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Mathematical modelling of stimulus-secretion coupling in the pancreatic B-cell. II. Calcium-stimulated calcium release
Authors:Y Scholler  V de Maertelaer  W J Malaisse
Institution:1. Graduate School of Frontier Sciences, University of Tokyo, 5-1-5 Kashiwanoha, Kashiwa 277-8562, Japan;2. Computational Biology Research Consortium (CBRC), in National Institute of Advanced Industrial Science and Technology (AIST), 2-41-6, Aomi, Koto-ku, Tokyo 135-0064, Japan;3. Department of Electrical Engineering and Bioscience, Faculty of Science and Engineering, Waseda University, 55 N-06-10, 3-4-1, Okubo Shinjuku-ku, Tokyo 169-8555, Japan
Abstract:An attempt was made to simulate in a mathematical model one of the two major effects of glucose upon 45Ca fractional outflow rate from prelabelled pancreatic islets, namely the increase in effluent radioactivity which is currently ascribed to the displacement of 45Ca from intracellular sites, as resulting from a facilitated influx of unlabelled 40Ca into the islet cells. The occurrence of such a rise in effluent radioactivity and its suppression in the absence of extracellular Ca2+ could only be simulated if the release of Ca by the vacuolar system was assumed to be stimulated by a rise in the cytosolic Ca concentration. It is proposed therefore that, in islets like in muscle, a process of Ca-stimulated Ca release may participate in the regulation of intracellular Ca distribution.
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