Evidence map›Paper›PMID 26904947›Full record

ArticleCell reports2016

MafA-Controlled Nicotinic Receptor Expression Is Essential for Insulin Secretion and Is Impaired in Patients with Type 2 Diabetes.

Elvira Ganic, Tania Singh, Cheng Luan, João Fadista, Jenny K Johansson, Holly Ann Cyphert, Hedvig Bennet, Petter Storm, Gaëlle Prost, Henrik Ahlenius and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 35 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

15 authors at 2 institutions in 2 countries.

Elvira GanicStem Cell Center, Lund University, Klinikgatan 26, Lund 22184, Sweden; Lund University Diabetes Center, Lund University, Klinikgatan 26, Lund 22184, Sweden.
Tania SinghStem Cell Center, Lund University, Klinikgatan 26, Lund 22184, Sweden; Lund University Diabetes Center, Lund University, Klinikgatan 26, Lund 22184, Sweden.
Cheng LuanLund University Diabetes Center, Lund University, Klinikgatan 26, Lund 22184, Sweden.
João FadistaLund University Diabetes Center, Lund University, Klinikgatan 26, Lund 22184, Sweden.
Jenny K JohanssonStem Cell Center, Lund University, Klinikgatan 26, Lund 22184, Sweden; Lund University Diabetes Center, Lund University, Klinikgatan 26, Lund 22184, Sweden.
Holly Ann CyphertDepartment of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Hedvig BennetLund University Diabetes Center, Lund University, Klinikgatan 26, Lund 22184, Sweden.
Petter StormLund University Diabetes Center, Lund University, Klinikgatan 26, Lund 22184, Sweden.
Gaëlle ProstStem Cell Center, Lund University, Klinikgatan 26, Lund 22184, Sweden.
Henrik AhleniusStem Cell Center, Lund University, Klinikgatan 26, Lund 22184, Sweden.
Erik RenströmLund University Diabetes Center, Lund University, Klinikgatan 26, Lund 22184, Sweden.
Roland SteinDepartment of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Leif GroopLund University Diabetes Center, Lund University, Klinikgatan 26, Lund 22184, Sweden.
Malin FexLund University Diabetes Center, Lund University, Klinikgatan 26, Lund 22184, Sweden.
Isabella ArtnerStem Cell Center, Lund University, Klinikgatan 26, Lund 22184, Sweden; Lund University Diabetes Center, Lund University, Klinikgatan 26, Lund 22184, Sweden. Electronic address: isabella.artner@med.lu.se.
Lund University · SEVanderbilt University Medical Center · US

Funding

Defining the Role of MafA in Islet Beta CellsR01DK090570 · NIDDK · VANDERBILT UNIVERSITY · PI PARENT, AUDREY, STEIN, ROLAND W · 2011 to 2025
$5.9M
NIDDK NIH HHS R01 DK090570
6 · The paper itself

Abstract

Monoamine and acetylcholine neurotransmitters from the autonomic nervous system (ANS) regulate insulin secretion in pancreatic islets. The molecular mechanisms controlling neurotransmitter signaling in islet β cells and their impact on diabetes development are only partially understood. Using a glucose-intolerant, MafA-deficient mouse model, we demonstrate that MAFA controls ANS-mediated insulin secretion by activating the transcription of nicotinic (ChrnB2 and ChrnB4) and adrenergic (Adra2A) receptor genes, which are integral parts of acetylcholine- and monoamine-signaling pathways. We show that acetylcholine-mediated insulin secretion requires nicotinic signaling and that nicotinic receptor expression is positively correlated with insulin secretion and glycemic control in human donor islets. Moreover, polymorphisms spanning MAFA-binding regions within the human CHRNB4 gene are associated with type 2 diabetes. Our data show that MAFA transcriptional activity is required for establishing β cell sensitivity to neurotransmitter signaling and identify nicotinic signaling as a modulator of insulin secretion impaired in type 2 diabetes.

Indexed as

AnimalsAutonomic Nervous SystemBinding SitesDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2FemaleGene Expression RegulationGlucose Tolerance TestHumansInsulinInsulin-Secreting CellsMaf Transcription Factors, LargeMiceMice, KnockoutNerve Tissue ProteinsPolymorphism, GeneticAdra2a protein, mouseChrnb4 protein, mouseInsulinMafa protein, mouseMaf Transcription Factors, LargeNerve Tissue ProteinsReceptors, Adrenergic, alpha-2Receptors, Nicotinic

Identifiers

PMID26904947
PMCPMC5918632
OpenAlexW2274238354

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.