Evidence map›Paper›PMID 15361491›Full record

ArticleGut2004

Enteropathy precedes type 1 diabetes in the BB rat.

S Graham, P Courtois, W J Malaisse, J Rozing, F W Scott, A Mc I Mowat

Open access · bronzeAbstract read
In one paragraph

Article in Gut, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

34 citing papers in PubMed, 83 citations in OpenAlex.

  1. Trial
  2. IL-22, a vital cytokine in autoimmune diseases.Clinical and experimental immunology · 2024
    Review
  3. Article
  4. Review
  5. Review
  6. Loss of gut barrier integrity triggers activation of islet-reactive T cells and autoimmune diabetes.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Epithelial Barrier Function in Gut-Bone Signaling.Advances in experimental medicine and biology · 2017
    Review
  12. Article
  13. The gut microbiota and Type 1 Diabetes.Clinical immunology (Orlando, Fla.) · 2015
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  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

6 authors at 4 institutions in 3 countries.

S GrahamDepartment of Immunology and Bacteriology, University of Glasgow, Western Infirmary, Glasgow G11 6NT, Scotland, UK.
P Courtois
W J Malaisse
J Rozing
F W Scott
A Mc I Mowat
University Medical Center Groningen · NLUniversity of Glasgow · GBUniversity of Ottawa · CAWestern Infirmary · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsThere is increasing evidence implicating intestinal immune responses to dietary proteins in the pathogenesis of type 1 autoimmune diabetes (T1D). Here we investigated the association between intestinal pathology and dietary factors in T1D by examining the mucosal architecture in the BB rat model.

methodsBB control (BBc) and diabetes prone (BBdp) rats were fed either a diabetes retardant hydrolysed casein based diet or one of two cereal based diets that promote the development of diabetes. Intestinal architecture was assessed in the jejunum by microdissection, histology, and immunohistology, and by measuring peroxidase activity and brush border invertase levels.

resultsEnteropathy was present in BBdp rats soon after weaning, as assessed by increases in crypt length and in the proliferative activity of crypt epithelial cells in the jejunum, and this remained constant until 120 days of age. There was also a decrease in invertase activity, as well as increased numbers of intraepithelial lymphocytes, increased levels of mucosal peroxidase activity, and infiltration of the mucosa by CD4(+) T lymphocytes. Equivalent enteropathy was present at all times in BBdp rats and was not influenced by the nature of the diet or by thymectomy at three weeks at age, procedures which prevent the development of diabetes.

conclusionEnteropathy is a consistent feature in the diabetes prone BB rat but it precedes the onset of insulitis and appears to be due to mechanisms distinct from those which cause diabetes. The beneficial effects of the diabetes retardant hydrolysed casein diet on diabetes are not due to an effect on intestinal architecture per se but mucosal damage may be necessary for the development of autoreactivity in the pancreas.

Indexed as

Animalsbeta-FructofuranosidaseDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1DietFemaleIntestinal DiseasesIntestinal MucosaJejunumMalePrediabetic StateRatsRats, Inbred BBThymus Glandbeta-Fructofuranosidase

Identifiers

PMID15361491
PMCPMC1774253
OpenAlexW2143292560

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.