[PDF] Physiology and Pathophysiology of the Islets of Langerhans Bernat Soria (auth.), Bernat Soria (eds.)

Preface: 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 Rolefor KATP Channels: ATP-Sensitive K+ Channel Closure Is not an Obligatory Step for Glucose-Induced Priming of Pancreatic B-Cell; N. Taguchi et al.IntracellularMessengers: 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 Diabetesmellitus): What Went Wrong? Mechanisms of B-Cell Destructionand 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 andTransportation: 52 Additional Articles. Index.