Evidence map›Paper›PMID 26488296›Full record

ArticlePloS one2015

Abscisic Acid Stimulates Glucagon-Like Peptide-1 Secretion from L-Cells and Its Oral Administration Increases Plasma Glucagon-Like Peptide-1 Levels in Rats.

Santina Bruzzone, Mirko Magnone, Elena Mannino, Giovanna Sociali, Laura Sturla, Chiara Fresia, Valeria Booz, Laura Emionite, Antonio De Flora, Elena Zocchi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 28 citations in OpenAlex.

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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

10 authors at 2 institutions in 1 country.

Santina BruzzoneDepartment of Experimental Medicine (DIMES), Section of Biochemistry, and CEBR, University of Genova, Genova, Italy.
Mirko MagnoneDepartment of Experimental Medicine (DIMES), Section of Biochemistry, and CEBR, University of Genova, Genova, Italy.
Elena ManninoDepartment of Experimental Medicine (DIMES), Section of Biochemistry, and CEBR, University of Genova, Genova, Italy.
Giovanna SocialiDepartment of Experimental Medicine (DIMES), Section of Biochemistry, and CEBR, University of Genova, Genova, Italy.
Laura SturlaDepartment of Experimental Medicine (DIMES), Section of Biochemistry, and CEBR, University of Genova, Genova, Italy.
Chiara FresiaDepartment of Experimental Medicine (DIMES), Section of Biochemistry, and CEBR, University of Genova, Genova, Italy.
Valeria BoozDepartment of Experimental Medicine (DIMES), Section of Biochemistry, and CEBR, University of Genova, Genova, Italy.
Laura EmioniteAnimal facility, IRCCS AOU San Martino - IST Istituto Nazionale per la Ricerca sul Cancro, Genova, Italy.
Antonio De FloraDepartment of Experimental Medicine (DIMES), Section of Biochemistry, and CEBR, University of Genova, Genova, Italy.
Elena ZocchiDepartment of Experimental Medicine (DIMES), Section of Biochemistry, and CEBR, University of Genova, Genova, Italy.
University of Genoa · ITOspedale Policlinico San Martino · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In recent years, Abscisic Acid (ABA) has been demonstrated to be involved in the regulation of glucose homeostasis in mammals as an endogenous hormone, by stimulating both insulin release and peripheral glucose uptake. In addition, ABA is released by glucose- or GLP-1-stimulated β-pancreatic cells. Here we investigated whether ABA can stimulate GLP-1 release. The human enteroendocrine L cell line hNCI-H716 was used to explore whether ABA stimulates in vitro GLP-1 secretion and/or transcription. ABA induced GLP-1 release in hNCI-H716 cells, through a cAMP/PKA-dependent mechanism. ABA also enhanced GLP-1 transcription. In addition, oral administration of ABA significantly increased plasma GLP-1 and insulin levels in rats. In conclusion, ABA can stimulate GLP-1 release: this result and the previous observation that GLP-1 stimulates ABA release from β -cells, suggest a positive feed-back mechanism between ABA and GLP-1, regulating glucose homeostasis. Type 2 diabetes treatments targeting the GLP-1 axis by either inhibiting its rapid clearance by dipeptidyl-peptidase IV or using GLP-1 mimetics are currently used. Moreover, the development of treatments aimed at stimulating GLP-1 release from L cells has been considered as an alternative approach. Accordingly, our finding that ABA increases GLP-1 release in vitro and in vivo may suggest ABA and/or ABA analogs as potential anti-diabetic treatments.

Indexed as

Abscisic AcidAdministration, OralAnimalsBlood GlucoseCell Line, TumorCyclic AMPEnteroendocrine CellsFemaleGlucagon-Like Peptide 1HumansHypoglycemic AgentsInsulinMembrane ProteinsNuclear ProteinsPhosphate-Binding ProteinsRatsAbscisic AcidBlood GlucoseCyclic AMPGlucagon-Like Peptide 1Hypoglycemic AgentsInsulinLANCL2 protein, humanMembrane ProteinsNuclear ProteinsPhosphate-Binding Proteins

Identifiers

PMID26488296
PMCPMC4619318
OpenAlexW2209954776

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Registered trials

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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.