Evidence map›Paper›PMID 27825441›Full record

ArticleDevelopmental cell2016

Neurotrophin Signaling Is Required for Glucose-Induced Insulin Secretion.

Jessica Houtz, Philip Borden, Alexis Ceasrine, Liliana Minichiello, Rejji Kuruvilla

Open access · bronzeAbstract read
In one paragraph

Article in Developmental cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
6.0field-weighted citation impact, top 4% 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

52 citing papers in PubMed, 86 citations in OpenAlex.

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  18. Diabetes as a Pancreatic Microvascular Disease-A Pericytic Perspective.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2024
    Review
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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

5 authors at 2 institutions in 2 countries.

Jessica HoutzDepartment of Biology, Johns Hopkins University, 3400 North Charles Street, 224 Mudd Hall, Baltimore, MD 21218, USA.
Philip BordenDepartment of Biology, Johns Hopkins University, 3400 North Charles Street, 224 Mudd Hall, Baltimore, MD 21218, USA.
Alexis CeasrineDepartment of Biology, Johns Hopkins University, 3400 North Charles Street, 224 Mudd Hall, Baltimore, MD 21218, USA.
Liliana MinichielloDepartment of Pharmacology, University of Oxford, OX1 3QT Oxford, UK.
Rejji KuruvillaDepartment of Biology, Johns Hopkins University, 3400 North Charles Street, 224 Mudd Hall, Baltimore, MD 21218, USA. Electronic address: rkuruvilla@jhu.edu.
Johns Hopkins University · USUniversity of Oxford · GB

Funding

CELLULAR AND MOLECULAR BIOLOGYT32GM007231 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI VAN DOREN, MARK B · 1985 to 2020
$18.4M
JHU-UMD Diabetes Research CenterP30DK079637 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI AHIMA, REXFORD S. · 2013 to 2017
$9.7M
Neurotrophin mechanisms in neural development and diseaseR01NS073751 · NINDS · JOHNS HOPKINS UNIVERSITY · PI KURUVILLA, REJJI · 2011 to 2015
$1.7M
Neurotrophins as new regulators of islet biologyR01DK108267 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI KURUVILLA, REJJI · 2016 to 2019
$1.4M
Acquisition of Sony Biotechnology iCyt Synergy SY3200 BSC Cell SorterS10OD016230 · OD · JOHNS HOPKINS UNIVERSITY · PI MCCAFFERY, J. MICHAEL · 2014 to 2014
$520k
NIDDK NIH HHS P30 DK079637NIDDK NIH HHS R01 DK108267NIGMS NIH HHS T32 GM007231NIH HHS S10 OD016230NINDS NIH HHS R01 NS073751
6 · The paper itself

Abstract

Insulin secretion by pancreatic islet β cells is critical for glucose homeostasis, and a blunted β cell secretory response is an early deficit in type 2 diabetes. Here, we uncover a regulatory mechanism by which glucose recruits vascular-derived neurotrophins to control insulin secretion. Nerve growth factor (NGF), a classical trophic factor for nerve cells, is expressed in pancreatic vasculature while its TrkA receptor is localized to islet β cells. High glucose rapidly enhances NGF secretion and increases TrkA phosphorylation in mouse and human islets. Tissue-specific deletion of NGF or TrkA, or acute disruption of TrkA signaling, impairs glucose tolerance and insulin secretion in mice. We show that internalized TrkA receptors promote insulin granule exocytosis via F-actin reorganization. Furthermore, NGF treatment augments glucose-induced insulin secretion in human islets. These findings reveal a non-neuronal role for neurotrophins and identify a new regulatory pathway in insulin secretion that can be targeted to ameliorate β cell dysfunction.

Indexed as

ActinsAnimalsEndocytosisExocytosisGene DeletionGlucoseGlucose IntoleranceGlucose Tolerance TestHomeostasisHumansInsulinInsulin SecretionIntegrasesMice, Inbred C57BLModels, BiologicalNerve Growth FactorActinsCre recombinaseGlucoseInsulinIntegrasesNerve Growth FactorReceptor, trkAactin remodelingendosomal signalingglucose homeostasishuman isletsinsulin secretionneurotrophinspancreatic vasculaturepericytes

Identifiers

PMID27825441
PMCPMC5123838
OpenAlexW2549063564

What OpenQuestion holds

Textmetadata
LicenceTDM
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.