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Insulin secretion: movement at all levels.

With this Second SERVIER-IGIS Symposium Diabetes Supplement, we, the members of the International Group on Insulin Secretion (IGIS), happily realize that we have been able to keep the promise made in the First SERVIER-IGIS Symposium ( Diabetes 50 [Suppl. 1], 2001): we are indeed initiating a tradition, with a yearly series of state-of-the-art collections on various aspects of islet biology, with the emphasis on type 2 diabetes. Without the logistics and the generous unrestricted educational grant put at our disposal by SERVIER, Paris, it is doubtful that we would ever embark on this project, let alone succeed in producing these high-quality publications.

The Second SERVIER-IGIS Symposium dealt with the “Kinetics of Insulin Release in Health and Type 2 Diabetes.” To optimally fulfill its preeminent role in glucose homeostasis, insulin secretion must not only be quantitatively appropriate, it must also follow a precise time course. It has indeed been known since the 1960s that insulin secretion is phasic; later work refined the definition of phasicity by the discovery of superimposed oscillations of varying frequencies. Many of these features are absent or disturbed in type 2 diabetic patients, sometimes before overt hyperglycemia is established. These convincing findings notwithstanding, the conditions required to demonstrate certain aspects of phasic insulin release are sometimes unphysiological. Just to mention the often used hyperglycemic clamp, in nature the β-cell is never exposed to a “jump” of the extracellular glucose concentration from 5 to 15–20 mmol/l within 2–3 min. It is therefore a legitimate question whether phasic insulin release is a bona fide biological characteristic of the β-cell. This supplement examines the question from several angles, at different levels of “magnification.” …