Evidence map›Paper›PMID 27421719›Full record

ReviewImmunologic research2017

On the pathogenesis of insulin-dependent diabetes mellitus: the role of microbiota.

Elena Gianchecchi, Alessandra Fierabracci

Abstract readReview
PubMed Publisher
In one paragraph

Review in Immunologic research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Review
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  3. Observational
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  10. Article
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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

2 authors.

Elena GianchecchiVismederi Srl, Siena, Italy.
Alessandra FierabracciInfectivology and Clinical Trials Area, Bambino Gesù Children's Hospital, IRCCS, Viale S. Paolo 15, 00146, Rome, Italy. alessandra.fierabracci@opbg.net.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 1 diabetes (T1D) is an autoimmune disorder characterized by the selective destruction of insulin-producing β cells as result of a complex interplay between genetic, stochastic and environmental factors in genetically susceptible individuals. An increasing amount of experimental data from animal models and humans has supported the role played by imbalanced gut microbiome in T1D pathogenesis. The commensal intestinal microbiota is fundamental for several physiologic mechanisms, including the establishment of immune homeostasis. Alterations in its composition have been correlated to changes in the gut immune system, including defective tolerance to food antigens, intestinal inflammation and enhanced gut permeability. Early findings reported differences in the intestinal microbiome of subjects affected by prediabetes or overt disease compared to healthy individuals. The present review focuses on microbiota-host homeostasis, its alterations, factors that influence microbiome composition and discusses their putative correlation with T1D development. Further studies are necessary to clarify the role played by microbiota modifications in the processes that cause enhanced permeability and the autoimmune mechanisms responsible for T1D onset.

Indexed as

Gastrointestinal MicrobiomeAnimalsDiabetes Mellitus, Type 1HumansImmunity, MucosalAutoimmune disordersEnvironmental factorsEtiopathogenesisMicrobiomePrevention treatmentT1D

Identifiers

PMID27421719

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.