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Impact of Treatment on Islet Function in Type 2 Diabetes

¹ Unit of Endocrinology and Metabolism, University of Louvain, Faculty of Medicine, Brussels, Belgium
² Institut National de la Santé et de la Recherche Médicale U342, St. Vincent de Paul Hospital, Paris, France
³ Department of Endocrinology and Metabolism, Hebrew University Hadassah Medical Center, Jerusalem, Israel
⁴ Metabolism Unit, CNR Institute of Clinical Physiology, University of Pisa, Pisa, Italy
⁵ Howard Hughes Medical Institute, University of Chicago, Chicago, Illinois
⁶ Department of Molecular Medicine, Division of Endocrinology & Diabetes, Karolinska Hospital, Stockholm, Sweden

The first 300 words of the full text of this article appear below.

Five years already! We, the members of the International Group on Insulin Secretion (IGIS), are very happy that the Servier-IGIS Symposium on insulin secretion and islet pathophysiology, which we first organized in 2000, has, beyond our expectations, become a traditional, awaited, and much appraised event. The pleasant venue and climate of the French Riviera in early spring undoubtedly contribute to the attractiveness of the symposium. However, we trust that the major reason for its success is the high quality of the presentations and scientific exchanges. These standards extend to the rapid publication of most contributions as refereed and edited review or original articles in a series of supplements to Diabetes (1–4). Both the symposium and the publication are made possible by a generous, unrestricted educational grant from Les Laboratoires Servier (Paris).

This fifth edition focused on therapeutic approaches of type 2 diabetes and their impact on islet function. Although their hypoglycemic properties had already been recognized in 1942, sulfonamides (carbutamide) started to be used in the treatment of type 2 diabetes in 1955 (5). If millions of diabetic patients have successfully been treated with sulfonylureas for 50 years, it is because these compounds luckily hit a key regulatory site of insulin secretion, the ATP-sensitive K⁺ channel (K_ATP channel) that was to be discovered about 30 years later (6,7) and whose structure was identified only 10 years ago (8,9). Several sessions of the symposium were dedicated to this target, its role in various tissues, and the perspective of designing novel drugs with high selectivity. Alternative ways to stimulate deficient insulin secretion were discussed as well as the impact that treatment, whether directly targeting ß-cells or not, may have on islet function and progression of diabetes. Whenever possible . . . [Full Text of this Article]

Address correspondence to Jean-Claude Henquin, MD, PhD, Université Catholique de Louvain, Endocrinology & Metabolism Unit, UCL 55 30 Faculty of Medicine, Avenue Hippocrate 55, Brussels 1200, Belgium. E-mail: henquin@endo.ucl.ac.be. Or Suad Efendic, MD, PhD, Department of Molecular Medicine, Karolinska Institute, SE-17176 Stockholm, Sweden. E-mail: suad.efendic@molmed.ki.se

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