Although its function in the regulation of glucose homeostasis in healthy subjects is recognized, the role of glucagon secreted by the α-cells of the pancreatic islets has long been underappreciated in the etiology of type 2 diabetes (T2D) compared with its rival hormone insulin. Numerous studies of recent decades highlight its key role in the development of fasting and postprandial hyperglycemia in T2D patients. The pathophysiology of T2D is characterized not only by insulin resistance and β-cell dysfunction, but also by hyperglucagonemia in the fasting state and lack of glucagon suppression following oral glucose and exaggerated glucagon responses to mixed meal ingestion. The XIIth Servier-IGIS Symposium sought to provide an update on glucagon expression and secretion and its fundamental role in physiology and in thepathology of T2D. It also reviewed the new therapeutic approaches opened up by knowledge of glucagon and α-cells, the exciting advances made in islet transplantation, generation of functional β-cells by α-cell reprogramming, to replace conventional exogenous insulin therapy, and the encouraging use of incretin in monotherapy or in combination therapy. The present Digest summarizes the main topics debated at the meeting.
“Pancreatic α-cells and glucagon—neglected metabolic actors”
I- Birth and death of the α-cell
II- Regulation of glucagon expression
III- Regulation of glucagon secretion
IV- Role of glucagon in metabolism
V- Therapeutic perspectives
Lectures during IGIS meeting and unpublished reviews