Evidence map›Paper›PMID 18820210›Full record

ReviewDiabetes2008

The "perfect storm" for type 1 diabetes: the complex interplay between intestinal microbiota, gut permeability, and mucosal immunity.

Outi Vaarala, Mark A Atkinson, Josef Neu

Registry-linked trialOpen access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Diabetes, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03032354 (Effect of Lactobacillus Rhamnosus GG and Bifidobacterium Lactis BB 12 on Beta-cell Function in Children With Newly Diagnosed Type 1 Diabetes - a Randomized Controlled Trial), which is not on this map. Cited by 243 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
243citing papers in PubMed, 2 pooled it
16.0field-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.

NCT03032354 phase4unknown statusnot on this mapstarted 2017, after this paper: background citation

Effect of Lactobacillus Rhamnosus GG and Bifidobacterium Lactis BB 12 on Beta-cell Function in Children With Newly Diagnosed Type 1 Diabetes - a Randomized Controlled Trial

TypeinterventionalSponsorMedical University of WarsawRan2017 to 2018Enrolled96ConditionsDiabetes Mellitus, Type 1ArmsLactobacillus rhamnosus GG and Bifidobacterium lactis BB12, Placebo, (Placebo group)
3 · Its place in the literature

Who cites it

243 citing papers in PubMed, 2 syntheses or guidelines pooled it, 491 citations in OpenAlex.

  1. Pooled it
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  10. Extracellular vesicles fromFrontiers in immunology · 2026
    Article
  11. Review
  12. OralWorld journal of diabetes · 2025
    Article
  13. Observational
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183 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

3 authors at 3 institutions in 3 countries.

Outi VaaralaLaboratory for Immunobiology, Department of Viral Diseases and Immunology, National Public Health Institute, Helsinki, Finland. outi.vaarala@ktl.fi
Mark A Atkinson
Josef Neu
Florida College · USInstitute for Molecular Medicine Finland · FIUniversity of Florida · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is often stated that type 1 diabetes results from a complex interplay between varying degrees of genetic susceptibility and environmental factors. While agreeing with this principal, our desire is that this Perspectives article will highlight another complex interplay potentially associated with this disease involving facets related to the gut, one where individual factors that, upon their interaction with each another, form a "perfect storm" critical to the development of type 1 diabetes. This trio of factors includes an aberrant intestinal microbiota, a "leaky" intestinal mucosal barrier, and altered intestinal immune responsiveness. Studies examining the microecology of the gastrointestinal tract have identified specific microorganisms whose presence appears related (either quantitatively or qualitatively) to disease; in type 1 diabetes, a role for microflora in the pathogenesis of disease has recently been suggested. Increased intestinal permeability has also been observed in animal models of type 1 diabetes as well as in humans with or at increased-risk for the disease. Finally, an altered mucosal immune system has been associated with the disease and is likely a major contributor to the failure to form tolerance, resulting in the autoimmunity that underlies type 1 diabetes. Herein, we discuss the complex interplay between these factors and raise testable hypotheses that form a fertile area for future investigations as to the role of the gut in the pathogenesis and prevention of type 1 diabetes.

Indexed as

AnimalsDiabetes Mellitus, Type 1Gastrointestinal TractHumansImmunity, MucosalIntestinal MucosaModels, Biological

Identifiers

PMID18820210
PMCPMC2551660
OpenAlexW2110785364

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

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.