Evidence map›Paper›PMID 32162764›Full record

ReviewDiabetes/metabolism research and reviews2020

Zonulin as a potential putative biomarker of risk for shared type 1 diabetes and celiac disease autoimmunity.

Lauren K Wood Heickman, Mark D DeBoer, Alessio Fasano

Open access · greenAbstract readReview
In one paragraph

Review in Diabetes/metabolism research and reviews, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
6.7field-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

38 citing papers in PubMed, 69 citations in OpenAlex.

  1. Review
  2. Article
  3. OralWorld journal of diabetes · 2025
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Global Approach to Follow-Up of Celiac Disease.Foods (Basel, Switzerland) · 2024
    Review
  13. Article
  14. Article
  15. Relationship between pathogenicFrontiers in cellular and infection microbiology · 2024
    Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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

3 authors at 2 institutions in 2 countries.

Lauren K Wood HeickmanDepartment of Pediatrics, Division of Endocrinology, University of Virginia, Charlottesville, Virginia, USA.ORCID 0000-0003-0998-3085
Mark D DeBoerDepartment of Pediatrics, Division of Endocrinology, University of Virginia, Charlottesville, Virginia, USA.
Alessio FasanoMucosal Immunology and Biology Research Center, Division of Pediatric Gastroenterology and Nutrition, Massachusetts General Hospital for Children, Harvard Medical School Boston, Boston, Massachusetts, USA.
University of Virginia · USBoston Children's Hospital · US

Funding

Zonulin as a putative biomarker of risk in Type 1 DiabetesF32DK117607 · NIDDK · UNIVERSITY OF VIRGINIA · PI WOOD HEICKMAN, LAUREN KAITLIN · 2018 to 2019
$106k
NIDDK NIH HHS F32 DK117607
6 · The paper itself

Abstract

The incidence of type 1 diabetes (T1D) is increasing annually, in addition to other childhood-onset autoimmune diseases. This review is inspired by recent strides in research defining the pathophysiology of autoimmunity in celiac disease, a disease that has significant genetic overlap with T1D. Population genetic studies have demonstrated an increased proportion of newly diagnosed young children with T1D also have a higher genetic risk of celiac disease, suggesting that shared environmental risk factors are driving the incidence of both diseases. The small intestine barrier forms a tightly regulated interface of the immune system with the outside world and largely controls the mucosal immune response to non-self-antigens, dictating the balance between tolerance and immune response. Zonulin is the only known physiological modulator of the intercellular tight junctions, important in antigen trafficking, and therefore, is a key player in regulation of the mucosal immune response. While usually tightly controlled, when the zonulin pathway is dysregulated by changes in microbiome composition and function, antigen trafficking control is lost, leading to loss of mucosal tolerance in genetically susceptible individuals. The tenant of this hypothesis is that loss of tolerance would not occur if the zonulin-dependent intestinal barrier function is restored, thereby preventing the influence of environmental triggers in individuals genetically susceptible to autoimmunity. This review outlines the current research and a structured hypothesis on how a dysregulated small intestinal epithelial barrier, a "leaky gut," may be important in the pathogenesis of autoimmunity in certain individuals at risk of both T1D and celiac disease.

Indexed as

AnimalsAutoimmune DiseasesBiomarkersCeliac DiseaseDiabetes Mellitus, Type 1HaptoglobinsHumansPrognosisProtein PrecursorsRisk FactorsBiomarkersHaptoglobinsProtein Precursorszonulinautoimmunityceliac diseaseintestinal permeabilityleaky guttype 1 diabetesZonulin

Identifiers

PMID32162764
PMCPMC7340576
OpenAlexW3011315383

What OpenQuestion holds

Textmetadata
LicenceTDM
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.