Evidence map›Paper›PMID 26401073›Full record

Observational studyWorld journal of gastroenterology2015

Increased catabolism and decreased unsaturation of ganglioside in patients with inflammatory bowel disease.

John J Miklavcic, Tasha D L Hart, Gordon M Lees, Glen K Shoemaker, Kareena L Schnabl, Bodil M K Larsen, Oliver F Bathe, Alan B R Thomson, Vera C Mazurak, M Tom Clandinin

Open access · hybridAbstract readObservational Study
In one paragraph

Observational study in World journal of gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 30% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Neu3 neuraminidase induction triggers intestinal inflammation and colitis in a model of recurrent human food-poisoning.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  7. Review
  8. Article
  9. Article
  10. 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

10 authors at 3 institutions in 1 country.

John J MiklavcicJohn J Miklavcic, Glen K Shoemaker, Vera C Mazurak, M Tom Clandinin, Alberta Institute for Human Nutrition, University of Alberta, Edmonton AB T6G 2R1, Canada.
Tasha D L HartJohn J Miklavcic, Glen K Shoemaker, Vera C Mazurak, M Tom Clandinin, Alberta Institute for Human Nutrition, University of Alberta, Edmonton AB T6G 2R1, Canada.
Gordon M LeesJohn J Miklavcic, Glen K Shoemaker, Vera C Mazurak, M Tom Clandinin, Alberta Institute for Human Nutrition, University of Alberta, Edmonton AB T6G 2R1, Canada.
Glen K ShoemakerJohn J Miklavcic, Glen K Shoemaker, Vera C Mazurak, M Tom Clandinin, Alberta Institute for Human Nutrition, University of Alberta, Edmonton AB T6G 2R1, Canada.
Kareena L SchnablJohn J Miklavcic, Glen K Shoemaker, Vera C Mazurak, M Tom Clandinin, Alberta Institute for Human Nutrition, University of Alberta, Edmonton AB T6G 2R1, Canada.
Bodil M K LarsenJohn J Miklavcic, Glen K Shoemaker, Vera C Mazurak, M Tom Clandinin, Alberta Institute for Human Nutrition, University of Alberta, Edmonton AB T6G 2R1, Canada.
Oliver F BatheJohn J Miklavcic, Glen K Shoemaker, Vera C Mazurak, M Tom Clandinin, Alberta Institute for Human Nutrition, University of Alberta, Edmonton AB T6G 2R1, Canada.
Alan B R ThomsonJohn J Miklavcic, Glen K Shoemaker, Vera C Mazurak, M Tom Clandinin, Alberta Institute for Human Nutrition, University of Alberta, Edmonton AB T6G 2R1, Canada.
Vera C MazurakJohn J Miklavcic, Glen K Shoemaker, Vera C Mazurak, M Tom Clandinin, Alberta Institute for Human Nutrition, University of Alberta, Edmonton AB T6G 2R1, Canada.
M Tom ClandininJohn J Miklavcic, Glen K Shoemaker, Vera C Mazurak, M Tom Clandinin, Alberta Institute for Human Nutrition, University of Alberta, Edmonton AB T6G 2R1, Canada.
University of Alberta · CAAlberta Health Services · CAWestern University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo investigate whether accelerated catabolism of ganglioside and decreased ganglioside content contribute to the etiology of pro-inflammatory intestinal disease.

methodsIntestinal mucosa from terminal ileum or colon was obtained from patients with ulcerative colitis or inflammatory Crohn's disease (n = 11) undergoing bowel resection and compared to control samples of normal intestine from patients with benign colon polyps (n = 6) and colorectal cancer (n = 12) in this observational case-control study. Gangliosides and phospholipids of intestinal mucosa were characterized by class and ceramide or fatty acid composition using liquid chromatography triple-quad mass spectrometry. Content and composition of ganglioside classes GM1, GM3, GD3, GD1a, GT1 and GT3 were compared among subject groups. Content and composition of phospholipid classes phosphatidylcholine (PC) and phosphatidylethanolamine were compared among subject groups. Unsaturation index of individual ganglioside and phospholipid classes was computed and compared among subject groups. Ganglioside catabolism enzymes beta-hexosaminidase A (HEXA) and sialidase-3 (NEU3) were measured in intestinal mucosa using western blot and compared among subject groups.

resultsRelative GM3 ganglioside content was 2-fold higher (P < 0.05) in intestine from patients with inflammatory bowel disease (IBD) compared to control intestine. The quantity of GM3 and ratio of GM3/GD3 was also higher in IBD intestine than control tissue (P < 0.05). Control intestine exhibited 3-fold higher (P < 0.01) relative GD1a ganglioside content than IBD intestine. GD3 and GD1a species of ganglioside containing three unsaturated bonds were present in control intestine, but were not detected in IBD intestine. The relative content of PC containing more than two unsaturated bonds was 30% lower in IBD intestine than control intestine (P < 0.05). The relative content of HEXA in IBD intestine was increased 1.7-fold (P < 0.05) and NEU3 was increased 8.3-fold (P < 0.01) compared to normal intestine. Intestinal mucosa in IBD is characterized by increased GM3 content, decreased GD1a, and a reduction in polyunsaturated fatty acid constituents in GD3, GD1a and PC.

conclusionThis study suggests a new paradigm by proposing that IBD occurs as a consequence of increased metabolism of specific gangliosides.

Indexed as

beta-Hexosaminidase alpha ChainCase-Control StudiesColitis, UlcerativeColonCrohn DiseaseFatty Acids, UnsaturatedGangliosidesG(M3) GangliosideHumansIleumIntestinal MucosaNeuraminidasePhosphatidylcholinesPhosphatidylethanolaminesbeta-Hexosaminidase alpha ChainFatty Acids, Unsaturatedganglioside, GD1aganglioside, GD3GangliosidesG(M3) GangliosideHEXA protein, humanNeu3 protein, humanNeuraminidasePhosphatidylcholinesPhosphatidylethanolaminesCrohn diseaseFatty acidGangliosideInflammationInflammatory bowel diseaseLipidNutritionPhospholipidUlcerative colitis

Identifiers

PMID26401073
PMCPMC4572789
OpenAlexW2413500179

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.