Evidence map›Paper›PMID 15367103›Full record

ArticleThe Biochemical journal2005

5-aminoimidazole-4-carboxamide riboside (AICAR) enhances GLUT2-dependent jejunal glucose transport: a possible role for AMPK.

John Walker, Humberto B Jijon, Hugo Diaz, Payam Salehi, Thomas Churchill, Karen L Madsen

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

56 citing papers in PubMed, 145 citations in OpenAlex.

  1. High and typical 18F-FDG bowel uptake in patients treated with metformin.European journal of nuclear medicine and molecular imaging · 2008 · on this map
    Trial
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  9. Metformin action in the gut-insight provided by [Diabetology international · 2022
    Article
  10. Biomedical reports · 2021
    Article
  11. Review
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  15. Article
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  18. Glucose transporters in the small intestine in health and disease.Pflugers Archiv : European journal of physiology · 2020
    Review
  19. Review
  20. 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

6 authors at 1 institution in 1 country.

John WalkerDivision of Gastroenterology, University of Alberta, 6146 Dentistry Pharmacy Building, Edmonton, Alberta, Canada T6G 2C2.
Humberto B Jijon
Hugo Diaz
Payam Salehi
Thomas Churchill
Karen L Madsen
University of Alberta · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AMPK (AMP-activated protein kinase) is a key sensor of energy status within the cell. Activated by an increase in the AMP/ATP ratio, AMPK acts to limit cellular energy depletion by down-regulating selective ATP-dependent processes. The purpose of the present study was to determine the role of AMPK in regulating intestinal glucose transport. [3H]3-O-methyl glucose fluxes were measured in murine jejunum in the presence and absence of the AMPK activators AICAR (5-aminoimidazole-4-carboxamide riboside) and metformin and the p38 inhibitor, SB203580. To differentiate between a sodium-coupled (SGLT1) and diffusive (GLUT2) route of entry, fluxes were measured in the presence of the SGLT1 and GLUT2 inhibitors phloridzin and phloretin. Glucose transporter mRNA levels were measured by reverse transcriptase-PCR, and localization by Western blotting. Surface-expressed GLUT2 was assessed by luminal biotinylation. Activation of p38 mitogen-activated protein kinase was analysed by Western blotting. We found that treatment of jejunal tissue with AICAR resulted in enhanced net glucose uptake and was associated with phosphorylation of p38 mitogen-activated protein kinase. Inhibition of p38 abrogated the stimulation of AICAR-stimulated glucose uptake. Phloretin abolished the AICAR-mediated increase in glucose flux, whereas phloridzin had no effect, suggesting the involvement of GLUT2. In addition, AICAR decreased total protein levels of SGLT1, concurrently increasing levels of GLUT2 in the brush-border membrane. The anti-diabetic drug metformin, a known activator of AMPK, also induced the localization of GLUT2 to the luminal surface. We conclude that the activation of AMPK results in an up-regulation of non-energy requiring glucose uptake by GLUT2 and a concurrent down-regulation of sodium-dependent glucose transport.

Indexed as

Aminoimidazole CarboxamideAMP-Activated Protein KinasesAnimalsBiological Transport, ActiveEnzyme ActivationGlucoseGlucose Transporter Type 2ImidazolesIntestinal MucosaJejunumMembrane GlycoproteinsMiceMice, Inbred StrainsMonosaccharide Transport ProteinsMultienzyme Complexesp38 Mitogen-Activated Protein KinasesacadesineAminoimidazole CarboxamideAMP-Activated Protein KinasesGlucoseGlucose Transporter Type 2ImidazolesMembrane GlycoproteinsMonosaccharide Transport ProteinsMultienzyme Complexesp38 Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesPyridinesRibonucleosidesRNA, MessengerSB 203580Slc5a1 protein, mouseSodium-Glucose Transporter 1

Identifiers

PMID15367103
PMCPMC1134720
OpenAlexW2066161326

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.