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Contributions of Physiology to the Understanding of Diabetes

Ten Essays in Memory of Albert E. Renold

  • Gaston R. Zahnd
  • Claes B. Wollheim

About this book

Introduction

Recent developments in research on diabetes mellitus embrace basic disciplines such as physiology, biochemistry, morphology, and evolving subspecialities. Fundamental studies on the heterogeneous diabetic syndrome are directed towards regulatory principles of cell metabolism, genetic control mechanisms of insulin biosynthesis, and secretion as well as autoimmune events implicated in selective destruction of the pancreatic ß-cell. At the same time, efforts are being made to better understand normal and impaired bilogical action of insulin and insulin-like growth factor I and the translocation process of glucose transporters in insulin-responsive target cells.
The above topics are presented in ten interrelated essays written by renowned experts. The authors offer an integrated view on the development of their work and perspectives in their fields.
The present volume is dedicated in reverence to the late Albert Renold, a founding father of the European Association for the Study of Diabetes, for his visionay leadership.

Keywords

Diabetes Diabetes mellitus Insulin Insulin Secretion biochemistry biology cell biology cells growth factor insulin-like metabolism physiology protein signal transduction signaling pathways

Editors and affiliations

  • Gaston R. Zahnd
    • 1
  • Claes B. Wollheim
    • 2
  1. 1.Fondation pour Recherches Médicales Faculté de MédecineUniversité de GenèveGenève 4Switzerland
  2. 2.Division de Biochimie clinique et de Diabétologie expérimentaleCentre Médical UniversitaireGenève 4Switzerland

Bibliographic information

  • DOI https://doi.org/10.1007/978-3-642-60475-1
  • Copyright Information Springer-Verlag Berlin Heidelberg 1997
  • Publisher Name Springer, Berlin, Heidelberg
  • eBook Packages Springer Book Archive
  • Print ISBN 978-3-642-64422-1
  • Online ISBN 978-3-642-60475-1
  • Buy this book on publisher's site
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