Evidence map›Paper›PMID 19885112›Full record

ArticleJournal of diabetes science and technology2007

Inflammation and glucose sensors: use of dexamethasone to extend glucose sensor function and life span in vivo.

Ulrike Klueh, Manjot Kaur, David C Montrose, Donald L Kreutzer

Open access · bronzeAbstract read
In one paragraph

Article in Journal of diabetes science and technology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.5field-weighted citation impact, top 27% 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

22 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Biomedical Implants with Charge-Transfer Monitoring and Regulating Abilities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021
    Review
  6. Review
  7. Review
  8. Article
  9. Dexamethasone-Enhanced Microdialysis and Penetration Injury.Frontiers in bioengineering and biotechnology · 2020
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Microdialysis sampling techniques applied to studies of the foreign body reaction.European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences · 2014
    Review
  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

4 authors at 1 institution in 1 country.

Ulrike KluehCenter for Molecular Tissue Engineering and Department of Surgery, University of Connecticut, School of Medicine, Farmington, Connecticut 06030, USA. klueh@nso.uchc.edu
Manjot Kaur
David C Montrose
Donald L Kreutzer
University of Connecticut · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIt has been generally accepted that the acute loss of sensor function is the consequence of sensor biofouling as a result of inflammation induced at sites of sensor implantation, as well as tissue trauma induced by the sensor and its implantation. Because anti-inflammatory therapies are used routinely to control inflammation in a wide variety of diseases, we hypothesized that anti-inflammatory therapy would likely extend glucose sensor function in vivo. To test this hypothesis, we utilized our recently developed mouse model of implantable glucose sensors and the potent anti-inflammatory steroid dexamethasone (DEX).

methodFor this study, glucose sensors were implanted subcutaneously into the head and neck area of mice and sensor function was determined up to 14 days postimplantation. These mice received a daily intraperitoneal injection of DEX at a dose of 1, 6, or 10 mg/kg body weight.

resultsMice not treated with DEX lost sensor functionality very rapidly, usually within the first 24 hours postimplantation. Mice treated with DEX at the various doses had an increased sensor life span of up to 2 weeks postimplantation. Additionally, sensitivity was maintained in DEX-treated mice as compared to control mice (non-DEX treated). Histologic evaluation of tissue surrounding the site of sensor implantation had almost no inflammatory cells in DEX-treated mice, whereas control mice had an intense band of inflammation surrounding the site of sensor implantation.

conclusionTo our knowledge this is the first study directly demonstrating that anti-inflammatory therapy can extend glucose sensor function in vivo and supports the key role of inflammation in loss of sensor function in vivo, as well as the uses of anti-inflammatory therapy as a potential key adjuvant in enhancing glucose sensor function and life span in vivo.

Indexed as

anti-inflammatory therapydexamethasonediabetesfibrosisimplantable glucose sensorinflammationmurine (mouse)sensor function in vivotissue responsesvessel regression

Identifiers

PMID19885112
PMCPMC2769643
OpenAlexW2137585122

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.