Evidence map›Paper›PMID 25346723›Full record

ReviewFrontiers in endocrinology2014

Insulin in the brain: its pathophysiological implications for States related with central insulin resistance, type 2 diabetes and Alzheimer's disease.

Enrique Blázquez, Esther Velázquez, Verónica Hurtado-Carneiro, Juan Miguel Ruiz-Albusac

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 232 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
232citing papers in PubMed, 4 pooled it
16.0field-weighted citation impact, top 1% 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

232 citing papers in PubMed, 4 syntheses or guidelines pooled it, 471 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Trial
  7. Trial
  8. Time- and Region-Specific Effects of Intranasal Insulin on Oxidative Stress Parameters in the Rat Brain.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  9. Review
  10. Article
  11. Article
  12. How does type 2 diabetes modify the risk of Alzheimer's disease?Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article

172 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

Enrique BlázquezDepartamento de Bioquímica y Biología Molecular III, Facultad de Medicina, Universidad Complutense , Madrid , Spain ; The Center for Biomedical Research in Diabetes and Associated Metabolic Disorders (CIBERDEM) , Madrid , Spain ; Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdiSSC) , Madrid , Spain.
Esther VelázquezDepartamento de Bioquímica y Biología Molecular III, Facultad de Medicina, Universidad Complutense , Madrid , Spain ; The Center for Biomedical Research in Diabetes and Associated Metabolic Disorders (CIBERDEM) , Madrid , Spain ; Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdiSSC) , Madrid , Spain.
Verónica Hurtado-CarneiroDepartamento de Bioquímica y Biología Molecular III, Facultad de Medicina, Universidad Complutense , Madrid , Spain ; The Center for Biomedical Research in Diabetes and Associated Metabolic Disorders (CIBERDEM) , Madrid , Spain ; Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdiSSC) , Madrid , Spain.
Juan Miguel Ruiz-AlbusacDepartamento de Bioquímica y Biología Molecular III, Facultad de Medicina, Universidad Complutense , Madrid , Spain ; The Center for Biomedical Research in Diabetes and Associated Metabolic Disorders (CIBERDEM) , Madrid , Spain ; Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdiSSC) , Madrid , Spain.
Instituto de Investigación Sanitaria del Hospital Clínico San Carlos · ESUniversidad Complutense de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although the brain has been considered an insulin-insensitive organ, recent reports on the location of insulin and its receptors in the brain have introduced new ways of considering this hormone responsible for several functions. The origin of insulin in the brain has been explained from peripheral or central sources, or both. Regardless of whether insulin is of peripheral origin or produced in the brain, this hormone may act through its own receptors present in the brain. The molecular events through which insulin functions in the brain are the same as those operating in the periphery. However, certain insulin actions are different in the central nervous system, such as hormone-induced glucose uptake due to a low insulin-sensitive GLUT-4 activity, and because of the predominant presence of GLUT-1 and GLUT-3. In addition, insulin in the brain contributes to the control of nutrient homeostasis, reproduction, cognition, and memory, as well as to neurotrophic, neuromodulatory, and neuroprotective effects. Alterations of these functional activities may contribute to the manifestation of several clinical entities, such as central insulin resistance, type 2 diabetes mellitus (T2DM), and Alzheimer's disease (AD). A close association between T2DM and AD has been reported, to the extent that AD is twice more frequent in diabetic patients, and some authors have proposed the name "type 3 diabetes" for this association. There are links between AD and T2DM through mitochondrial alterations and oxidative stress, altered energy and glucose metabolism, cholesterol modifications, dysfunctional protein O-GlcNAcylation, formation of amyloid plaques, altered Aβ metabolism, and tau hyperphosphorylation. Advances in the knowledge of preclinical AD and T2DM may be a major stimulus for the development of treatment for preventing the pathogenic events of these disorders, mainly those focused on reducing brain insulin resistance, which is seems to be a common ground for both pathological entities.

Indexed as

Alzheimer’s diseasebiological actionsbraincentral insulin resistanceinsulinpathophysiological implicationsreceptorstype 2 diabetes

Identifiers

PMID25346723
PMCPMC4191295
OpenAlexW2135591161

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.