Evidence map›Paper›PMID 31756973›Full record

ArticleMolecules (Basel, Switzerland)2019

Deficiency of Urokinase Plasminogen Activator May Impair β Cells Regeneration and Insulin Secretion in Type 2 Diabetes Mellitus.

Chung-Ze Wu, Shih-Hsiang Ou, Li-Chien Chang, Yuh-Feng Lin, Dee Pei, Jin-Shuen Chen

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 32% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Icariin Protects Mouse Insulinoma Min6 Cell Function by Activating the PI3K/AKT Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  4. Oxidative medicine and cellular longevity · 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

6 authors at 4 institutions in 1 country.

Chung-Ze WuDivision of Endocrinology and Metabolism, Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan.
Shih-Hsiang OuDivision of Nephrology, Department of Internal Medicine, Kaohsiung Veterans General Hospital, Kaohsiung 81362, Taiwan.
Li-Chien ChangSchool of Pharmacy, National Defense Medical Center, Taipei 11490, Taiwan.
Yuh-Feng LinGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan.
Dee PeiDivision of Endocrinology and Metabolism, Department of Internal Medicine, Fu Jen Catholic University Hospital, New Taipei City 24352, Taiwan.
Jin-Shuen ChenDepartment of Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung 81362, Taiwan.
Kaohsiung Veterans General Hospital · TWTaipei Medical University-Shuang Ho Hospital · TWFu Jen Catholic University · TWNational Defense Medical Center · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

methodsIn mice models, wild-type and uPA knockout (uPA-/-) BALB/c mice were used for induction of T2DM. In cell models, insulin secretion rate and β cell proliferation were assessed in normal and high glucose after treating uPA siRNA, uPA, or anti-uPA antibody. In our clinical study, patients with T2DM received an oral glucose-tolerance test, and the relationship between uPA and insulin secretion was assessed.

resultsInsulin particles and insulin secretion were mildly restored one month after induction in wild-type mice, but not in uPA-/- mice. In cell models, insulin secretion rate and cell proliferation declined in high glucose after uPA silencing either by siRNA or by anti-uPA antibody. After treatment with uPA, β cell proliferation increased in normal glucose. In clinical study, patients with T2DM and higher uPA levels had better ability of insulin secretion than those with lower uPA levels.

conclusionuPA may play a substantial role in insulin secretion, β cell regeneration, and progressive development of T2DM. Supplementation of uPA might be a novel approach for prevention and treatment of T2DM in the future.

Indexed as

RegenerationAnimalsDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Insulin-Secreting CellsMiceMice, Inbred BALB CMice, KnockoutUrokinase-Type Plasminogen ActivatorUrokinase-Type Plasminogen Activatorinsulin secretiontype 2 diabetes mellitusurokinase plasminogen activatorβ cell regeneration

Identifiers

PMID31756973
PMCPMC6930534
OpenAlexW2990341393

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.