Evidence map›Paper›PMID 38628834›Full record

ArticleBasic and clinical neuroscience

Hepatic Acyl CoA Oxidase1 Inhibition Modifies Brain Lipids and Electrical Properties of Dentate Gyrus.

Shahrbanoo Rafiei, Fariba Khodagholi, Hamid Gholami Pourbadie, Leila Dargahi, Fereshteh Motamedi

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Article in Basic and clinical neuroscience. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.1field-weighted citation impact, top 55% 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

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

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

5 authors at 2 institutions in 1 country.

Shahrbanoo RafieiNeuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID https://orcid.org/0000-0003-1591-6866
Fariba KhodagholiNeurobiology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID https://orcid.org/0000-0002-4911-4530
Hamid Gholami PourbadieDepartment of Physiology and Pharmacology, Pasteur Institute of Iran, Tehran, Iran.ORCID https://orcid.org/0000-0002-7634-7428
Leila DargahiNeuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID https://orcid.org/0000-0001-7777-5435
Fereshteh MotamediNeuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID https://orcid.org/0000-0003-4030-8627
Shahid Beheshti University of Medical Sciences · IRPasteur Institute of Iran · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Peroxisomes are essential organelles in lipid metabolism. They contain enzymes for β-oxidation of very long-chain fatty acids (VLCFA) that cannot be broken down in mitochondria. Reduced expression in hepatic acyl-CoA oxidase 1 (ACOX1), a peroxisome β-oxidation enzyme, followed by modification of the brain fatty acid profile has been observed in aged rodents. These studies have suggested a potential role for peroxisome β-oxidation in brain aging. This study was designed to examine the effect of hepatic ACOX1 inhibition on brain fatty acid composition and neuronal cell activities of young rats (200-250 g). Methods: A specific ACOX1 inhibitor, 10, 12- tricosadiynoic acid (TDYA), 100 μg/kg (in olive oil) was administered by daily gavage for 25 days in male Wistar rats. The brain fatty acid composition and electrophysiological properties of dentate gyrus granule cells were determined using gas chromatography and whole-cell patch-clamp, respectively. Results: A significant increase in C20, C22, C18:1, C20:1, and a decrease of C18, C24, C20:3n6, and C22:6n3 were found in 10, 12- tricosadiynoic acid (TDYA) treated rats compared to the control group. The results showed that ACOX1 inhibition changes fatty acid composition similar to old rats. ACOX1 inhibition caused hyperpolarization of resting membrane potential, and also reduction of input resistance, action potential duration, and spike firing. Moreover, ACOX1 inhibition increased rheobase current and afterhyperpolarization amplitude in granule cells. Conclusion: The results indicated that systemic inhibition of ACOX1 causes hypo-excitability of neuronal cells. These results provide new evidence on the involvement of peroxisome function and hepatic ACOX1 activity in brain fatty acid profile and the electrophysiological properties of dentate gyrus cells.

Indexed as

Brain lipidsDentate gyrusFatty acid β-oxidationNeuronal activity

Identifiers

PMID38628834
PMCPMC11016873
OpenAlexW3210644093

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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.