Evidence map›Paper›PMID 32258556›Full record

ReviewPorto biomedical journal

Regulation of colonic epithelial butyrate transport: Focus on colorectal cancer.

Pedro Gonçalves, Fátima Martel

Open access · diamondAbstract readReview
In one paragraph

Review in Porto biomedical journal. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
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  11. Article
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  13. MAFLD and Celiac Disease in Children.International journal of molecular sciences · 2023
    Review
  14. Article
  15. Review
  16. Article
  17. Sodium butyrate in both prevention and supportive treatment of colorectal cancer.Frontiers in cellular and infection microbiology · 2022
    Review
  18. Review
  19. Review
  20. The Immunomodulatory Functions of Butyrate.Journal of inflammation research · 2021
    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

2 authors at 2 institutions in 2 countries.

Pedro GonçalvesInnate Immunity Unit, Institut Pasteur, and the Institut National de la Santé et de la Recherche Médicale (INSERM) U668, Paris, France.
Fátima MartelDepartment of Biochemistry, Faculty of Medicine, and Institute for Research and Innovation in Health Sciences, University of Porto, Porto, Portugal.
i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto · PTInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

highlightsFermentation of the dietary fiber by intestinal microflora results in production of butyrate.Butyrate possesses anticarcinogenic effect at the colonic level.Three transporters (MCT1, SMCT1 and BCRP) regulate the intracellular concentration of BT in colonic epithelial cells.Changes in the expression of these transporters occur in colorectal cancer. ABSTRACT: Colorectal cancer (CRC) is one of the most common solid tumors worldwide. Consumption of dietary fiber is associated with a low risk of developing CRC. The fermentation of the dietary fiber by intestinal microflora results in production of butyrate (BT). This short-chain fatty acid is an important metabolic substrate in normal colonic epithelial cells and has important homeostatic functions at the colonic level. Because the cellular effects of BT (e.g. inhibition of histone deacetylases) are dependent on its intracellular concentration, knowledge on the mechanisms involved in BT membrane transport and its regulation seems particularly relevant. In this review, we will present the carrier-mediated mechanisms involved in BT membrane transport at the colonic epithelial level and their regulation, with an emphasis on CRC. Several xenobiotics known to modulate the risk for developing CRC are able to interfere with BT transport at the intestinal level. Thus, interference with BT transport certainly contributes to the anticarcinogenic or procarcinogenic effect of these compounds and these compounds may interfere with the anticarcinogenic effect of BT. Finally, we suggest that differences in BT transport between normal colonocytes and tumoral cells contribute to the "BT paradox" (the apparent opposing effect of BT in CRC cells and normal colonocytes).

Indexed as

BCRPButyrateColorectal cancerMCT1SMCT1

Identifiers

PMID32258556
PMCPMC6806744
OpenAlexW2467234435

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.