Evidence map›Paper›PMID 32708537›Full record

ArticleBiomolecules2020

The Constitutive Lack of α7 Nicotinic Receptor Leads to Metabolic Disorders in Mouse.

Blandine Gausserès, Junjun Liu, Ewout Foppen, Cécile Tourrel-Cuzin, Ana Rodriguez Sanchez-Archidona, Etienne Delangre, Céline Cruciani-Guglielmacci, Stéphanie Pons, Uwe Maskos, Bernard Thorens and 3 more

Open access · goldAbstract read
In one paragraph

Article in Biomolecules, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

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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

13 authors at 2 institutions in 2 countries.

Blandine GausserèsBiology and Pathology of the Endocrine Pancreas, Université de Paris, BFA, UMR 8251, CNRS, F-75013 Paris, France.
Junjun LiuBiology and Pathology of the Endocrine Pancreas, Université de Paris, BFA, UMR 8251, CNRS, F-75013 Paris, France.ORCID 0000-0002-3763-730X
Ewout FoppenRegulation of Glycemia by Central Nervous System, Université de Paris, BFA, UMR 8251, CNRS, F-75013 Paris, France.
Cécile Tourrel-CuzinBiology and Pathology of the Endocrine Pancreas, Université de Paris, BFA, UMR 8251, CNRS, F-75013 Paris, France.
Ana Rodriguez Sanchez-ArchidonaCenter for Integrative Genomics, University of Lausanne, CH-1015 Lausanne, Switzerland.ORCID 0000-0001-6002-2779
Etienne DelangreBiology and Pathology of the Endocrine Pancreas, Université de Paris, BFA, UMR 8251, CNRS, F-75013 Paris, France.
Céline Cruciani-GuglielmacciRegulation of Glycemia by Central Nervous System, Université de Paris, BFA, UMR 8251, CNRS, F-75013 Paris, France.ORCID 0000-0002-2562-5360
Stéphanie PonsInstitut Pasteur, UMR 3571, CNRS, Department of Neuroscience, Integrative Neurobiology of Cholinergic Systems, CEDEX 15, 75724 Paris, France.
Uwe MaskosInstitut Pasteur, UMR 3571, CNRS, Department of Neuroscience, Integrative Neurobiology of Cholinergic Systems, CEDEX 15, 75724 Paris, France.
Bernard ThorensCenter for Integrative Genomics, University of Lausanne, CH-1015 Lausanne, Switzerland.
Christophe MagnanRegulation of Glycemia by Central Nervous System, Université de Paris, BFA, UMR 8251, CNRS, F-75013 Paris, France.ORCID 0000-0002-7044-2571
Jamileh MovassatBiology and Pathology of the Endocrine Pancreas, Université de Paris, BFA, UMR 8251, CNRS, F-75013 Paris, France.
Kamel MaoucheBiology and Pathology of the Endocrine Pancreas, Université de Paris, BFA, UMR 8251, CNRS, F-75013 Paris, France.ORCID 0000-0001-5723-6338
Centre National de la Recherche Scientifique · FRUniversity of Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveType 2 diabetes (T2D) occurs by deterioration in pancreatic β-cell function and/or progressive loss of pancreatic β-cell mass under the context of insulin resistance. α7 nicotinic acetylcholine receptor (nAChR) may contribute to insulin sensitivity but its role in the pathogenesis of T2D remains undefined. We investigated whether the systemic lack of α7 nAChR was sufficient to impair glucose homeostasis.

methodsWe used an α7 nAChR knock-out (α7

resultsYoung α7

conclusionOur work highlights the important role of α7 nAChR in glucose homeostasis. The constitutive lack of α7 nAChR suggests a novel pathway influencing the pathogenesis of T2D.

Indexed as

Insulin Resistancealpha7 Nicotinic Acetylcholine ReceptorAnimalsCell LineDiabetes Mellitus, Type 2FemaleGene DeletionGlucoseGlucose IntoleranceHyperglycemiaMaleMiceMice, Inbred C57BLMice, KnockoutRatsalpha7 Nicotinic Acetylcholine ReceptorGlucosefat masshigh glycemiainsulin resistanceα7 nAChRβ-cell mass

Identifiers

PMID32708537
PMCPMC7408520
OpenAlexW3043461101

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.