Evidence map›Paper›PMID 17306374›Full record

ReviewPharmacology & therapeutics2007

Mechanisms of action of glucagon-like peptide 1 in the pancreas.

Máire E Doyle, Josephine M Egan

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

Review in Pharmacology & therapeutics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 291 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
291citing papers in PubMed, 4 pooled it
10.2field-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

291 citing papers in PubMed, 4 syntheses or guidelines pooled it, 663 citations in OpenAlex.

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  9. Glucagon-Like Peptide-1 Receptor PET/CT with 68Ga-NOTA-Exendin-4 for Detecting Localized Insulinoma: A Prospective Cohort Study.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2016
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231 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

2 authors at 2 institutions in 1 country.

Máire E DoyleDepartment of Pathology, Immunology & Laboratory Medicine, College of Medicine, University of Florida, Gainesville, FL, USA.
Josephine M Egan
National Institute on Aging · USUniversity of Florida · US

Funding

EXENDIN-4 AS A TREATMENT FOR DIABETES MELLITUSZ01AG000905 · NIA · NATIONAL INSTITUTE ON AGING · PI EGAN, JOSEPHINE M · 1997 to 2008
$1.5M
USE OF AN IN VIVO MODEL SYSTEM TO INVESTIGATE NIDDMZ01AG000214 · NIA · NATIONAL INSTITUTE ON AGING · PI EGAN, JOSEPHINE M · 1991 to 2008
$693k
Effects Of GLP-1 On Glucose HomeostasisZ01AG000906 · NIA · NATIONAL INSTITUTE ON AGING · PI EGAN, JOSEPHINE M · 1997 to 2008
$74k
Intramural NIH HHS Z01 AG000214Intramural NIH HHS Z01 AG000905Intramural NIH HHS Z01 AG000906
6 · The paper itself

Abstract

Glucagon-like peptide 1 (GLP-1) is a hormone that is encoded in the proglucagon gene. It is mainly produced in enteroendocrine L cells of the gut and is secreted into the blood stream when food containing fat, protein hydrolysate, and/or glucose enters the duodenum. Its particular effects on insulin and glucagon secretion have generated a flurry of research activity over the past 20 years culminating in a naturally occurring GLP-1 receptor (GLP-1R) agonist, exendin 4 (Ex-4), now being used to treat type 2 diabetes mellitus (T2DM). GLP-1 engages a specific guanine nucleotide-binding protein (G-protein) coupled receptor (GPCR) that is present in tissues other than the pancreas (brain, kidney, lung, heart, and major blood vessels). The most widely studied cell activated by GLP-1 is the insulin-secreting beta cell where its defining action is augmentation of glucose-induced insulin secretion. Upon GLP-1R activation, adenylyl cyclase (AC) is activated and cAMP is generated, leading, in turn, to cAMP-dependent activation of second messenger pathways, such as the protein kinase A (PKA) and Epac pathways. As well as short-term effects of enhancing glucose-induced insulin secretion, continuous GLP-1R activation also increases insulin synthesis, beta cell proliferation, and neogenesis. Although these latter effects cannot be currently monitored in humans, there are substantial improvements in glucose tolerance and increases in both first phase and plateau phase insulin secretory responses in T2DM patients treated with Ex-4. This review will focus on the effects resulting from GLP-1R activation in the pancreas.

Indexed as

AnimalsDiabetes Mellitus, Type 2Enteroendocrine CellsExenatideGlucagonGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorGlucoseHumansHypoglycemic AgentsInsulinInsulin-Secreting CellsInsulin SecretionPancreasPeptidesReceptors, GlucagonExenatideGLP1R protein, humanGlucagonGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorGlucoseHypoglycemic AgentsInsulinPeptidesReceptors, GlucagonVenoms

Identifiers

PMID17306374
PMCPMC1934514
OpenAlexW1012070930

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.