Evidence map›Paper›PMID 35487889›Full record

ArticleTranslational psychiatry2022

Effects of pharmacological treatment on metabolomic alterations in animal models of depression.

Juncai Pu, Yiyun Liu, Siwen Gui, Lu Tian, Yue Yu, Dongfang Wang, Xiaogang Zhong, Weiyi Chen, Xiaopeng Chen, Yue Chen and 6 more

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.7field-weighted citation impact, top 8% 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

28 citing papers in PubMed, 44 citations in OpenAlex.

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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

16 authors at 2 institutions in 2 countries.

Juncai Pu *Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Yiyun Liu *NHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Siwen GuiNHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Lu TianNHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Yue YuDepartment of Health Sciences Research, Mayo Clinic, MN, 55901, USA.
Dongfang WangNHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.ORCID 0000-0002-7517-3972
Xiaogang ZhongNHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.ORCID 0000-0002-6648-4461
Weiyi ChenDepartment of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Xiaopeng ChenDepartment of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Yue ChenDepartment of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Xiang ChenDepartment of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Xue GongDepartment of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Lanxiang LiuDepartment of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Wenxia LiDepartment of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Haiyang WangDepartment of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Peng XieDepartment of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China. xiepeng@cqmu.edu.cn.ORCID 0000-0002-0081-6048
The Affiliated Yongchuan Hospital of Chongqing Medical University · CNMayo Clinic Health System · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Numerous studies have investigated metabolite alterations resulting from pharmacological treatment in depression models although few quantitative studies explored metabolites exhibiting constant alterations. This study aimed to identify consistently dysregulated metabolites across such studies using a knowledgebase-driven approach. This study was based on 157 studies that identified an assembly of 2757 differential metabolites in the brain, blood, urine, liver, and feces samples of depression models with pharmacological medication. The use of a vote-counting approach to identify consistently upregulated and downregulated metabolites showed that serotonin, dopamine, norepinephrine, gamma-aminobutyric acid, anandamide, tryptophan, hypoxanthine, and 3-methoxytyramine were upregulated in the brain, while quinolinic acid, glutamic acid, 5-hydroxyindoleacetic acid, myo-inositol, lactic acid, and the kynurenine/tryptophan ratio were downregulated. Circulating levels of trimethylamine N-oxide, isoleucine, leucine, tryptophan, creatine, serotonin, valine, betaine, and low-density lipoprotein were elevated. In contrast, levels of alpha-D-glucose, lactic acid, N-acetyl glycoprotein, glutamine, beta-D-glucose, corticosterone, alanine, phenylacetylglycine, glycine, high-density lipoprotein, arachidonic acid, myo-inositol, allantoin, and taurine were decreased. Moreover, 12 metabolites in urine and nine metabolites in the liver were dysregulated after treatment. Pharmacological treatment also increased fecal levels of butyric acid, acetic acid, propionic acid, and isovaleric acid. Collectively, metabolite disturbances induced by depression were reversed by pharmacological treatment. Pharmacological medication reversed the reduction of brain neurotransmitters caused by depression, modulated disturbance of the tryptophan-kynurenine pathway and inflammatory activation, and alleviated abnormalities of amino acid metabolism, energy metabolism, lipid metabolism, and gut microbiota-derived metabolites.

Indexed as

KynurenineTryptophanAnimalsDepressionGlucoseInositolLactic AcidModels, AnimalSerotoninGlucoseInositolKynurenineLactic AcidSerotoninTryptophan

Identifiers

PMID35487889
PMCPMC9055046
OpenAlexW4225121626

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.