[Pancreatic glucagon: physiological signal of postprandial satiety]

Pancreatic glucagon, in addition to its metabolic effects, appears to accelerate postprandial satiety which controls meal size. Glucagon is released during meals. Administration of glucagon at the beginning of meals reduces the size of test meals in animals and humans, and reduces the size of spontaneous meals in rats. This effect is behaviorally indistinguishable from normal satiety in rats and subjectively indistinguishable from normal satiety in humans. Antagonism of the action of endogenous glucagon during meals by administration of glucagon antibodies increases both test meals and spontaneous meals. These results indicate that glucagon is a physiological satiety signal. The possible mechanisms through which glucagon's effect is transduced into a neural signal and relayed to the brain are also reviewed. Finally, we discuss the possible, but not yet clear, role of glucagon in obesity, and as a potential therapeutic tool for the treatment of eating disorders.