Evidence map›Paper›PMID 22473784›Full record

ArticleThe Journal of physiology2012

'Metabolic syndrome' in the brain: deficiency in omega-3 fatty acid exacerbates dysfunctions in insulin receptor signalling and cognition.

Rahul Agrawal, Fernando Gomez-Pinilla

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed
12.6field-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

95 citing papers in PubMed, 217 citations in OpenAlex.

  1. Trial
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  6. Protective Potential ofCurrent issues in molecular biology · 2025
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  18. Lifestyle Adjustment: Influential Risk Factors in Cognitive Aging.Advances in experimental medicine and biology · 2023
    Article
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Rahul AgrawalDepartment of Integrative Biology and Physiology, University of California Los Angeles (UCLA), Los Angeles, CA 90095, USA.
Fernando Gomez-Pinilla
University of California, Los Angeles · US

Funding

Restoration of Homeostasis After Brain TraumaR01NS050465 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI GOMEZ-PINILLA, FERNANDO · 2005 to 2019
$5.5M
Neurotrophins Support Spinal Cord Learning and RehabilitationR01NS056413 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI GOMEZ-PINILLA, FERNANDO · 2009 to 2013
$1.8M
NINDS NIH HHS NS50465NINDS NIH HHS NS56413.NINDS NIH HHS R01 NS050465NINDS NIH HHS R01 NS056413
6 · The paper itself

Abstract

We pursued studies to determine the effects of the metabolic syndrome (MetS) on brain, and the possibility of modulating these effects by dietary interventions. In addition, we have assessed potential mechanisms by which brain metabolic disorders can impact synaptic plasticity and cognition. We report that high-dietary fructose consumption leads to an increase in insulin resistance index, and insulin and triglyceride levels, which characterize MetS. Rats fed on an n-3 deficient diet showed memory deficits in a Barnes maze, which were further exacerbated by fructose intake. In turn, an n-3 deficient diet and fructose interventions disrupted insulin receptor signalling in hippocampus as evidenced by a decrease in phosphorylation of the insulin receptor and its downstream effector Akt. We found that high fructose consumption with an n-3 deficient diet disrupts membrane homeostasis as evidenced by an increase in the ratio of n-6/n-3 fatty acids and levels of 4-hydroxynonenal, a marker of lipid peroxidation. Disturbances in brain energy metabolism due to n-3 deficiency and fructose treatments were evidenced by a significant decrease in AMPK phosphorylation and its upstream modulator LKB1 as well as a decrease in Sir2 levels. The decrease in phosphorylation of CREB, synapsin I and synaptophysin levels by n-3 deficiency and fructose shows the impact of metabolic dysfunction on synaptic plasticity. All parameters of metabolic dysfunction related to the fructose treatment were ameliorated by the presence of dietary n-3 fatty acid. Results showed that dietary n-3 fatty acid deficiency elevates the vulnerability to metabolic dysfunction and impaired cognitive functions by modulating insulin receptor signalling and synaptic plasticity.

Indexed as

AnimalsBrainCognitionDietDisease Models, AnimalFatty Acids, Omega-3FructoseMaleMaze LearningMetabolic SyndromeRatsRats, Sprague-DawleyReceptor, InsulinFatty Acids, Omega-3FructoseReceptor, Insulin

Identifiers

PMID22473784
PMCPMC3424766
OpenAlexW2113039508

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.