Evidence map›Paper›PMID 32080229›Full record

ArticleScientific reports2020

Inhibition of IL-1beta improves Glycaemia in a Mouse Model for Gestational Diabetes.

Friederike Schulze, Josua Wehner, Denise V Kratschmar, Valmir Makshana, Daniel T Meier, Stéphanie P Häuselmann, Elise Dalmas, Constanze Thienel, Erez Dror, Sophia J Wiedemann and 9 more

Abstract read
PubMed Full text at PMC Publisher
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. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. Trial
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  11. Inhibitory effects ofHeliyon · 2023
    Article
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  18. Observational
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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

19 authors.

Friederike Schulze *Clinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland and Department of Biomedicine, University of Basel, Basel, Switzerland. schulze.fritzi@gmail.com.
Josua Wehner *Clinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland and Department of Biomedicine, University of Basel, Basel, Switzerland.
Denise V KratschmarDivision of Molecular and Systems Toxicology, Department of Pharmaceutical Sciences, University of Basel, Basel, Switzerland.
Valmir MakshanaClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland and Department of Biomedicine, University of Basel, Basel, Switzerland.
Daniel T MeierClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland and Department of Biomedicine, University of Basel, Basel, Switzerland.
Stéphanie P HäuselmannClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland and Department of Biomedicine, University of Basel, Basel, Switzerland.
Elise DalmasClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland and Department of Biomedicine, University of Basel, Basel, Switzerland.
Constanze ThienelClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland and Department of Biomedicine, University of Basel, Basel, Switzerland.
Erez DrorClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland and Department of Biomedicine, University of Basel, Basel, Switzerland.
Sophia J WiedemannClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland and Department of Biomedicine, University of Basel, Basel, Switzerland.
Shuyang TraubClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland and Department of Biomedicine, University of Basel, Basel, Switzerland.
Thierry M NordmannClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland and Department of Biomedicine, University of Basel, Basel, Switzerland.
Leila RachidClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland and Department of Biomedicine, University of Basel, Basel, Switzerland.
Axel De BaatClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland and Department of Biomedicine, University of Basel, Basel, Switzerland.
Theresa V RohmClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland and Department of Biomedicine, University of Basel, Basel, Switzerland.
Cheng ZhaoClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland and Department of Biomedicine, University of Basel, Basel, Switzerland.
Alex OdermattDivision of Molecular and Systems Toxicology, Department of Pharmaceutical Sciences, University of Basel, Basel, Switzerland.
Marianne Böni-SchnetzlerClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland and Department of Biomedicine, University of Basel, Basel, Switzerland.
Marc Y DonathClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland and Department of Biomedicine, University of Basel, Basel, Switzerland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gestational diabetes mellitus (GDM) is one of the most common diseases associated with pregnancy, however, the underlying mechanisms remain unclear. Based on the well documented role of inflammation in type 2 diabetes, the aim was to investigate the role of inflammation in GDM. We established a mouse model for GDM on the basis of its two major risk factors, obesity and aging. In these GDM mice, we observed increased Interleukin-1β (IL-1β) expression in the uterus and the placenta along with elevated circulating IL-1β concentrations compared to normoglycemic pregnant mice. Treatment with an anti-IL-1β antibody improved glucose-tolerance of GDM mice without apparent deleterious effects for the fetus. Finally, IL-1β antagonism showed a tendency for reduced plasma corticosterone concentrations, possibly explaining the metabolic improvement. We conclude that IL-1β is a causal driver of impaired glucose tolerance in GDM.

Indexed as

AnimalsDiabetes, GestationalDisease Models, AnimalFemaleHormonesHyperglycemiaInterleukin-1betaMice, Inbred C57BLPregnancySteroidsHormonesInterleukin-1betaSteroids

Identifiers

PMID32080229
PMCPMC7033251

What OpenQuestion holds

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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.