Evidence map›Paper›PMID 25177166›Full record

ArticleThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology2014

Exendin-4 Improves Nonalcoholic Fatty Liver Disease by Regulating Glucose Transporter 4 Expression in ob/ob Mice.

Seok Kim, Jaehoon Jung, Hwajin Kim, Rok Won Heo, Chin-Ok Yi, Jung Eun Lee, Byeong Tak Jeon, Won-Ho Kim, Jong Ryeal Hahm, Gu Seob Roh

Open access · hybridAbstract read
In one paragraph

Article in The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  10. Journal of clinical medicine · 2018
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  13. Anti-diabetic activities of catalpol in db/db mice.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2016
    Article
  14. Myeloid-specific SIRT1 Deletion Aggravates Hepatic Inflammation and Steatosis in High-fat Diet-fed Mice.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2015
    Article
  15. EGCG Blocked Phenylephrin-Induced Hypertrophy in H9C2 Cardiomyocytes, by Activating AMPK-Dependent Pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2015
    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 1 institution in 1 country.

Seok KimDepartment of Anatomy and Convergence Medical Science, Institutes of Health Science, Gyeongsnag National University School of Medicine, Jinju 660-751, Korea.
Jaehoon JungDepartment of Internal Medicine, Institutes of Health Science, Gyeongsnag National University School of Medicine, Jinju 660-751, Korea.
Hwajin KimDepartment of Anatomy and Convergence Medical Science, Institutes of Health Science, Gyeongsnag National University School of Medicine, Jinju 660-751, Korea.
Rok Won HeoDepartment of Anatomy and Convergence Medical Science, Institutes of Health Science, Gyeongsnag National University School of Medicine, Jinju 660-751, Korea.
Chin-Ok YiDepartment of Anatomy and Convergence Medical Science, Institutes of Health Science, Gyeongsnag National University School of Medicine, Jinju 660-751, Korea.
Jung Eun LeeDepartment of Thoracic and Cardiovascular Surgery, Institutes of Health Science, Gyeongsnag National University School of Medicine, Jinju 660-751, Korea.
Byeong Tak JeonDepartment of Neurologic Surgery, Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.
Won-Ho KimDivision of Metabolic Diseases, Center for Biomedical Sciences, National Institutes of Health, Cheongwon-gun 363-700, Korea.
Jong Ryeal HahmDepartment of Internal Medicine, Institutes of Health Science, Gyeongsnag National University School of Medicine, Jinju 660-751, Korea.
Gu Seob RohDepartment of Anatomy and Convergence Medical Science, Institutes of Health Science, Gyeongsnag National University School of Medicine, Jinju 660-751, Korea.
Mayo Clinic · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exendin-4 (Ex-4), a glucagon-like peptide-1 receptor (GLP-1R) agonist, has been known to reverse hepatic steatosis in ob/ob mice. Although many studies have evaluated molecular targets of Ex-4, its mechanism of action on hepatic steatosis and fibrosis has not fully been determined. In the liver, glucose transporter 4 (GLUT4) is mainly expressed in hepatocytes, endothelial cells and hepatic stellate cells (HSCs). In the present study, the effects of Ex-4 on GLUT4 expression were determined in the liver of ob/ob mice. Ob/ob mice were treated with Ex-4 for 10 weeks. Serum metabolic parameters, hepatic triglyceride levels, and liver tissues were evaluated for hepatic steatosis. The weights of the whole body and liver in ob/ob mice were reduced by long-term Ex-4 treatment. Serum metabolic parameters, hepatic steatosis, and hepatic fibrosis in ob/ob mice were reduced by Ex-4. Particularly, Ex-4 improved hepatic steatosis by enhancing GLUT4 via GLP-1R activation in ob/ob mice. Ex-4 treatment also inhibited hepatic fibrosis by decreasing expression of connective tissue growth factor in HSCs of ob/ob mice. Our data suggest that GLP-1 agonists exert a protective effect on hepatic steatosis and fibrosis in obesity and type 2 diabetes.

Indexed as

Exendin-4Glucose transporter 4Nonalcoholic fatty liver diseaseob/ob

Identifiers

PMID25177166
PMCPMC4146636
OpenAlexW2041802771

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

Registered trials

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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.