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. 2014 Oct 31;6(3):e949195. doi: 10.4161/19382014.2014.949195

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© 2014 The Author(s). Published with license by Taylor & Francis Group, LLC

© Gerardo J Félix-Martínez and J Rafael Godínez-Fernández

This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License http://creativecommons.org/licenses/by-nc/3.0/, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.

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Figure 1. — Glucose-stimulated insulin secretion (GSIS). After glucose is transported into the cell by the GLUT transporters, it is metabolized, potentiating the production of ATP and the closure of the ATP-sensitive K⁺ channels (K_ATP). The membrane is depolarized and voltage-dependent Ca²⁺ channels (VDCCs) are activated, allowing the influx of Ca²⁺. The increase of the intracellular Ca²⁺ concentration ([Ca²⁺]_i) stimulates Ca²⁺-dependent insulin secretion.