ArticleDiabetologia2013
Pharmacological inhibition of Eph receptors enhances glucose-stimulated insulin secretion from mouse and human pancreatic islets.
Article in Diabetologia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 31 citations in OpenAlex.
- E-Cadherin Is Important in the In Vitro Postnatal Development and Function of Pig Islets.Biomedicines · 2025Article
- Advances and current concepts on Eph receptors and ephrins in upper digestive tract cancers.Frontiers in oncology · 2024Review
- Ephrin-Eph receptor tyrosine kinases for potential therapeutics against hepatic pathologies.Journal of cell communication and signaling · 2023Review
- Article
- Diverse roles for axon guidance pathways in adult tissue architecture and function.Natural sciences (Weinheim, Germany) · 2022Article
- Heterogeneous Development of β-Cell Populations in Diabetes-Resistant and -Susceptible Mice.Diabetes · 2022Article
- Genome wide association study identifies novel candidate genes for growth and body conformation traits in goats.Scientific reports · 2022Article
- Article
- Axon Guidance Molecules in the Islets of Langerhans.Frontiers in endocrinology · 2022Review
- Roles of Eph-Ephrin Signaling in the Eye Lens Cataractogenesis, Biomechanics, and Homeostasis.Frontiers in cell and developmental biology · 2022Review
- Distinct Molecular Signatures of Clinical Clusters in People With Type 2 Diabetes: An IMI-RHAPSODY Study.Diabetes · 2021Article
- Intercellular Communication in the Islet of Langerhans in Health and Disease.Comprehensive Physiology · 2021Article
- Atypical teratoid/rhabdoid tumors (ATRTs) with SMARCA4 mutation are molecularly distinct from SMARCB1-deficient cases.Acta neuropathologica · 2021Article
- Harnessing the Power of Eph/ephrin Biosemiotics for Theranostic Applications.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Article
- Glucose homeostasis is regulated by pancreatic β-cell cilia via endosomal EphA-processing.Nature communications · 2019Article
- β-Cell Receptor Tyrosine Kinases in Controlling Insulin Secretion and Exocytotic Machinery: c-Kit and Insulin Receptor.Endocrinology · 2018Review
- Novel members of quinoline compound family enhance insulin secretion in RIN-5AH beta cells and in rat pancreatic islet microtissue.Scientific reports · 2017Article
- Characterization of pancreatic NMDA receptors as possible drug targets for diabetes treatment.Nature medicine · 2015Article
- Protein-tyrosine phosphatase 1B substrates and metabolic regulation.Seminars in cell & developmental biology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisType 2 diabetes is characterised by impaired glucose-stimulated insulin secretion (GSIS) from pancreatic islets. Since erythropoietin-producing hepatoma (Eph)-ephrin bidirectional signalling fine-tunes GSIS from pancreatic beta cells, we investigated Eph receptor tyrosine kinases (RTK) as potential drug targets for selectively increasing GSIS.
methodsInsulin secretion assays were carried out using mouse and human pancreatic islets as well as mouse insulinoma (MIN6) cells in the presence or absence of two Eph RTK inhibitors. Furthermore, the most potent inhibitor was injected into mice to evaluate its effects on glucose tolerance and plasma insulin levels.
resultsWe showed that the Eph RTK inhibitors selectively increased GSIS from MIN6 cells as well as mouse and human islets. Our results also showed that the insulin secretory effects of these compounds required Eph-ephrin signalling. Finally, pharmacological inhibition of Eph receptor signalling improved glucose tolerance in mice. CONCLUSIONS/
interpretationWe showed for the first time that Eph RTKs represent targets for small molecules to selectively increase GSIS and improve glucose tolerance.
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