Evidence map›Paper›PMID 17483192›Full record

ArticleGut2007

Impairment of mitochondrial acetoacetyl CoA thiolase activity in the colonic mucosa of patients with ulcerative colitis.

Srikanth Santhanam, Aparna Venkatraman, Balakrishnan S Ramakrishna

Open access · bronzeAbstract read
In one paragraph

Article in Gut, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 2 pooled it
2.4field-weighted citation impact, top 12% 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

41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 78 citations in OpenAlex.

  1. Pooled it
  2. Role of Mitochondria in Inflammatory Bowel Diseases: A Systematic Review.International journal of molecular sciences · 2023
    Pooled it
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Ulcerative colitis: Timeline to a cure.World journal of gastroenterology · 2025
    Article
  13. Review
  14. Review
  15. Article
  16. Mitochondrial function and gastrointestinal diseases.Nature reviews. Gastroenterology & hepatology · 2024
    Review
  17. Article
  18. Article
  19. Review
  20. Review
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 1 institution in 1 country.

Srikanth SanthanamWellcome Trust Research Laboratory, Department of Gastrointestinal Sciences, Christian Medical College, Vellore, India.
Aparna Venkatraman
Balakrishnan S Ramakrishna
Christian Medical College & Hospital · IN

Funding

Wellcome Trust
6 · The paper itself

Abstract

BACKGROUND AND

aimsButyrate oxidation by colonocytes is impaired in ulcerative colitis. This study examined the activity of enzymes involved in butyrate oxidation in ulcerative colitis.

methodsActivities of mitochondrial acetoacetyl coenzyme A (CoA) thiolase, crotonase and beta-hydroxy butyryl CoA dehydrogenase were estimated spectrophotometrically in rectosigmoid mucosal biopsies from patients with ulcerative colitis and Crohn's colitis, and control subjects undergoing colonoscopy for colon cancer or rectal bleeding.

resultsThe activity of mitochondrial acetoacetyl CoA thiolase was decreased by 80% in ulcerative colitis (3.4 (0.58) mumol/min/g wet weight, n = 30) compared with control (16.9 (3.5), n = 18) and with Crohn's colitis (17.6 (3.1), n = 12) (p<0.0001). The activity of two other mitochondrial butyrate oxidation enzymes--crotonase and beta-hydroxy butyryl CoA dehydrogenase--as well as of cytoplasmic thiolase was normal in ulcerative colitis. Mitochondrial thiolase activity in ulcerative colitis did not correlate with clinical, endoscopic or histological indices of disease severity. Mitochondrial thiolase activity was reduced in the normal right colon mucosa of patients with left-sided ulcerative colitis. Enzyme kinetic studies revealed a lowered V(max), suggesting inhibition at a site distinct from the catalytic site. Reduced thiolase activity in ulcerative colitis was returned to normal by exposure to 0.3 mM beta-mercaptoethanol, a reductant. Using normal colon mucosal biopsies, redox modulation of thiolase activity by hydrogen peroxide, a mitochondrial oxidant, could be shown. A significant increase in hydrogen peroxide formation was observed in ulcerative colitis biopsies.

conclusionA defect of mitochondrial acetoacetyl CoA thiolase occurs in ulcerative colitis. Increased reactive oxygen species generation in mitochondria of epithelial cells in ulcerative colitis may underlie this defect.

Indexed as

Acetyl-CoA C-AcetyltransferaseAdolescentAdultButyryl-CoA DehydrogenaseColitis, UlcerativeEnoyl-CoA HydrataseFemaleHumansIntestinal MucosaMaleMercaptoethanolMiddle AgedMitochondriaMitochondrial DiseasesOxidation-ReductionAcetyl-CoA C-AcetyltransferaseButyryl-CoA DehydrogenaseEnoyl-CoA HydrataseMercaptoethanol

Identifiers

PMID17483192
PMCPMC2095666
OpenAlexW2111939870

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.