Evidence map›Paper›PMID 22776039›Full record

ReviewDiabetes, obesity & metabolism2013

GLP-1 receptor activated insulin secretion from pancreatic β-cells: mechanism and glucose dependence.

A R Meloni, M B DeYoung, C Lowe, D G Parkes

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

Review in Diabetes, obesity & metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 202 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
202citing papers in PubMed, 8 pooled it
8.0field-weighted citation impact, top 2% 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

202 citing papers in PubMed, 8 syntheses or guidelines pooled it, 364 citations in OpenAlex.

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  11. Semaglutide Added to Basal Insulin in Type 2 Diabetes (SUSTAIN 5): A Randomized, Controlled Trial.The Journal of clinical endocrinology and metabolism · 2018 · on this map
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  19. An RNA thermogenic therapy to preserve lean mass and enhance metabolic health during GLP-1 weight loss.Proceedings of the National Academy of Sciences of the United States of America · 2026
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142 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

4 authors.

A R MeloniAmylin Pharmaceuticals, Inc., San Diego, CA 92121, USA. alison.meloni@amylin.com
M B DeYoung
C Lowe
D G Parkes

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The major goal in the treatment of type 2 diabetes mellitus is to control the hyperglycaemia characteristic of the disease. However, treatment with common therapies such as insulin or insulinotrophic sulphonylureas (SU), while effective in reducing hyperglycaemia, may impose a greater risk of hypoglycaemia, as neither therapy is self-regulated by ambient blood glucose concentrations. Hypoglycaemia has been associated with adverse physical and psychological outcomes and may contribute to negative cardiovascular events; hence minimization of hypoglycaemia risk is clinically advantageous. Stimulation of insulin secretion from pancreatic β-cells by glucagon-like peptide 1 receptor (GLP-1R) agonists is known to be glucose-dependent. GLP-1R agonists potentiate glucose-stimulated insulin secretion and have little or no activity on insulin secretion in the absence of elevated blood glucose concentrations. This 'glucose-regulated' activity of GLP-1R agonists makes them useful and potentially safer therapeutics for overall glucose control compared to non-regulated therapies; hyperglycaemia can be reduced with minimal hypoglycaemia. While the inherent mechanism of action of GLP-1R agonists mediates their glucose dependence, studies in rats suggest that SUs may uncouple this dependence. This hypothesis is supported by clinical studies showing that the majority of events of hypoglycaemia in patients treated with GLP-1R agonists occur in patients treated with a concomitant SU. This review aims to discuss the current understanding of the mechanisms by which GLP-1R signalling promotes insulin secretion from pancreatic β-cells via a glucose-dependent process.

Indexed as

Blood GlucoseDiabetes Mellitus, Type 2Dipeptidyl-Peptidase IV InhibitorsFemaleGlucagon-Like Peptide-1 ReceptorGlycated HemoglobinHumansHyperglycemiaInsulinInsulin-Secreting CellsInsulin SecretionMaleReceptors, GlucagonBlood GlucoseDipeptidyl-Peptidase IV InhibitorsGLP1R protein, humanGlp1r protein, ratGlucagon-Like Peptide-1 ReceptorGlycated Hemoglobinhemoglobin A1c protein, humanInsulinReceptors, Glucagon

Identifiers

PMID22776039
PMCPMC3556522
OpenAlexW2060476230

What OpenQuestion holds

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LicenceCC BY
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.