Evidence map›Paper›PMID 29524296›Full record

ArticleJournal of cellular and molecular medicine2018

Liraglutide, a human glucagon-like peptide-1 analogue, stimulates AKT-dependent survival signalling and inhibits pancreatic β-cell apoptosis.

Katerina Kapodistria, Effie-Photini Tsilibary, Eleni Kotsopoulou, Petros Moustardas, Paraskevi Kitsiou

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Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
6.9field-weighted citation impact, top 3% 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

41 citing papers in PubMed, 65 citations in OpenAlex.

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  15. Signaling pathways in obesity: mechanisms and therapeutic interventions.Signal transduction and targeted therapy · 2022
    Review
  16. Intracellular ATP Signaling Contributes to FAM3A-Induced PDX1 Upregulation in Pancreatic Beta Cells.Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association · 2022
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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

5 authors at 2 institutions in 1 country.

Katerina KapodistriaInstitute of Biosciences and Applications, National Centre for Scientific Research, N.C.S.R. "Demokritos", Terma Patriarchou Grigoriou & Neapoleos, Attiki, Greece.
Effie-Photini TsilibaryInstitute of Biosciences and Applications, National Centre for Scientific Research, N.C.S.R. "Demokritos", Terma Patriarchou Grigoriou & Neapoleos, Attiki, Greece.
Eleni KotsopoulouInstitute of Biosciences and Applications, National Centre for Scientific Research, N.C.S.R. "Demokritos", Terma Patriarchou Grigoriou & Neapoleos, Attiki, Greece.
Petros MoustardasCenter for Clinical, Experimental Surgery and Translational Research, Biomedical Research Foundation Academy of Athens (BRFAA), Athens, Greece.
Paraskevi KitsiouInstitute of Biosciences and Applications, National Centre for Scientific Research, N.C.S.R. "Demokritos", Terma Patriarchou Grigoriou & Neapoleos, Attiki, Greece.ORCID 0000-0003-4135-1715
National Centre of Scientific Research "Demokritos" · GRAcademy of Athens · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liraglutide, a human long-lasting GLP-1 analogue, is currently regarded as a powerful treatment option for type 2 diabetes. Apart from glucoregulatory and insulinotropic actions, liraglutide increases β-cell mass through stimulation of β-cell proliferation and islet neogenesis, as well as inhibition of β-cell apoptosis. However, the underline molecular mechanisms have not been fully characterized. In this study, we investigated the mechanism by which liraglutide preserves islet β-cells in an animal model of overt diabetes, the obese db/db mice, and protects a mouse pancreatic β-cell line (βTC-6 cells) against apoptosis. Treatment of 12-week-old diabetic mice with liraglutide for 2 weeks had no appreciable effects on blood non-fasting glucose concentration, islet insulin content and body weight. However, morphological and biochemical examination of diabetic mouse pancreatic islets demonstrated that liraglutide restores islet size, reduces islet β-cell apoptosis and improves nephrin expression, a protein involved in β-cell survival signalling. Our results indicated that liraglutide protects βTC-6 cells from serum withdrawal-induced apoptosis through inhibition of caspase-3 activation. The molecular mechanism of the anti-apoptotic action of liraglutide in βTC-6-cells comprises stimulation of PI3-kinase-dependent AKT phosphorylation leading to the phosphorylation, hence inactivation of the pro-apoptotic protein BAD and inhibition of FoxO1 transcription factor. In conclusion, we provided evidence that the GLP-1 analogue liraglutide exerts important beneficial effects on pancreatic islet architecture and β-cell survival by protecting cells against apoptosis. These findings extend our understanding of the actions of liraglutide and further support the use of GLP-1R agonists in the treatment of patients with type 2 diabetes.

Indexed as

AnimalsApoptosisCell LineCell ProliferationCell SurvivalDiabetes Mellitus, Type 2Forkhead Box Protein O1Glucagon-Like Peptide 1HumansHypoglycemic AgentsInsulinInsulin-Secreting CellsLiraglutideMiceMice, ObesePhosphatidylinositol 3-KinasesForkhead Box Protein O1Glucagon-Like Peptide 1Hypoglycemic AgentsInsulinLiraglutidePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktapoptosisBAD inactivationdb/db diabetic mouseFoxO1 inhibitionLiraglutideNephrinPancreatic β-cellsPI3K-AKT survival signalling

Identifiers

PMID29524296
PMCPMC5980190
OpenAlexW2792524495

What OpenQuestion holds

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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.