Evidence map›Paper›PMID 34599147›Full record

ArticleTranslational psychiatry2021

Alterations of kynurenine pathway in alcohol use disorder and abstinence: a link with gut microbiota, peripheral inflammation and psychological symptoms.

Sophie Leclercq, Markus Schwarz, Nathalie M Delzenne, Peter Stärkel, Philippe de Timary

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06636227 (Optimal Dosing, Tolerability, and Initial Efficacy of Diclofenac as a KMO Inhibitor in Individuals With Alcohol Use Disorder), which is not on this map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
4.3field-weighted citation impact, top 4% 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.

NCT06636227 phase1recruitingnot on this mapstarted 2024, after this paper: background citation

Optimal Dosing, Tolerability, and Initial Efficacy of Diclofenac as a KMO Inhibitor in Individuals With Alcohol Use Disorder

TypeinterventionalSponsorUniversity of Maryland, BaltimoreRan2024 to 2026Enrolled24ConditionsAlcohol Use Disorder (AUD), Alcohol-Related DisordersArmsDiclofenac 100mg, Diclofenac 75mg, Diclofenac 50mg, Placebo control
3 · Its place in the literature

Who cites it

58 citing papers in PubMed, 86 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

5 authors at 3 institutions in 2 countries.

Sophie LeclercqInstitute of Neuroscience, Université catholique de Louvain (UCLouvain), Brussels, Belgium.ORCID 0000-0002-2894-5220
Markus SchwarzInstitute of Laboratory Medicine, LMU Klinikum Munich, Munich, Germany.
Nathalie M DelzenneMetabolism and Nutrition Research Group, Louvain Drug Research Institute, Université catholique de Louvain (UCLouvain), Brussels, Belgium.ORCID 0000-0003-2115-6082
Peter StärkelLaboratory of Hepato-Gastroenterology, Institute of Experimental and Clinical Research, Université catholique de Louvain (UCLouvain), Brussels, Belgium.ORCID 0000-0003-2938-4442
Philippe de TimaryInstitute of Neuroscience, Université catholique de Louvain (UCLouvain), Brussels, Belgium. philippe.detimary@uclouvain.be.ORCID 0000-0003-3956-6848
Cliniques Universitaires Saint-Luc · BEUCLouvain · BELMU Klinikum · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The gut-brain communication is mostly driven by the immune, metabolic and neural pathways which remained poorly explored in patients with alcohol use disorder (AUD). The metabolites arising from the tryptophan-kynurenine pathway have gained considerable attention since they are at the interface between intestinal bacteria, host immune response and brain functions. This study described the circulating levels of kynurenine metabolites in AUD patients, at the onset (T1) and end (T2) of a 3-week detoxification program, and tested correlations between those metabolites and inflammatory markers, the gut microbiota and the psychological symptoms. Increased concentration of the neurotoxic metabolite quinolinic acid (QUIN) and decreased levels of the neuroprotector metabolite kynurenic acid (KYNA) which both modulate glutamatergic neurotransmission were observed in AUD patients, particularly at T2. The inflammatory marker hsCRP was associated with several metabolic ratios of the kynurenine pathway. Tryptophan, KYNA and QUIN were correlated with depression, alcohol craving and reaction time, respectively. Analysis of gut microbiota revealed that bacteria known as short-chain fatty acid producers, as well as bacterial metabolites including butyrate and medium-chain fatty acids were associated with some metabolites of the tryptophan-kynurenine pathway. Targeting the glutamatergic neurotransmission through the modulation of the kynurenine pathway, by manipulating the gut microbiota, might represent an interesting alternative for modulating alcohol-related behavior.

Indexed as

AlcoholismGastrointestinal MicrobiomeHumansInflammationKynurenic AcidKynurenineQuinolinic AcidKynurenic AcidKynurenineQuinolinic Acid

Identifiers

PMID34599147
PMCPMC8486842
OpenAlexW3203796687

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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.