Evidence map›Paper›PMID 19023563›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2009

Modulation of butyrate transport in Caco-2 cells.

Pedro Gonçalves, João Ricardo Araújo, Maria João Pinho, Fátima Martel

Abstract read
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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
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  3. Article
  4. Article
  5. Article
  6. Article
  7. The transport mechanism of monocarboxylate transporter on spinosin in Caco-2 cells.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2016
    Article
  8. Article
  9. Article
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  12. Article
  13. 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

4 authors at 1 institution in 1 country.

Pedro GonçalvesDepartment of Biochemistry (U38-FCT), Faculty of Medicine, University of Porto, 4200-319, Porto, Portugal.
João Ricardo Araújo
Maria João Pinho
Fátima Martel
Universidade do Porto · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of this study was to investigate the putative influence of some pharmacological agents and drugs of abuse upon the apical uptake of butyrate (BT) into Caco-2 cells. The apical uptake of (14)C-BT by Caco-2 cells was (1) time and concentration dependent, (2) pH dependent, (3) Na(+) independent and Cl(-) dependent, (4) energy dependent, (5) inhibited by several BT structural analogues (acetate, propionate, alpha-ketobutyrate, pyruvate, lactate), (6) insensitive to the anion exchange inhibitors DIDS and SITS and (7) inhibited by the monocarboxylate transport (MCT) inhibitors NPPB and pCMB. These characteristics are compatible with an involvement of MCT1-mediated transport. Acutely, uptake of a low concentration of (14)C-BT (10 microM) was reduced by acetaldehyde, acetylsalicylic acid, indomethacin, caffeine and theophylline and increased by MDMA. Chronically, uptake was increased by caffeine and decreased by tetrahydrocannabinol and MDMA; reverse transcription quantitative real-time PCR analysis showed that these three compounds decreased the mRNA levels of MCT1. Acutely, acetaldehyde, indomethacin and MDMA reduced the uptake of a high concentration of (14)C-BT (20 mM), and acetylsalicylic acid increased it. Chronically, none of the compounds affected uptake. Acetaldehyde, indomethacin and propionate seem to be competitive inhibitors of (14)C-BT uptake. Acetylsalicylic acid simultaneously increased the K (m) and the V (max) of (14)C-BT uptake. In conclusion, MCT1-mediated transport of (14)C-BT in Caco-2 cells is modulated by either acute or chronic exposure to some pharmacological agents and drugs of abuse (acetaldehyde, acetylsalicylic acid, indomethacin, caffeine, theophylline and the drugs of abuse tetrahydrocannabinol and MDMA).

Indexed as

2,4-Dinitrophenol4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic AcidAcetaldehydeAcids, AcyclicAspirinBiological Transport, ActiveButyratesCaco-2 CellsCaffeineCell SurvivalDronabinolGene ExpressionHumansHydrogen-Ion ConcentrationIndomethacin2,4-Dinitrophenol4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic AcidAcetaldehydeAcids, AcyclicAspirinButyratesCaffeineDronabinolIndomethacinIonsMonocarboxylate Transport Protein 1Monocarboxylic Acid TransportersN-Methyl-3,4-methylenedioxyamphetamineSodium AzideSymportersTheophylline

Identifiers

PMID19023563
OpenAlexW2090394846

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.