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Role of Transient Receptor Potential Melastatin-like Subtype 5 Channel in Insulin Secretion From Rat beta-Cells
Karolinska Institutet.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
2014 (English)In: Pancreas, ISSN 0885-3177, E-ISSN 1536-4828, Vol. 43, no 4, 597-604 p.Article in journal (Refereed) Published
Abstract [en]

Objective Several studies have reported that the transient receptor potential melastatin-like subtype 5 (TRPM5) channel, a Ca2+-activated monovalent cation channel, is involved in the stimulus-secretion coupling in the mouse pancreatic beta-cells. We have studied the role of the TRPM5 channel in regulating insulin secretion and cytoplasmic free Ca2+ concentration ([Ca2+](i)) in the rat beta-cells by using triphenylphosphine oxide, a selective inhibitor of the channel. Methods Insulin secretion from islets from Sprague-Dawley rats was measured in batch incubations. Cytoplasmic free Ca2+ concentration was measured from single beta-cells by fura-2-based microfluorometry. Results Triphenylphosphine oxide did not alter insulin secretion and [Ca2+](i) response triggered by KCl or fructose. It inhibited insulin secretion in response to glucose, l-arginine, and glucagon-like peptide 1. It also inhibited glucose-induced insulin secretion by mechanisms that are independent of the adenosine triphosphate-sensitive potassium channels and [Ca2+](i) increase. Conclusions Our results suggest that in the rat islets, TRPM5 is involved in mediating insulin secretion by glucose and l-arginine and in potentiating the glucose-induced insulin secretion by glucagon-like peptide 1.

Place, publisher, year, edition, pages
2014. Vol. 43, no 4, 597-604 p.
Keyword [en]
insulin secretion, islets of Langerhans, transient receptor potential channels, calcium signaling, pancreatic beta-cells, TRPM5
National Category
Gastroenterology and Hepatology
URN: urn:nbn:se:uu:diva-225009DOI: 10.1097/MPA.0000000000000027ISI: 000334787400016OAI: oai:DiVA.org:uu-225009DiVA: diva2:719642
Available from: 2014-05-26 Created: 2014-05-26 Last updated: 2014-09-17Bibliographically approved

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