Evidence map›Paper›PMID 26606859›Full record

ArticleLife sciences2016

GSK-3β mediates dexamethasone-induced pancreatic β cell apoptosis.

Bin Guo, Wenjian Zhang, Shiqing Xu, Jinning Lou, Shuxia Wang, Xiuli Men

Abstract read
In one paragraph

Article in Life sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
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  9. The Effects of ProbioticInternational journal of molecular sciences · 2023
    Article
  10. Review
  11. Review
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  13. Article
  14. Article
  15. Review
  16. Article
  17. Molecular Mechanisms of Glucocorticoid-Induced Insulin Resistance.International journal of molecular sciences · 2021
    Review
  18. Review
  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

6 authors at 3 institutions in 2 countries.

Bin GuoDepartment of Pathophysiology, North China University of Science and Technology,Tangshan 063000, People's Republic of China.
Wenjian ZhangInstitute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing 100029, People's Republic of China.
Shiqing XuInstitute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing 100029, People's Republic of China.
Jinning LouInstitute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing 100029, People's Republic of China.
Shuxia WangDepartment of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, KY 40536, USA. Electronic address: swang7@uky.edu.
Xiuli MenDepartment of Pathophysiology, North China University of Science and Technology,Tangshan 063000, People's Republic of China. Electronic address: xiulimen@126.com.
China-Japan Friendship Hospital · CNNorth China University of Science and Technology · CNUniversity of Kentucky · US

Funding

Thrombospondin 1 in obesity associated inflammation and insulin resistanceR01DK098176 · NIDDK · UNIVERSITY OF KENTUCKY · PI WANG, SHUXIA · 2014 to 2017
$1.2M
NIDDK NIH HHS DK098176NIDDK NIH HHS R01 DK098176
6 · The paper itself

Abstract

aimsGlucocorticoids, such as dexamethasone, are widely used anti-inflammatory drugs. Their use is frequently associated with the development of steroid- associated diabetes. Pancreatic β-cell dysfunction has been suggested to be one of the main causes of steroid-associated diabetes. However, the mechanism is not fully understood. Glycogen synthase kinase-3β (GSK-3β) is a multifunctional serine/threonine kinase and plays an important role in energy metabolism, cell growth and apoptosis. Therefore, the contribution of GSK-3β in dexamethasone-induced pancreatic β-cell apoptosis was determined in the present study. MAIN

methodsThe effect of dexamethasone treatment on rat pancreatic β-cell line (INS-1) apoptosis (determined by TUNEL and Flow Cytometry), generation of reactive oxidative stress (ROS), and the phosphorylation status of GSK-3β was determined. The inhibitory effect of GSK-3β inhibitor-lithium chloride (LiCl) on dexamethasone-induced β-cell apoptosis was also evaluated. KEY

findingsDexamethasone (0.1 μM) treatment induced INS-1 apoptosis, which was associated with increased GSK-3β activation and increased NOX4-derived ROS generation. Pretreatment of INS-1 with LiCl inhibited dexamethasone induced ROS generation and INS-1 apoptosis. SIGNIFICANCE: This study provides a new mechanism of Dex induced pancreatic β cell apoptosis and may serve as a new therapeutic option for treating GC induced diabetes.

Indexed as

AnimalsApoptosisCell LineCell ProliferationDexamethasoneEnzyme ActivationEnzyme InhibitorsGlucocorticoidsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaInsulin-Secreting CellsLithium ChlorideNADPH Oxidase 4NADPH OxidasesOxidative StressPhosphorylationDexamethasoneEnzyme InhibitorsGlucocorticoidsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, ratLithium ChlorideNADPH Oxidase 4NADPH OxidasesNox4 protein, ratReactive Oxygen SpeciesApoptosisDexamethasoneGSK-3βROS

Identifiers

PMID26606859
PMCPMC4703461
OpenAlexW2178571345

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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.