Evidence map›Paper›PMID 21782840›Full record

ReviewProgress in biophysics and molecular biology2011

Molecular physiology of glucagon-like peptide-1 insulin secretagogue action in pancreatic β cells.

Colin A Leech, Igor Dzhura, Oleg G Chepurny, Guoxin Kang, Frank Schwede, Hans-G Genieser, George G Holz

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Progress in biophysics and molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 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.

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

74 citing papers in PubMed, 1 synthesis or guideline pooled it, 123 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. GLP-1: The Progenitor Hormone.Obesity surgery · 2025
    Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Liraglutide increases islet CaDiabetes, obesity & metabolism · 2022
    Article
  20. Article

14 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

7 authors at 3 institutions in 2 countries.

Colin A LeechDepartment of Medicine, State University of New York Upstate Medical University, Syracuse, NY, USA. leechc@upstate.edu
Igor Dzhura
Oleg G Chepurny
Guoxin Kang
Frank Schwede
Hans-G Genieser
George G Holz
SUNY Upstate Medical University · USBiolog Life Science Institute · DENew York University · US

Funding

Insulinotropin: A Modulator Of B-Cell Glucose SignalingR01DK045817 · NIDDK · UPSTATE MEDICAL UNIVERSITY · PI HOLZ, GEORGE G · 2001 to 2008
$3.0M
Molecular Basis of Antidiabetogenic Hormone ActionR01DK069575 · NIDDK · UPSTATE MEDICAL UNIVERSITY · PI HOLZ, GEORGE G · 2007 to 2017
$2.9M
NIDDK NIH HHS R01 DK045817NIDDK NIH HHS R01-DK045817NIDDK NIH HHS R01 DK069575NIDDK NIH HHS R01-DK069575
6 · The paper itself

Abstract

Insulin secretion from pancreatic β cells is stimulated by glucagon-like peptide-1 (GLP-1), a blood glucose-lowering hormone that is released from enteroendocrine L cells of the distal intestine after the ingestion of a meal. GLP-1 mimetics (e.g., Byetta) and GLP-1 analogs (e.g., Victoza) activate the β cell GLP-1 receptor (GLP-1R), and these compounds stimulate insulin secretion while also lowering levels of blood glucose in patients diagnosed with type 2 diabetes mellitus (T2DM). An additional option for the treatment of T2DM involves the administration of dipeptidyl peptidase-IV (DPP-IV) inhibitors (e.g., Januvia, Galvus). These compounds slow metabolic degradation of intestinally released GLP-1, thereby raising post-prandial levels of circulating GLP-1 substantially. Investigational compounds that stimulate GLP-1 secretion also exist, and in this regard a noteworthy advance is the demonstration that small molecule GPR119 agonists (e.g., AR231453) stimulate L cell GLP-1 secretion while also directly stimulating β cell insulin release. In this review, we summarize what is currently known concerning the signal transduction properties of the β cell GLP-1R as they relate to insulin secretion. Emphasized are the cyclic AMP, protein kinase A, and Epac2-mediated actions of GLP-1 to regulate ATP-sensitive K⁺ channels, voltage-dependent K⁺ channels, TRPM2 cation channels, intracellular Ca⁺ release channels, and Ca⁺-dependent exocytosis. We also discuss new evidence that provides a conceptual framework with which to understand why GLP-1R agonists are less likely to induce hypoglycemia when they are administered for the treatment of T2DM.

Indexed as

AnimalsDiabetes Mellitus, Type 2Glucagon-Like Peptide 1HumansIncretinsInsulinInsulin-Secreting CellsInsulin SecretionGlucagon-Like Peptide 1IncretinsInsulin

Identifiers

PMID21782840
PMCPMC3200499
OpenAlexW2046913589

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.