, Jinshan Hospital of Fudan University, Shanghai, China.
Yuqing MaoDepartment of Gastroenterology and Hepatology, Jinshan Hospital of Fudan University, Shanghai, China.
Xiaoming FanDepartment of Gastroenterology and Hepatology, Jinshan Hospital of Fudan University, Shanghai, China.
Jinshan Hospital of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNonalcoholic fatty liver disease (NAFLD) has been considered the most commonly occurring chronic hepatopathy in the world. Ghrelin MATERIALS AND

methodsHuman LO2 cells were pretreated with siRNA-GOAT to induce liver steatosis using free fatty acids (FFAs). A chronic NAFLD model was established by feeding male mice C57bl/6 with high-fat diet (HFD) for 56 days with GO-CoA-Tat administrated subcutaneously. Lipid droplets were identified by Oil Red O stains. Body weight (BW) of mice was measured every week. Autophagy, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), serum biochemical indicators (glucose [Glu], total cholesterol [TC], triglyceride [TG], aspartate aminotransferase [AST], alanine aminotransferase [ALT]) and signaling pathway proteins of phosphorylated AMPK-mTOR were measured.

resultsThe TG contents of the FFA and HFD groups were decreased by the inhibition of GOAT. Among mice treated with GO-CoA-Tat and siRNA-GOAT, IL-6 and TNF-α concentrations were remarkably decreased. Indicators of liver injury such as ALT and AST were also remarkably decreased among mice treated with GO-CoA-Tat. Likewise, GO-CoA-Tat significantly reduced the BW of mice and serum TG, TC and Glu. Autophagy was induced along with reduced lipids in the cells of the FFA and HFD groups. The inhibition of GOAT upregulated autophagy via AMPK-mTOR restoration.

conclusionThese results indicate that the inhibition of GOAT attenuates lipotoxicity by autophagy stimulation via AMPK-mTOR restoration and offers innovative evidence for using GO-CoA-Tat or siRNA-GOAT in NAFLD clinically.

Indexed as

AcyltransferasesAMP-Activated Protein KinasesAnimalsAutophagyCells, CulturedHepatocytesHumansLipidsMaleMembrane ProteinsMiceMice, Inbred C57BLRNA, MessengerSignal TransductionTOR Serine-Threonine KinasesAcyltransferasesAMP-Activated Protein KinasesLipidsMBOAT4 protein, humanMboat4 protein, mouseMembrane ProteinsMTOR protein, humanmTOR protein, mouseRNA, MessengerTOR Serine-Threonine KinasesFFAfree fatty acidghrelin o-acyltransferaseGOATHFDhigh-fat dietNAFLDnonalcoholic fatty liver disease

Identifiers

PMID29713145
PMCPMC5912383
OpenAlexW2801670879

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.