Evidence map›Paper›PMID 27631195›Full record

ArticleJournal of neuroendocrinology2016

Deciphering Brain Insulin Receptor and Insulin-Like Growth Factor 1 Receptor Signalling.

A Kleinridders

Registry-linked trialOpen access · hybridAbstract read
In one paragraph

Article in Journal of neuroendocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04118920 (Safety of Topical Insulin Eye Drops for the Treatment of Open-angle Glaucoma), which is not on this map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
5.0field-weighted citation impact, top 5% 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.

NCT04118920 phase1active not recruitingnot on this mapstarted 2023, after this paper: background citation

Safety of Topical Insulin Eye Drops for the Treatment of Open-angle Glaucoma

TypeinterventionalSponsorCentre hospitalier de l'Université de Montréal (CHUM)Ran2023 to 2024Enrolled18ConditionsGlaucomaArmsTopical insulin (4 units), Topical insulin (20 units), Artificial tears
3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. The Role ofNutrients · 2025
    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

1 author at 1 institution in 1 country.

A KleinriddersGerman Institute of Human Nutrition Potsdam-Rehbruecke, Central Regulation of Metabolism, Nuthetal, Germany.
German Institute of Human Nutrition · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin receptor (IR) and insulin-like growth factor 1 receptor (IGF1R) are highly conserved receptor tyrosine kinases that share signalling proteins and are ubiquitously expressed in the brain. Central application of insulin or IGF1 exerts several similar physiological outcomes, varying in strength, whereas disruption of the corresponding receptors in the brain leads to remarkably different effects on brain size and physiology, thus highlighting the unique effects of the corresponding hormone receptors. Central insulin/IGF1 resistance impacts upon various levels of the IR/IGF1R signalling pathways and is a feature of the metabolic syndrome and neurodegenerative diseases such as Alzheimer's disease. The intricacy of brain insulin and IGF1 signalling represents a challenge for the identification of specific IR and IGF1R signalling differences in pathophysiological conditions. The present perspective sheds light on signalling differences and methodologies for specifically deciphering brain IR and IGF1R signalling.

Indexed as

Signal TransductionAnimalsAntigens, CDBrainHumansReceptor, IGF Type 1Receptor, InsulinAntigens, CDINSR protein, humanReceptor, IGF Type 1Receptor, Insulinbraindiabetesinsulin and IGF1 receptors

Identifiers

PMID27631195
PMCPMC5129466
OpenAlexW2557026142

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

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.