Evidence map›Paper›PMID 32179763›Full record

ArticleScientific reports2020

Effect of induced hypoglycemia on inflammation and oxidative stress in type 2 diabetes and control subjects.

Hassan Kahal, Anna Halama, Ahmed Aburima, Aditya M Bhagwat, Alexandra E Butler, Johannes Graumann, Karsten Suhre, Thozhukat Sathyapalan, Stephen L Atkin

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 89 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 2 pooled it
9.5field-weighted citation impact, top 1% 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

89 citing papers in PubMed, 2 syntheses or guidelines pooled it, 106 citations in OpenAlex.

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29 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 4 countries.

Hassan Kahal *Academic Endocrinology, Diabetes and Metabolism, Hull York Medical School, Hull, UK.
Anna Halama *Weill Cornell Medicine Qatar, Education City, PO, 24144, Doha, Qatar.
Ahmed AburimaCentre for Cardiovascular and Metabolic Research, Hull York Medical School, Hull, UK.
Aditya M BhagwatWeill Cornell Medicine Qatar, Education City, PO, 24144, Doha, Qatar.
Alexandra E ButlerDiabetes Research Center (DRC), Qatar Biomedical Research Institute (QBRI), Hamad Bin Khalifa University (HBKU), Qatar Foundation (QF), PO Box, 34110, Doha, Qatar. abutler@hbku.edu.qa.
Johannes GraumannProteomics Core, Weill Cornell Medicine-Qatar, Education City, PO Box, 24144, Doha, Qatar.
Karsten SuhreProteomics Core, Weill Cornell Medicine-Qatar, Education City, PO Box, 24144, Doha, Qatar.
Thozhukat SathyapalanAcademic Endocrinology, Diabetes and Metabolism, Hull York Medical School, Hull, UK.
Stephen L AtkinRoyal College of Surgeon in Ireland, Manama, Bahrain.
Hull York Medical School · GBWeill Cornell Medical College in Qatar · QAHamad bin Khalifa University · QAMax Planck Institute for Heart and Lung Research · DERoyal College of Surgeons in Ireland - Bahrain · BH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intensive diabetes control has been associated with increased mortality in type 2 diabetes (T2DM); this has been suggested to be due to increased hypoglycemia. We measured hypoglycemia-induced changes in endothelial parameters, oxidative stress markers and inflammation at baseline and after a 24-hour period in type 2 diabetic (T2DM) subjects versus age-matched controls. Case-control study: 10 T2DM and 8 control subjects. Blood glucose was reduced from 5 (90 mg/dl) to hypoglycemic levels of 2.8 mmol/L (50 mg/dl) for 1 hour by incremental hyperinsulinemic clamps using baseline and 24 hour samples. Measures of endothelial parameters, oxidative stress and inflammation at baseline and at 24-hours post hypoglycemia were performed: proteomic (Somalogic) analysis for inflammatory markers complemented by C-reactive protein (hsCRP) measurement, and proteomic markers and urinary isoprostanes for oxidative measures, together with endothelial function. Between baseline and 24 -hours after hypoglycemia, 15 of 140 inflammatory proteins differed in T2DM whilst only 1 of 140 differed in controls; all returned to baseline at 24-hours. However, elevated hsCRP levels were seen at 24-hours in T2DM (2.4 mg/L (1.2-5.4) vs. 3.9 mg/L (1.8-6.1), Baseline vs 24-hours, P < 0.05). In patients with T2DM, between baseline and 24-hour after hypoglycemia, only one of 15 oxidative stress proteins differed and this was not seen in controls. An increase (P = 0.016) from baseline (73.4 ng/mL) to 24 hours after hypoglycemia (91.7 ng/mL) was seen for urinary isoprostanes. Hypoglycemia resulted in inflammatory and oxidative stress markers being elevated in T2DM subjects but not controls 24-hours after the event.

Indexed as

Oxidative StressAdultBiomarkersBlood GlucoseCase-Control StudiesC-Reactive ProteinDiabetes Mellitus, Type 2FemaleHumansHypoglycemiaHypoglycemic AgentsInflammationMaleMiddle AgedTime FactorsBiomarkersBlood GlucoseC-Reactive ProteinHypoglycemic Agents

Identifiers

PMID32179763
PMCPMC7075968
OpenAlexW3010856774

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.