Evidence map›Paper›PMID 39427219›Full record

ArticleGut pathogens2024

Fecal glycoprotein 2 is a marker of gut microbiota dysbiosis and systemic inflammation.

Fabian Frost, Stefan Weiss, Johannes Hertel, Malte Rühlemann, Corinna Bang, Andre Franke, Matthias Nauck, Marcus Dörr, Henry Völzke, Dirk Roggenbuck and 7 more

Abstract read
In one paragraph

Article in Gut pathogens, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

17 authors.

Fabian FrostDepartment of Medicine A, University Medicine Greifswald, Ferdinand-Sauerbruch- Straße, 17475, Greifswald, Germany.
Stefan WeissDepartment of Medicine A, University Medicine Greifswald, Ferdinand-Sauerbruch- Straße, 17475, Greifswald, Germany.
Johannes HertelDepartment of Psychiatry and Psychotherapy, University Medicine Greifswald, Greifswald, Germany.
Malte RühlemannInstitute of Clinical Molecular Biology, Kiel University, Kiel, Germany.
Corinna BangInstitute of Clinical Molecular Biology, Kiel University, Kiel, Germany.
Andre FrankeInstitute of Clinical Molecular Biology, Kiel University, Kiel, Germany.
Matthias NauckInstitute of Clinical Chemistry and Laboratory Medicine, University Medicine Greifswald, Greifswald, Germany.
Marcus DörrDepartment of Internal Medicine B, University Medicine Greifswald, Greifswald, Germany.
Henry VölzkeInstitute for Community Medicine, University Medicine Greifswald, Greifswald, Germany.
Dirk RoggenbuckInstitute of Biotechnology, Faculty Environment and Natural Sciences, Brandenburg University of Technology Cottbus-Senftenberg, Senftenberg, Germany.
Peter SchierackInstitute of Biotechnology, Faculty Environment and Natural Sciences, Brandenburg University of Technology Cottbus-Senftenberg, Senftenberg, Germany.
Uwe VölkerDepartment of Functional Genomics, Interfaculty Institute for Genetics and Functional Genomics, University Medicine Greifswald, Greifswald, Germany.
Georg HomuthDepartment of Functional Genomics, Interfaculty Institute for Genetics and Functional Genomics, University Medicine Greifswald, Greifswald, Germany.
Ali A AghdassiDepartment of Medicine A, University Medicine Greifswald, Ferdinand-Sauerbruch- Straße, 17475, Greifswald, Germany.
Matthias SendlerDepartment of Medicine A, University Medicine Greifswald, Ferdinand-Sauerbruch- Straße, 17475, Greifswald, Germany.
Markus M LerchDepartment of Medicine A, University Medicine Greifswald, Ferdinand-Sauerbruch- Straße, 17475, Greifswald, Germany.
Frank U WeissDepartment of Medicine A, University Medicine Greifswald, Ferdinand-Sauerbruch- Straße, 17475, Greifswald, Germany. ulrich.weiss@med.uni-greifswald.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAntimicrobial autoantigenic glycoprotein 2 (GP2) is an important component of the innate immune system which originates from the exocrine pancreas as well as from the small intestines. The relationship of GP2 with the intestinal microbiome as well as the systemic implications of increased fecal GP2 levels are, however, still unclear. Therefore, fecal samples from 2,812 individuals of the Study of Health in Pomerania (SHIP) were collected to determine GP2 levels (enzyme-linked immunosorbent assay) and gut microbiota profiles (16 S rRNA gene sequencing). These data were correlated and associated with highly standardised and comprehensive phenotypic data of the study participants.

resultsFecal GP2 levels were increased in individuals with higher body mass index and smokers, whereas lower levels were found in case of preserved exocrine pancreatic function, female sex or a healthier diet. Moreover, higher GP2 levels were associated with increased serum levels of high-sensitivity C-reactive protein, loss of gut microbial diversity and an increase of potentially detrimental bacteria (Streptococcus, Haemophilus, Clostridium XIVa, or Collinsella). At the same time, predicted microbial pathways for the biosynthesis of beneficial short-chain fatty acids or lactic acid were depleted in individuals with high fecal GP2. Of note, GP2 exhibited a stronger association to overall microbiome variation than calprotectin.

conclusionFecal GP2 is a biomarker of gut microbiota dysbiosis and associated with increased systemic inflammation. The intestines may be more important as origin for GP2 than pancreatic acinar cells. Future studies need to investigate the potential clinical value in disease specific patient cohorts.

Indexed as

BiomarkerExocrineGP2IBDPancreasPancreatitis

Identifiers

PMID39427219
PMCPMC11490104

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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.