Evidence map›Paper›PMID 26152281›Full record

ArticleBMC gastroenterology2015

IGF-1 decreases portal vein endotoxin via regulating intestinal tight junctions and plays a role in attenuating portal hypertension of cirrhotic rats.

Tian-Yu Zhao, Li-Ping Su, Chun-Ye Ma, Xiao-Han Zhai, Zhi-Jun Duan, Ying Zhu, Gang Zhao, Chun-Yan Li, Li-Xia Wang, Dong Yang

Open access · goldAbstract read
In one paragraph

Article in BMC gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 2 pooled it
1.3field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Effects ofWorld journal of gastroenterology · 2019
    Article
  15. Article
  16. Advances in therapeutic options for portal hypertension.Therapeutic advances in gastroenterology · 2018
    Review
  17. Article
  18. 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 3 institutions in 1 country.

Tian-Yu ZhaoDepartment of Gastroenterology, The First Affiliated Hospital of Dalian Medical University, 116000, Dalian, Liaoning province, China. wwwdxycnbbs@163.com.
Li-Ping SuDepartment of Gastroenterology, The First Affiliated Hospital of Dalian Medical University, 116000, Dalian, Liaoning province, China. 1304133485@qq.com.
Chun-Ye MaDepartment of Neurology, The Second Affiliated Hospital of Dalian Medical University, 116023, Dalian, Liaoning province, China. machuye2008@163.com.
Xiao-Han ZhaiDepartment of Clinical Pharmacology, The First Affiliated Hospital of Dalian Medical University, 116000, Dalian, Liaoning province, China. hanhanjiayoudl@163.com.
Zhi-Jun DuanDepartment of Gastroenterology, The First Affiliated Hospital of Dalian Medical University, 116000, Dalian, Liaoning province, China. cathydoctor@sina.com.
Ying ZhuDepartment of Infectious Diseases, The First Affiliated Hospital of Dalian Medical University, 116000, Dalian, Liaoning province, China. zhuyingsh52@126.com.
Gang ZhaoDepartment of Gastroenterology, The First Affiliated Hospital of Dalian Medical University, 116000, Dalian, Liaoning province, China. zhaogang_59@263.net.
Chun-Yan LiDepartment of Gastroenterology, The First Affiliated Hospital of Dalian Medical University, 116000, Dalian, Liaoning province, China. Chunyanlidl@163.com.
Li-Xia WangDepartment of Gastroenterology, The First Affiliated Hospital of Dalian Medical University, 116000, Dalian, Liaoning province, China. wenwensl@yeah.net.
Dong YangDepartment of Gastroenterology, The First Affiliated Hospital of Dalian Medical University, 116000, Dalian, Liaoning province, China. yd613@163.com.
Dalian Medical University · CNFirst Affiliated Hospital of Dalian Medical University · CNSecond Affiliated Hospital of Dalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIntestinal barrier dysfunction is not only the consequence of liver cirrhosis, but also an active participant in the development of liver cirrhosis. Previous studies showed that external administration of insulin-like growth factor 1 (IGF-1) improved intestinal barrier function in liver cirrhosis. However, the mechanism of IGF-1 on intestinal barrier in liver cirrhosis is not fully elucidated. The present study aims to investigate the mechanisms of IGF-1 improving intestinal barrier function via regulating tight junctions in intestines.

methodsWe used carbon tetrachloride induced liver cirrhotic rats to investigate the effect of IGF-1 on intestinal claudin-1 and occludin expressions, serum alanine transaminase (ALT) and aspartate transaminase (AST) levels, severity of liver fibrosis, portal pressures, enterocytic apoptosis and lipopolysaccharides (LPS) levels in portal vein. The changes of IGF-1 in serum during the development of rat liver cirrhosis were also evaluated. Additionally, we assessed the effect of IGF-1 on claudin-1 and occludin expressions, changes of transepithelial electrical resistance (TEER) and apoptosis in Caco-2 cells to confirm in vivo findings.

resultsSerum IGF-1 levels were decreased in the development of rat liver cirrhosis, and external administration of IGF-1 restored serum IGF-1 levels. External administration of IGF-1 reduced serum ALT and AST levels, severity of liver fibrosis, LPS levels in portal vein, enterocytic apoptosis and portal pressure in cirrhotic rats. External administration of IGF-1 increased the expressions of claudin-1 and occludin in enterocytes, and attenuated tight junction dysfunction in intestines of cirrhotic rats. LPS decreased TEER in Caco-2 cell monolayer. LPS also decreased claudin-1 and occludin expressions and increased apoptosis in Caco-2 cells. Furthermore, IGF-1 attenuated the effect of LPS on TEER, claudin-1 expression, occludin expression and apoptosis in Caco-2 cells.

conclusionsTight junction dysfunction develops during the development of liver cirrhosis, and endotoxemia will develop subsequently. Correspondingly, increased endotoxin in portal system worsens tight junction dysfunction via decreasing intestinal occludin and claudin-1 expressions and increasing enterocytic apoptosis. Endotoxemia and intestinal barrier dysfunction form a vicious circle. External administration of IGF-1 breaks this vicious circle. Improvement of tight junctions might be one possible mechanism of the restoration of intestinal barrier function mediated by IGF-1.

Indexed as

AnimalsApoptosisCaco-2 CellsCarbon TetrachlorideClaudin-1EndotoxinsHumansHypertension, PortalInsulin-Like Growth Factor IIntestinesLipopolysaccharidesLiver Cirrhosis, ExperimentalMaleOccludinPortal PressurePortal VeinCarbon TetrachlorideClaudin-1EndotoxinsInsulin-Like Growth Factor ILipopolysaccharidesOccludin

Identifiers

PMID26152281
PMCPMC4495682
OpenAlexW1503957772

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.