Physiology and Pathophysiology of the Islets of Langerhans [Paperback]

Proceedings of the First International Meeting of the Pancreatic Islet Study Group held in the Alicante, Spain, November 25-28 1994Preface: Why are Islets so Important? B. Soriat. Stimulus-Secretion Coupling: Are KATP Channels Enough?: Glucose Recognition: Hexose Recognition by the Pancreatic B-Cell and the Gustatory Cell; A. Niki, H. Niki. Glucose-Induced Time-Dependent Potentiation and `Run Down' of Insulin Secretion in Islets of Young Rats; C.R. Bliss, G.W.G. Sharp. The Role for KATP Channels: ATP-Sensitive K+ Channel Closure Is not an Obligatory Step for Glucose-Induced Priming of Pancreatic B-Cell; N. Taguchi et al. Intracellular Messengers: Intracellular Second Messengers; S.J.H. Ashcroft. Modulation of Islet Release: Extracellular Messengers for Pancreatic B-Cells; T. Yada. B-Cell Metabolism and [Ca2+]: Reciprocal Links between Metabolism and Ionic Events in Islet Cells; W.J. Malaisse. B-Cell Heterogeneity. Building an Homogeneous Response from an Heterogeneous Population: Heterogeneity of beta-Cell Secretion: Possible Involvement of KATP Channels; M. Faehling, F.M. Ashcroft. IDDM (Insulin Dependent Diabetes mellitus): What Went Wrong? Mechanisms of B-Cell Destruction and Defence: New Aspects to Functioning and Regeneration of Pancreatic beta-Cells: Cyclic ADP-Ribose and Reg Gene; H. Okamoto. Pathophysiology of the NIDDM: Islet Growth, Regeneration and Transportation: 52 Additional Articles. Index.Springer Book Archives