Homologous and heterologous asynchronicity between identified α‐, β‐ and δ‐cells within intact islets of Langerhans in the mouse

• Published in: The Journal of physiology 1999-05, Vol.517 (1), p.85-93
• Main Authors: Nadal, Angel, Quesada, Ivan, Soria, Bernat
• Format: Article
• Language: English
• Subjects: Animals; Calcium Signaling - drug effects; Calcium Signaling - physiology; Glucagon - metabolism; Glucose - pharmacology; Immunohistochemistry; In Vitro Techniques; Insulin - metabolism; Insulin Secretion; Islets of Langerhans - cytology; Islets of Langerhans - drug effects; Islets of Langerhans - physiology; Mice; Microscopy, Confocal; Original; Oscillometry; Somatostatin - metabolism
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1111/j.1469-7793.1999.0085z.x

1 Using laser scanning confocal microscopy to image [Ca2+]i within intact murine islets of Langerhans, we analysed the [Ca2+]i signals generated by glucose in immunocytochemically identified α‐, β‐ and δ‐cells. 2 Glucagon‐containing α‐cells exhibited [Ca2+]i oscillations in the absence of glucose, which petered out when islets were exposed to high glucose concentrations. 3 Somatostatin‐containing δ‐cells were silent in the absence of glucose but concentrations of glucose as low as 3 mM elicited oscillations. 4 In pancreatic β‐cells, a characteristic oscillatory calcium pattern was evoked when glucose levels were raised from 3 to 11 mM and this was synchronized throughout the β‐cell population. Remarkably, [Ca2+]i oscillations in non‐β‐cells were completely asynchronous, both with respect to each other and to β‐cells. 5 These results demonstrate that the islet of Langerhans behaves as a functional syncytium only in terms of β‐cells, implying a pulsatile secretion of insulin. However, the lack of a co‐ordinated calcium signal in α‐ and δ‐cells implies that each cell acts as an independent functional unit and the concerted activity of these units results in a smoothly graded secretion of glucagon and somatostatin. Understanding the calcium signals underlying glucagon and somatostatin secretion may be of importance in the treatment of non‐insulin‐dependent diabetes mellitus since both glucagon and somatostatin appear to regulate insulin release in a paracrine fashion.