Evidence map›Paper›PMID 24998196›Full record

ArticleBrain, behavior, and immunity2014

High-fat diet consumption disrupts memory and primes elevations in hippocampal IL-1β, an effect that can be prevented with dietary reversal or IL-1 receptor antagonism.

Julia L Sobesky, Ruth M Barrientos, Henning S De May, Brittany M Thompson, Michael D Weber, Linda R Watkins, Steven F Maier

Abstract read
In one paragraph

Article in Brain, behavior, and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed, 1 pooled it
8.9field-weighted citation impact, top 2% 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

100 citing papers in PubMed, 1 synthesis or guideline pooled it, 156 citations in OpenAlex.

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40 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

7 authors at 1 institution in 1 country.

Julia L SobeskyDepartment of Psychology and Neuroscience, Center for Neuroscience, University of Colorado Boulder, Boulder, CO 80309, USA. Electronic address: julia.sobesky@colorado.edu.
Ruth M BarrientosDepartment of Psychology and Neuroscience, Center for Neuroscience, University of Colorado Boulder, Boulder, CO 80309, USA.
Henning S De MayDepartment of Psychology and Neuroscience, Center for Neuroscience, University of Colorado Boulder, Boulder, CO 80309, USA.
Brittany M ThompsonDepartment of Psychology and Neuroscience, Center for Neuroscience, University of Colorado Boulder, Boulder, CO 80309, USA.
Michael D WeberDepartment of Psychology and Neuroscience, Center for Neuroscience, University of Colorado Boulder, Boulder, CO 80309, USA.
Linda R WatkinsDepartment of Psychology and Neuroscience, Center for Neuroscience, University of Colorado Boulder, Boulder, CO 80309, USA.
Steven F MaierDepartment of Psychology and Neuroscience, Center for Neuroscience, University of Colorado Boulder, Boulder, CO 80309, USA.
University of Colorado Boulder · US

Funding

Preventing Transition of Acute-to-Chronic Neuropathic Pain: Models, Mechanisms &R01DE021966 · NIDCR · UNIVERSITY OF COLORADO · PI BARTH, DANIEL S., FLESHNER, MONIKA · 2011 to 2015
$2.0M
NIDCR NIH HHS R01 DE021966
6 · The paper itself

Abstract

High-fat diet (HFD)-induced obesity is reaching worldwide proportions. In addition to causing obesity, HFDs also induce a variety of health disorders, which includes cognitive decline. Hippocampal function may be particularly vulnerable to the negative consequences of HFD, and it is suspected that 'primed' neuroinflammatory processes may mediate this response. To examine the link between diet, hippocampal function and neuroinflammation, male Wistar rats were fed a medium or HFD. Hippocampal memory function was measured using contextual pre-exposure fear conditioning (CPE-FC). Rats fed a HFD demonstrated impaired memory, an effect that was augmented with longer duration of HFD consumption. HFD-induced memory impairments were linked to potentiated levels of interleukin-1 beta (IL-1β) protein in the hippocampus 2h after the foot-shock that occurs during CPE-FC. Central IL-1 receptor antagonism, with intracisterna magna (ICM) administration of hIL-1RA prior to the foot-shock prevented the diet-induced memory disruption, suggesting a critical role for IL-1β in this phenomenon. Additionally, obese animals whose diet regimen was reversed from HFD back to standard chow recovered memory function and did not demonstrate a foot-shock-induced hippocampal IL-1β increase. Interestingly, dietary reversal neutralized the negative impact of HFD on memory and IL-1β, yet animals maintained physiological evidence of obesity (increased body mass and serum leptin), indicating that dietary components, not body mass, may mediate the negative effects on memory.

Indexed as

Diet, High-FatAnimalsConditioning, PsychologicalFearHippocampusInterleukin-1betaMaleMemoryMemory DisordersRatsRats, WistarReceptors, Interleukin-1Interleukin-1betaReceptors, Interleukin-1Dietary reversalFear conditioningHigh-fat diethIL-1RAHippocampusInterleukin-1βMemory

Identifiers

PMID24998196
PMCPMC5652296
OpenAlexW1987478242

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.