Evidence map›Paper›PMID 27792405›Full record

ArticleEndocrinology2017

Circulating Insulin-Like Growth Factor I Regulates Its Receptor in the Brain of Male Mice.

A Trueba-Saiz, A M Fernandez, T Nishijima, M Mecha, A Santi, V Munive, I Torres Aleman

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 2 pooled it
3.7field-weighted citation impact, top 6% 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

18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Insulin- Like Growth Factor-1 as Brain-Body Connector.Advances in experimental medicine and biology · 2025
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Preclinical and clinical evidence of IGF-1 as a prognostic marker and acute intervention with ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Insulin transport into the brain.American journal of physiology. Cell physiology · 2018
    Review
  16. Review
  17. Article
  18. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

A Trueba-SaizCajal Institute, CSIC, and Ciberned , Madrid, Spain.
A M FernandezCajal Institute, CSIC, and Ciberned , Madrid, Spain.
T NishijimaCajal Institute, CSIC, and Ciberned , Madrid, Spain.
M MechaCajal Institute, CSIC, and Ciberned , Madrid, Spain.
A SantiCajal Institute, CSIC, and Ciberned , Madrid, Spain.
V MuniveCajal Institute, CSIC, and Ciberned , Madrid, Spain.
I Torres AlemanCajal Institute, CSIC, and Ciberned , Madrid, Spain.
Instituto Cajal · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of IGF-1 and its receptor (IGF-1R) in brain pathology is still unclear. Thus, either reduction of IGF-IR or treatment with IGF-1, two apparently opposite actions, has proven beneficial in brain diseases such as Alzheimer's dementia. A possible explanation of this discrepancy is that IGF-1 down-regulates brain IGF-1R levels, as previously seen in a mouse Alzheimer's dementia model. We now explored whether under normal conditions IGF-1 modulates its receptor. We first observed that in vitro, IGF-1 reduced IGF-1R mRNA levels in all types of brain cells including neurons, astrocytes, microglia, endothelial cells, and oligodendrocytes. IGF-1 also inhibited its own expression in neurons and brain endothelium. Next, we analyzed the in vivo actions of IGF-1. Because serum IGF-1 can enter the brain, we injected mice with IGF-1 ip. As soon as 1 hour after the injection, decreased hippocampal IGF-1 levels were observed, followed by increased IGF-1 and IGF-1R mRNAs 6 hours later. Because environmental enrichment (EE) stimulates the entrance of serum IGF-1 into the brain, we analyzed whether a physiological entrance of IGF-1 also produced changes in brain IGF-1R. Stimulation of IGF-1R by EE triggered a gradual decrease in hippocampal IGF-1 levels. After 6 hours of EE exposure, IGF-1 levels reached a significant decrease in parallel with increased IGF-1R expression. After longer times, IGF-1R mRNA levels returned to baseline. Thus, under nonpathological conditions, IGF-1 regulates brain IGF-1R. Because baseline IGF-1R levels are rapidly restored, a tight control of brain IGF-1R expression seems to operate under physiological conditions.

Indexed as

AnimalsBrainCells, CulturedInsulin-Like Growth Factor IMaleMice, Inbred C57BLReceptor, IGF Type 1Insulin-Like Growth Factor IReceptor, IGF Type 1

Identifiers

PMID27792405
OpenAlexW2544307470

What OpenQuestion holds

Textmetadata
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.