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A TRPM4 Inhibitor 9-Phenanthrol Inhibits Glucose- and Glucagon-Like Peptide 1-Induced Insulin Secretion from Rat Islets of Langerhans
Karolinska Institutet, Karolinska University Hospital, Department of Molecular Medicine and Surgery.
Karolinska Institutet, Karolinska University Hospital, Department of Molecular Medicine and Surgery.
Karolinska Institutet, Research Center, Södersjukhuset, Department of Clinical Science and Education; Uppsala University Hospital, Department of Emergency Care and Internal Medicine.ORCID iD: 0000-0002-9016-1881
2017 (English)In: Journal of Diabetes Research, ISSN 2314-6745, E-ISSN 2314-6753, article id 5131785Article in journal (Refereed) Published
Abstract [en]

Pancreatic beta-cells express several ion channels of the transient receptor potential family, which play important roles in mediating the stimulus-secretion coupling. One of these channels, the TRPM4 is a Ca2+-activated monovalent cation channel. This channel is inhibited by 9-phenanthrol, which also inhibits the TMEM16a Cl- channel, and activates the Ca2+-activated K+ channel, K(ca)3.1. The net effects of ion-channel modulation by 9-phenantherol on the insulin secretion remain unclear. We tested the effects of 9-phenanthrol on glucose-and GLP-1-induced insulin secretion from isolated rat islets in static incubations. When applied to the islets in the presence of 3.3mM glucose, 9-phenanthrol caused a small increase in insulin secretion (similar to 7% of the insulin secretion stimulated by 10mM glucose). 10 mu M 9-phenanthrol did not inhibit glucose-or GLP-1-induced insulin secretion. 20 mu M and 30 mu M 9-phenanthrol inhibited glucose-induced insulin secretion by similar to 80% and similar to 85%, respectively. Inhibition of the GLP-1-induced insulin secretion by 20 mu M and 30 mu M 9-phenanthrol was 65% and 94%, respectively. Our study shows that the major effect of 9-phenanthrol on the islets is a strong inhibition of insulin secretion, and we speculate that compounds related to 9-phenanthrol may be potentially useful in treating the pancreatogenous hyperinsulinemic hypoglycemia syndromes.

Place, publisher, year, edition, pages
2017. article id 5131785
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Endocrinology and Diabetes Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-336657DOI: 10.1155/2017/5131785ISI: 000412184900001OAI: oai:DiVA.org:uu-336657DiVA, id: diva2:1170700
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The Karolinska Institutet's Research FoundationAvailable from: 2018-01-04 Created: 2018-01-04 Last updated: 2018-01-04

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