Evidence map›Paper›PMID 19625695›Full record

ArticleThe Journal of nutrition2009

Butyrate enhances the intestinal barrier by facilitating tight junction assembly via activation of AMP-activated protein kinase in Caco-2 cell monolayers.

Luying Peng, Zhong-Rong Li, Robert S Green, Ian R Holzman, Jing Lin

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in The Journal of nutrition, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03032354 (Effect of Lactobacillus Rhamnosus GG and Bifidobacterium Lactis BB 12 on Beta-cell Function in Children With Newly Diagnosed Type 1 Diabetes - a Randomized Controlled Trial), which is not on this map. Cited by 1,122 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1,122citing papers in PubMed, 5 pooled it
11.5field-weighted citation impact, top 1% 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.

NCT03032354 phase4unknown statusnot on this mapstarted 2017, after this paper: background citation

Effect of Lactobacillus Rhamnosus GG and Bifidobacterium Lactis BB 12 on Beta-cell Function in Children With Newly Diagnosed Type 1 Diabetes - a Randomized Controlled Trial

TypeinterventionalSponsorMedical University of WarsawRan2017 to 2018Enrolled96ConditionsDiabetes Mellitus, Type 1ArmsLactobacillus rhamnosus GG and Bifidobacterium lactis BB12, Placebo, (Placebo group)
3 · Its place in the literature

Who cites it

1,122 citing papers in PubMed, 5 syntheses or guidelines pooled it, 1,952 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Trial
  7. Trial
  8. Trial
  9. Trial
  10. Trial
  11. Trial
  12. Review
  13. Review
  14. Review
  15. Bridging the gap:Gut microbes · 2026
    Review
  16. Review
  17. Gut microbes · 2026
    Article
  18. Review
  19. Article
  20. Review

1,062 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 2 countries.

Luying PengDepartment of Pediatrics, Mount Sinai School of Medicine, New York, NY 10029-6574, USA.
Zhong-Rong Li
Robert S Green
Ian R Holzman
Jing Lin
Icahn School of Medicine at Mount Sinai · USTongji University · CNWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Butyrate, one of the SCFA, promotes the development of the intestinal barrier. However, the molecular mechanisms underlying the butyrate regulation of the intestinal barrier are unknown. To test the hypothesis that the effect of butyrate on the intestinal barrier is mediated by the regulation of the assembly of tight junctions involving the activation of the AMP-activated protein kinase (AMPK), we determined the effect of butyrate on the intestinal barrier by measuring the transepithelial electrical resistance (TER) and inulin permeability in a Caco-2 cell monolayer model. We further used a calcium switch assay to study the assembly of epithelial tight junctions and determined the effect of butyrate on the assembly of epithelial tight junctions and AMPK activity. We demonstrated that the butyrate treatment increased AMPK activity and accelerated the assembly of tight junctions as shown by the reorganization of tight junction proteins, as well as the development of TER. AMPK activity was also upregulated by butyrate during calcium switch-induced tight junction assembly. Compound C, a specific AMPK inhibitor, inhibited the butyrate-induced activation of AMPK. The facilitating effect of butyrate on the increases in TER in standard culture media, as well as after calcium switch, was abolished by compound C. We conclude that butyrate enhances the intestinal barrier by regulating the assembly of tight junctions. This dynamic process is mediated by the activation of AMPK. These results suggest an intriguing link between SCFA and the intracellular energy sensor for the development of the intestinal barrier.

Indexed as

AMP-Activated Protein KinasesButyratesCaco-2 CellsElectric ImpedanceEpitheliumHumansIntestinal MucosaInulinMembrane ProteinsPermeabilityPhosphorylationProtein Kinase InhibitorsTight JunctionsUp-RegulationAMP-Activated Protein KinasesButyratesInulinMembrane ProteinsProtein Kinase Inhibitors

Identifiers

PMID19625695
PMCPMC2728689
OpenAlexW2155770880

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.