Evidence map›Paper›PMID 29028817›Full record

ArticlePloS one2017

Mitochondrial dysfunction in the gastrointestinal mucosa of children with autism: A blinded case-control study.

Shannon Rose, Sirish C Bennuri, Katherine F Murray, Timothy Buie, Harland Winter, Richard Eugene Frye

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 86 citations in OpenAlex.

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  19. Recent advances in mitochondrial diseases: From molecular insights to therapeutic perspectives.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2022
    Review
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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

6 authors at 3 institutions in 1 country.

Shannon RoseAutism Research Program, Arkansas Children's Research Institute, Little Rock, Arkansas, United States of America.
Sirish C BennuriAutism Research Program, Arkansas Children's Research Institute, Little Rock, Arkansas, United States of America.
Katherine F MurrayDepartment of Pediatric Gastroenterology and Nutrition, MassGeneral Hospital for Children, Boston, Massachusetts, United States of America.
Timothy BuieDepartment of Gastroenterology, Boston Children's Hospital, Boston, Massachusetts, United States of America.
Harland WinterDepartment of Pediatric Gastroenterology and Nutrition, MassGeneral Hospital for Children, Boston, Massachusetts, United States of America.
Richard Eugene FryeAutism Research Program, Arkansas Children's Research Institute, Little Rock, Arkansas, United States of America.ORCID http://orcid.org/0000-0003-4442-2937
Arkansas Children's Hospital · USMassachusetts General Hospital · USBoston Children's Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastrointestinal (GI) symptoms are prevalent in autism spectrum disorder (ASD) but the pathophysiology is poorly understood. Imbalances in the enteric microbiome have been associated with ASD and can cause GI dysfunction potentially through disruption of mitochondrial function as microbiome metabolites modulate mitochondrial function and mitochondrial dysfunction is highly associated with GI symptoms. In this study, we compared mitochondrial function in rectal and cecum biopsies under the assumption that certain microbiome metabolites, such as butyrate and propionic acid, are more abundant in the cecum as compared to the rectum. Rectal and cecum mucosal biopsies were collected during elective diagnostic colonoscopy. Using a single-blind case-control design, complex I and IV and citrate synthase activities and complex I-V protein quantity from 10 children with ASD, 10 children with Crohn's disease and 10 neurotypical children with nonspecific GI complaints were measured. The protein for all complexes, except complex II, in the cecum as compared to the rectum was significantly higher in ASD samples as compared to other groups. For both rectal and cecum biopsies, ASD samples demonstrated higher complex I activity, but not complex IV or citrate synthase activity, compared to other groups. Mitochondrial function in the gut mucosa from children with ASD was found to be significantly different than other groups who manifested similar GI symptomatology suggesting a unique pathophysiology for GI symptoms in children with ASD. Abnormalities localized to the cecum suggest a role for imbalances in the microbiome, potentially in the production of butyrate, in children with ASD.

Indexed as

AdolescentAutistic DisorderCase-Control StudiesChildElectron Transport Chain Complex ProteinsFemaleGastrointestinal TractHumansMaleElectron Transport Chain Complex Proteins

Identifiers

PMID29028817
PMCPMC5640251
OpenAlexW2762265991

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.