ArticlePharmacology research & perspectives2021
Rat prostaglandin EP3 receptor is highly promiscuous and is the sole prostanoid receptor family member that regulates INS-1 (832/3) cell glucose-stimulated insulin secretion.
Article in Pharmacology research & perspectives, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- GαJournal of the Endocrine Society · 2024Article
- The prostaglandin EAmerican journal of physiology. Endocrinology and metabolism · 2024Article
- Article
- Review
- Noncanonical Regulation of cAMP-Dependent Insulin Secretion and Its Implications in Type 2 Diabetes.Comprehensive Physiology · 2023Article
- Plasma Prostaglandin EMetabolites · 2022Article
- Review
- Pharmacological blockade of the EP3 prostaglandin EMolecular metabolism · 2021Article
- Prostaglandin EP3 receptor signaling is required to prevent insulin hypersecretion and metabolic dysfunction in a non-obese mouse model of insulin resistance.American journal of physiology. Endocrinology and metabolism · 2021Article
- Human Islet Expression Levels of Prostaglandin EACS pharmacology & translational science · 2021Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Chronic elevations in fatty acid metabolites termed prostaglandins can be found in circulation and in pancreatic islets from mice or humans with diabetes and have been suggested as contributing to the β-cell dysfunction of the disease. Two-series prostaglandins bind to a family of G-protein-coupled receptors, each with different biochemical and pharmacological properties. Prostaglandin E receptor (EP) subfamily agonists and antagonists have been shown to influence β-cell insulin secretion, replication, and/or survival. Here, we define EP3 as the sole prostanoid receptor family member expressed in a rat β-cell-derived line that regulates glucose-stimulated insulin secretion. Several other agonists classically understood as selective for other prostanoid receptor family members also reduce glucose-stimulated insulin secretion, but these effects are only observed at relatively high concentrations, and, using a well-characterized EP3-specific antagonist, are mediated solely by cross-reactivity with rat EP3. Our findings confirm the critical role of EP3 in regulating β-cell function, but are also of general interest, as many agonists supposedly selective for other prostanoid receptor family members are also full and efficacious agonists of EP3. Therefore, care must be taken when interpreting experimental results from cells or cell lines that also express EP3.
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