Evidence map›Paper›PMID 25550456›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2015

Gut microbes promote colonic serotonin production through an effect of short-chain fatty acids on enterochromaffin cells.

Christopher S Reigstad, Charles E Salmonson, John F Rainey, Joseph H Szurszewski, David R Linden, Justin L Sonnenburg, Gianrico Farrugia, Purna C Kashyap

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 693 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
693citing papers in PubMed, 8 pooled it
24.2field-weighted citation impact, top 1% 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

693 citing papers in PubMed, 8 syntheses or guidelines pooled it, 1,238 citations in OpenAlex.

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  20. Irritable bowel syndrome.Nature reviews. Disease primers · 2026
    Review

633 more citing papers are in PubMed but not listed here.

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

8 authors at 3 institutions in 1 country.

Christopher S Reigstad*Enteric NeuroScience Program, Division of Gastroenterology and Hepatology, and Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA; and Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California, USA.
Charles E Salmonson*Enteric NeuroScience Program, Division of Gastroenterology and Hepatology, and Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA; and Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California, USA.
John F Rainey*Enteric NeuroScience Program, Division of Gastroenterology and Hepatology, and Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA; and Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California, USA.
Joseph H Szurszewski*Enteric NeuroScience Program, Division of Gastroenterology and Hepatology, and Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA; and Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California, USA.
David R Linden*Enteric NeuroScience Program, Division of Gastroenterology and Hepatology, and Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA; and Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California, USA.
Justin L Sonnenburg*Enteric NeuroScience Program, Division of Gastroenterology and Hepatology, and Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA; and Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California, USA.
Gianrico Farrugia*Enteric NeuroScience Program, Division of Gastroenterology and Hepatology, and Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA; and Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California, USA.
Purna C Kashyap*Enteric NeuroScience Program, Division of Gastroenterology and Hepatology, and Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA; and Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California, USA kashyap.purna@mayo.edu.
Mayo Clinic in Florida · USMayo Clinic · USStanford University · US

Funding

PILOT AND FEASIBILTY PROGRAMP30DK084567 · NIDDK · MAYO CLINIC ROCHESTER · PI Tamas Ordog · 2009 to 2026
$22.2M
Impact of Diet on Intestinal Microbiota-Host DynamicsR01DK085025 · NIDDK · STANFORD UNIVERSITY · PI JUSTIN L SONNENBURG · 2010 to 2026
$6.4M
MECHANISMS OF ALTERATION OF GASTROINTESTINAL MOTILITY BY GUT MICROBIOTAK08DK100638 · NIDDK · MAYO CLINIC ROCHESTER · PI KASHYAP, PURNA C · 2014 to 2017
$610k
NIDDK NIH HHS K08 DK100638NIDDK NIH HHS K08DK100638NIDDK NIH HHS P30 DK084567NIDDK NIH HHS P30DK84567NIDDK NIH HHS R01 DK085025
6 · The paper itself

Abstract

Gut microbiota alterations have been described in several diseases with altered gastrointestinal (GI) motility, and awareness is increasing regarding the role of the gut microbiome in modulating GI function. Serotonin [5-hydroxytryptamine (5-HT)] is a key regulator of GI motility and secretion. To determine the relationship among gut microbes, colonic contractility, and host serotonergic gene expression, we evaluated mice that were germ-free (GF) or humanized (HM; ex-GF colonized with human gut microbiota). 5-HT reduced contractile duration in both GF and HM colons. Microbiota from HM and conventionally raised (CR) mice significantly increased colonic mRNAs Tph1 [(tryptophan hydroxylase) 1, rate limiting for mucosal 5-HT synthesis; P < 0.01] and chromogranin A (neuroendocrine secretion; P < 0.01), with no effect on monoamine oxidase A (serotonin catabolism), serotonin receptor 5-HT4, or mouse serotonin transporter. HM and CR mice also had increased colonic Tph1 protein (P < 0.05) and 5-HT concentrations (GF, 17 ± 3 ng/mg; HM, 25 ± 2 ng/mg; and CR, 35 ± 3 ng/mg; P < 0.05). Enterochromaffin (EC) cell numbers (cells producing 5-HT) were unchanged. Short-chain fatty acids (SCFAs) promoted TPH1 transcription in BON cells (human EC cell model). Thus, gut microbiota acting through SCFAs are important determinants of enteric 5-HT production and homeostasis.

Indexed as

AnimalsCell CountCell LineChromogranin AColonDigestive SystemEnterochromaffin CellsFatty Acids, VolatileFemaleGastrointestinal MotilityGerm-Free LifeHumansMaleMiceMicrobiotaRNA, MessengerChromogranin Achromogranin A, mouseFatty Acids, VolatileRNA, MessengerSerotoninTPH1 protein, humanTph1 protein, mouseTryptophan Hydroxylase5-hydroxytryptaminegnotobioticgut motilityhost-microbe interactionmicrobiome

Identifiers

PMID25550456
PMCPMC4396604
OpenAlexW1997608252

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.