Le Sauter J, Geary N
Department of Psychology, Barnard Collège of Columbia University, New York, NY 10027.
Ann Endocrinol (Paris). 1993;54(3):149-61.
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.
除了其代谢作用外，胰高血糖素似乎还能加速餐后饱腹感，而饱腹感可控制进餐量。进食期间会释放胰高血糖素。在进餐开始时给予胰高血糖素可减少动物和人类的试验餐量，并减少大鼠的自发进餐量。这种作用在行为上与大鼠的正常饱腹感无法区分，在主观上与人类的正常饱腹感也无法区分。通过给予胰高血糖素抗体来拮抗进餐期间内源性胰高血糖素的作用，会增加试验餐量和自发进餐量。这些结果表明，胰高血糖素是一种生理性饱腹感信号。本文还综述了胰高血糖素的作用被转化为神经信号并传递至大脑的可能机制。最后，我们讨论了胰高血糖素在肥胖症中可能但尚不明确的作用，以及作为治疗饮食失调潜在治疗工具的可能性。
