Evidence map›Paper›PMID 38961712›Full record

ArticleGut microbes

Oral histidine affects gut microbiota and MAIT cells improving glycemic control in type 2 diabetes patients.

Moritz V Warmbrunn, Ilias Attaye, Judith Aron-Wisnewsky, Elena Rampanelli, Eduard W J van der Vossen, Youling Hao, Annefleur Koopen, Per-Olof Bergh, Daniela Stols-Gonçalves, Nadia Mohamed and 13 more

Abstract read
In one paragraph

Article in Gut microbes. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

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  16. Alterations in the Gut Microbiota Composition in Obesity with and without Type 2 Diabetes: A Pilot Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
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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

23 authors.

Moritz V WarmbrunnDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Ilias AttayeDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Judith Aron-WisnewskyAssistante Publique Hôpitaux de Paris, Nutrition Department, Pitié-Salpêtrière Hospital, CRNH Ile de France, Paris, France.
Elena RampanelliDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Eduard W J van der VossenDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Youling HaoDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Annefleur KoopenDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Per-Olof BerghDepartment of Molecular and Clinical Medicine/Wallenberg Laboratory, Institute of Medicine, University of Gothenburg and Sahlgrenska, Gothenburg, Sweden.
Daniela Stols-GonçalvesDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Nadia MohamedDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Marleen KemperDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Xanthe VerdoesDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Koen WortelboerDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Mark DavidsDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Eugeni BeldaAssistante Publique Hôpitaux de Paris, Nutrition Department, Pitié-Salpêtrière Hospital, CRNH Ile de France, Paris, France.
Sébastien AndréAssistante Publique Hôpitaux de Paris, Nutrition Department, Pitié-Salpêtrière Hospital, CRNH Ile de France, Paris, France.
Stanley HazenDepartment of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Karine ClementAssistante Publique Hôpitaux de Paris, Nutrition Department, Pitié-Salpêtrière Hospital, CRNH Ile de France, Paris, France.
Bert GroenDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Daniel H van RaalteDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Hilde HerremaDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Fredrik BackhedDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Max NieuwdorpDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amino acids, metabolized by host cells as well as commensal gut bacteria, have signaling effects on host metabolism. Oral supplementation of the essential amino acid histidine has been shown to exert metabolic benefits. To investigate whether dietary histidine aids glycemic control, we performed a case-controlled parallel clinical intervention study in participants with type 2 diabetes (T2D) and healthy controls. Participants received oral histidine for seven weeks. After 2 weeks of histidine supplementation, the microbiome was depleted by antibiotics to determine the microbial contribution to histidine metabolism. We assessed glycemic control, immunophenotyping of peripheral blood mononucelar cells (PBMC), DNA methylation of PBMCs and fecal gut microbiota composition. Histidine improves several markers of glycemic control, including postprandial glucose levels with a concordant increase in the proportion of MAIT cells after two weeks of histidine supplementation. The increase in MAIT cells was associated with changes in gut microbial pathways such as riboflavin biosynthesis and epigenetic changes in the amino acid transporter SLC7A5. Associations between the microbiome and MAIT cells were replicated in the MetaCardis cohort. We propose a conceptual framework for how oral histidine may affect MAIT cells via altered gut microbiota composition and SLC7A5 expression in MAIT cells directly and thereby influencing glycemic control. Future studies should focus on the role of flavin biosynthesis intermediates and SLC7A5 modulation in MAIT cells to modulate glycemic control.

Indexed as

Diabetes Mellitus, Type 2Gastrointestinal MicrobiomeHistidineMucosal-Associated Invariant T CellsAdministration, OralAdultAgedBacteriaBlood GlucoseCase-Control StudiesDietary SupplementsDNA MethylationFecesFemaleGlycemic ControlHumansBlood GlucoseHistidinediabeteshistidineinsulin resistanceMicrobiomemonocytes

Identifiers

PMID38961712
PMCPMC11225920

What OpenQuestion holds

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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.