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Diabetes 55:2463-2469, 2006
DOI: 10.2337/db06-0272
© 2006 by the American Diabetes Association
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Glucose Induces Opposite Intracellular Ca2+ Concentration Oscillatory Patterns in Identified {alpha}- and ß-Cells Within Intact Human Islets of Langerhans

Ivan Quesada1, Mariana G. Todorova1, Paloma Alonso-Magdalena1, Marta Beltrá1, Everardo M. Carneiro4, Franz Martin2, Angel Nadal1, and Bernat Soria3

1 Institute of Bioengineering, Miguel Hernandez University, Sant Joan d’Alacant, Spain
2 Andalusian Center of Developmental Biology, University Pablo Olavide, Seville, Spain
3 CABIMER (Andalusian Center for Molecular Biology and Regenerative Medicine), Seville, Spain
4 Department of Physiology and Biology, State University of Campinas, Campinas, Brazil

Address correspondence and reprint requests to Ivan Quesada, PhD, Institute of Bioengineering, Miguel Hernandez University, Ctra. N-332, Km. 87, 03550 Sant Joan d’Alacant, Spain. E-mail: ivanq{at}umh.es

Correspondence and reprint requests may also be addressed to Bernat Soria, MD, PhD, CABIMER, Andalusian Center for Molecular Biology and Regenerative Medicine, Avda. Américo Vespucio s/n, Isla de la Cartuja, 41092 Seville, Spain. E-mail: bernat.soria{at}juntadeandalucia.es

Abbreviations: [Ca2+]i, intracellular Ca2+ concentration

Homeostasis of blood glucose is mainly regulated by the coordinated secretion of glucagon and insulin from {alpha}- and ß-cells within the islets of Langerhans. The release of both hormones is Ca2+ dependent. In the current study, we used confocal microscopy and immunocytochemistry to unequivocally characterize the glucose-induced Ca2+ signals in {alpha}- and ß-cells within intact human islets. Extracellular glucose stimulation induced an opposite response in these two cell types. Although the intracellular Ca2+ concentration ([Ca2+]i) in ß-cells remained stable at low glucose concentrations, {alpha}-cells exhibited an oscillatory [Ca2+]i response. Conversely, the elevation of extracellular glucose elicited an oscillatory [Ca2+]i pattern in ß-cells but inhibited low-glucose–induced [Ca2+]i signals in {alpha}-cells. These Ca2+ signals were synchronic among ß-cells grouped in clusters within the islet, although they were not coordinated among the whole ß-cell population. The response of {alpha}-cells was totally asynchronic. Therefore, both the {alpha}- and ß-cell populations within human islets did not work as a syncitium in response to glucose. A deeper knowledge of {alpha}- and ß-cell behavior within intact human islets is important to better understand the physiology of the human endocrine pancreas and may be useful to select high-quality islets for transplantation.


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