Evidence map›Paper›PMID 29649429›Full record

ArticleExperimental neurology2018

Deletion of the insulin receptor in sensory neurons increases pancreatic insulin levels.

Caleb W Grote, Natalie M Wilson, Natalie K Katz, Brianne L Guilford, Janelle M Ryals, Lesya Novikova, Lisa Stehno-Bittel, Douglas E Wright

Abstract read
In one paragraph

Article in Experimental neurology, 2018. 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
1.2field-weighted citation impact, top 22% 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, 16 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. The Effects of Insulin on Immortalized Rat Schwann Cells, IFRS1.International journal of molecular sciences · 2021
    Article
  9. Review
  10. Article
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

8 authors at 2 institutions in 1 country.

Caleb W GroteDepartment of Orthopedic Surgery, University of Kansas Medical Center, United States.
Natalie M WilsonDepartment of Anatomy and Cell Biology, University of Kansas Medical Center, United States.
Natalie K KatzDepartment of Anatomy and Cell Biology, University of Kansas Medical Center, United States.
Brianne L GuilfordDepartment of Applied Health, Southern Illinois University Edwardsville, United States.
Janelle M RyalsDepartment of Anatomy and Cell Biology, University of Kansas Medical Center, United States.
Lesya NovikovaPhysical Therapy & Rehabilitation Science, University of Kansas Medical Center, Southern Illinois University Edwardsville, United States.
Lisa Stehno-BittelPhysical Therapy & Rehabilitation Science, University of Kansas Medical Center, Southern Illinois University Edwardsville, United States.
Douglas E WrightDepartment of Anatomy and Cell Biology, University of Kansas Medical Center, United States. Electronic address: dwright@kumc.edu.
University of Kansas Medical Center · USSouthern Illinois University Edwardsville · US

Funding

Mentoring CoreP20GM103418 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI Douglas E Wright · 2012 to 2026
$63.0M
Painful Versus Insensate Diabetic NeuropathyR01NS043314 · NINDS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI Douglas E Wright · 2003 to 2026
$6.7M
Using PCORnet to Expand the DS-CONNECT Cohort Through Healthcare System Recruitment, Incorporating Electronic Health Records, and Assessing Self-DeterminationU54HD090216 · NICHD · UNIVERSITY OF KANSAS LAWRENCE · PI COLOMBO, JOHN A. · 2016 to 2020
$6.2M
NICHD NIH HHS U54 HD090216NIGMS NIH HHS P20 GM103418NINDS NIH HHS R01 NS043314
6 · The paper itself

Abstract

Insulin is known to have neurotrophic properties and loss of insulin support to sensory neurons may contribute to peripheral diabetic neuropathy (PDN). Here, genetically-modified mice were generated in which peripheral sensory neurons lacked the insulin receptor (SNIRKO mice) to determine whether disrupted sensory neuron insulin signaling plays a crucial role in the development of PDN and whether SNIRKO mice develop symptoms of PDN due to reduced insulin neurotrophic support. Our results revealed that SNIRKO mice were euglycemic and never displayed significant changes in a wide range of sensorimotor behaviors, nerve conduction velocity or intraepidermal nerve fiber density. However, SNIRKO mice displayed elevated serum insulin levels, glucose intolerance, and increased insulin content in the islets of Langerhans of the pancreas. These results contribute to the growing idea that sensory innervation of pancreatic islets is key to regulating islet function and that a negative feedback loop of sensory neuron insulin signaling keeps this regulation in balance. Our results suggest that a loss of insulin receptors in sensory neurons does not lead to peripheral nerve dysfunction. The SNIRKO mice will be a powerful tool to investigate sensory neuron insulin signaling and may give a unique insight into the role that sensory neurons play in modifying islet physiology.

Indexed as

Gene DeletionAnimalsBlood GlucoseFemaleInsulinMaleMiceMice, KnockoutMice, TransgenicMicrofilament ProteinsPancreasReceptor, InsulinSensory Receptor CellsAvil protein, mouseBlood GlucoseInsulinMicrofilament ProteinsReceptor, InsulinBeta cellDorsal root gangliaGene deletionInsulinInsulin receptorIsletMouse modelsNeuropathyPancreasSensory neuron

Identifiers

PMID29649429
PMCPMC5963702
OpenAlexW2796810669

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.