Evidence map›Paper›PMID 41024160›Full record

ArticleJournal of translational medicine2025

Screening of metabolic markers in pediatric epilepsy disorders.

Yu Chen, Shuo Kong, Yuhui Wang, Yansheng Ding, Biwen Peng, Jian Xu

Abstract read
In one paragraph

Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
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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

6 authors.

Yu ChenDepartment of Genetics, Shandong Second Medical University, Weifang, 261053, Shandong, China.
Shuo KongDepartment of Physiology, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Yuhui WangDepartment of Clinical Laboratory, Weifang People's Hospital, Weifang, 261000, Shandong, China.
Yansheng DingDepartment of Clinical Laboratory, Weifang Maternal and Child Health Hospital, Weifang, 261011, Shandong, China.
Biwen PengDepartment of Physiology, Hubei Provincial Key Laboratory of Developmentally Originated Disease, School of Basic Medical Sciences, Wuhan University, Wuhan, China. pengbiwen@whu.edu.cn.
Jian XuDepartment of Clinical Laboratory, Weifang Maternal and Child Health Hospital, Wuhan University School of Basic Medical Sciences-Weifang Children's Neurological Diseases and Innovation Transformation Joint Research Center, Weifang, 261011, Shandong, China. ydukongjian@163.com.

Funding

Natural Science Foundation of Shandong Province Grant No. ZR2019BH056
6 · The paper itself

Abstract

backgroundThe ketogenic diet (KD) has been shown to effectively reduce seizures. Ketogenic medium-chain triglycerides (MCTs) enhance brain energy metabolism in adults with neurological disorders, but their effect on peripheral metabolites in children with epilepsy is unclear. The function and mechanisms of MCTs in pediatric epilepsy remain poorly understood.

methodsWe performed untargeted LC-MS metabolomics on blood samples from children with epilepsy (n = 14) and healthy controls (n = 20), identifying octanoic acid (OA) as significantly elevated. To explore its potential role, OA was administered in a PTZ-induced seizure model in juvenile mice. Behavioral analysis, Nissl staining, and immunofluorescence demonstrated that OA modulated seizure susceptibility and activated GPR40, a receptor expressed in neurons.

results(1) A total of 518 metabolites were examined in plasma samples, with the top 20 metabolites selected, of which 14 were upregulated and 6 were downregulated. (2) In the PTZ-induced epilepsy model, OA significantly prolonged seizure latency by 59.86 ± 7.032 s (P < 0.0001), without affecting seizure grade or duration. Mechanistically, OA enhanced GPR40 activation and inhibited astrocyte activation in the hippocampus.

conclusionThis study identified and validated peripheral blood metabolites in children with epilepsy. OA was found to exert a protective effect via GPR40 activation, enhancing neuroprotection. These findings suggest that OA may play a critical role in neuroprotection and could serve as a potential therapeutic target for pediatric epilepsy.

Indexed as

BiomarkersEpilepsyMetabolomicsAdolescentAnimalsAstrocytesCaprylatesChildChild, PreschoolDisease Models, AnimalFemaleHippocampusHumansMaleMiceReceptors, G-Protein-CoupledBiomarkersCaprylatesoctanoic acidReceptors, G-Protein-CoupledEpilepsyGPR40MarkersMetabolomicsOctanoic acid

Identifiers

PMID41024160
PMCPMC12482065

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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.