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Journal of Diabetes Research
Volume 2016, Article ID 3142175, 9 pages
Research Article

Potentiation of Calcium Influx and Insulin Secretion in Pancreatic Beta Cell by the Specific TREK-1 Blocker Spadin

1CNRS, Inserm, IPMC, Université Côte d’Azur, Valbonne, France
2CNRS, CHU Lille, Institut Pasteur de Lille, UMR 8199-EGID, Université Lille, 59000 Lille, France
3Département de Physiologie, Institut de Génomique Fonctionnelle (IGF), CNRS/INSERM UMR5203, Université de Montpellier, Montpellier, France

Received 3 August 2016; Revised 21 November 2016; Accepted 29 November 2016

Academic Editor: Eusebio Chiefari

Copyright © 2016 Céline Hivelin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Inhibition of the potassium channels TREK-1 by spadin (SPA) is currently thought to be a promising therapeutic target for the treatment of depression. Since these channels are expressed in pancreatic β-cells, we investigated their role in the control of insulin secretion and glucose homeostasis. In this study, we confirmed the expression of TREK-1 channels in the insulin secreting MIN6-B1 β-cell line and in mouse islets. We found that their blockade by SPA potentiated insulin secretion induced by potassium chloride dependent membrane depolarization. Inhibition of TREK-1 by SPA induced a decrease of the resting membrane potential ( mV) and increased the cytosolic calcium concentration. In mice, administration of SPA enhanced the plasma insulin level stimulated by glucose, confirming its secretagogue effect observed in vitro. Taken together, this work identifies SPA as a novel potential pharmacological agent able to control insulin secretion and glucose homeostasis.