Evidence map›Paper›PMID 17318626›Full record

ArticleDiabetologia2007

Regulation of pancreatic islet cell survival and replication by gamma-aminobutyric acid.

B Ligon, J Yang, S B Morin, M F Ruberti, M L Steer

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Diabetologia, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.9field-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

20 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Pancreatic β-cell heterogeneity in health and diabetes: classes, sources, and subtypes.American journal of physiology. Endocrinology and metabolism · 2021
    Review
  5. Insulin resistance and the role of gamma-aminobutyric acid.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2021
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. GABAergic system in the endocrine pancreas: a new target for diabetes treatment.Diabetes, metabolic syndrome and obesity : targets and therapy · 2015
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Paracrine interactions within islets of Langerhans.Journal of molecular neuroscience : MN · 2012
    Review
  18. GABA exerts protective and regenerative effects on islet beta cells and reverses diabetes.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  19. Article
  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

5 authors at 2 institutions in 1 country.

B LigonDepartment of Neuroscience, Tufts University School of Medicine, 136 Harrison Ave., Boston, MA 02111, USA. b.ligon@mitokine.com
J Yang
S B Morin
M F Ruberti
M L Steer
Tufts Medical Center · USTufts University · US

Funding

PILOT AND FEASIBILITY STUDIESP30DK034928 · NIDDK · TUFTS MEDICAL CENTER · PI JEFFERSON, DOUGLAS M. · 1986 to 2007
$8.5M
GABA-B Receptors as Regulators of Islet BiologyR01DK063344 · NIDDK · TUFTS MEDICAL CENTER · PI DUNLAP, KATHLEEN · 2002 to 2003
$810k
PHYSIOLOGIC ROLES OF CA++ CHANNELS IN ISLET BETA CELLSK08NS001923 · NINDS · TUFTS UNIVERSITY BOSTON · PI LIGON, B BROOKE · 1997 to 2001
$239k
NIDDK NIH HHS DK34928NIDDK NIH HHS DK63344NINDS NIH HHS K08-NS01923
6 · The paper itself

Abstract

aims/hypothesisPancreatic islets have evolved remarkable, though poorly understood mechanisms to modify beta cell mass when nutrient intake fluctuates or cells are damaged. We hypothesised that appropriate and timely adjustments in cell number occur because beta cells release proliferative signals to surrounding cells when stimulated by nutrients and 'bleed' these growth factors upon injury. MATERIALS AND

methodsIn rat pancreatic islets, we measured DNA content, insulin content, insulin secretion after treatment, immunoblots of apoptotic proteins and the uptake of nucleoside analogues to assess the ability of gamma-aminobutyric acid (GABA), which is highly concentrated in beta cells, to act as a growth and survival factor. This focus is supported by work from others demonstrating that GABA increases cell proliferation in the developing nervous system, acts as a survival factor for differentiated neurons and, interestingly, protects plants under stress.

resultsOur results show that DNA, insulin content and insulin secretion are higher in freshly isolated islets treated with GABA or GABA B receptor agonists. Exposure to GABA upregulated the anti-apoptotic protein B-cell chronic lymphocytic leukaemia XL and limited activation of caspase 3 in islets. The cellular proliferation rate in GABA-treated islets was twice that of untreated controls. CONCLUSIONS/

interpretationWe conclude that GABA serves diverse purposes in the islet, meeting a number of functional criteria to act as an endogenous co-regulator of beta cell mass.

Indexed as

AnimalsCell ProliferationCell SurvivalDNAgamma-Aminobutyric AcidImmunohistochemistryInsulinInsulin-Secreting CellsInsulin SecretionIslets of LangerhansMaleMicroscopy, ConfocalRatsRats, Sprague-DawleyReceptors, GABA-AReceptors, GABA-BDNAgamma-Aminobutyric AcidInsulinReceptors, GABA-AReceptors, GABA-BThymidine

Identifiers

PMID17318626
OpenAlexW2019278833

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.