Geary N
Psychology Department, Columbia University, New York, NY 10027.
Neurosci Biobehav Rev. 1990 Fall;14(3):323-38. doi: 10.1016/s0149-7634(05)80042-9.
The hypothesis that prandial increases in circulating pancreatic glucagon initiates an important peripheral satiety signal is reviewed. Glucagon administration at the beginning of meals reduces the size of test meals in animals and humans and reduces the size of spontaneous meals in rats. Exogenous glucagon may also interact synergistically with cholecystokinin to inhibit feeding. These appear to be satiety effects because they are behaviorally specific in rats and subjectively specific in humans. Glucagon's pharmacological satiety effect is complemented by compelling evidence for a necessary contribution of endogenous glucagon to the control of meal size: administration of glucagon antibodies increases both test and spontaneous meal size in rats. Under many, but not all, conditions exogenous glucagon's satiety effect appears to originate in the liver and to be relayed to the brain via hepatic vagal afferents. Analysis of the central processing of this signal, however, has barely begun. How glucagon changes are transduced into neural afferent signals also remains an open question. The only hypothesis that has been extensively tested is that stimulation of hepatic glucose production initiates the satiety signal, but this is neither convincingly supported nor clearly rejected by currently available data. It is also not yet clear whether glucagon contributes to some forms of obesity or has potential use as a therapeutic tool in the control of eating disorders. Of the several proposed controls of hunger and satiety, glucagon appears to be one of the most likely to be physiologically relevant. This encourages further analysis of its behavioral characteristics, its neural mechanisms, and its clinical potential.
本文综述了一个假说，即进餐时循环中胰高血糖素的升高会启动一个重要的外周饱腹感信号。在动物和人类进食开始时给予胰高血糖素，会减小试验餐的量，在大鼠中还会减小自发进食的量。外源性胰高血糖素也可能与胆囊收缩素协同作用以抑制进食。这些似乎是饱腹感效应，因为它们在大鼠中具有行为特异性，在人类中具有主观特异性。胰高血糖素的药理学饱腹感效应得到了内源性胰高血糖素对进食量控制有必要作用的确凿证据的补充：给予胰高血糖素抗体可增加大鼠的试验餐和自发进食量。在许多但并非所有情况下，外源性胰高血糖素的饱腹感效应似乎起源于肝脏，并通过肝迷走神经传入纤维传递至大脑。然而，对该信号的中枢处理分析才刚刚开始。胰高血糖素的变化如何转化为神经传入信号仍是一个悬而未决的问题。唯一经过广泛测试的假说是肝脏葡萄糖生成的刺激启动了饱腹感信号，但目前可得的数据既未令人信服地支持这一假说，也未明确否定它。胰高血糖素是否与某些形式的肥胖有关，或者是否有作为控制饮食失调的治疗工具的潜力，目前也尚不清楚。在几种提出的饥饿和饱腹感控制机制中，胰高血糖素似乎是最有可能具有生理相关性的机制之一。这鼓励进一步分析其行为特征、神经机制及其临床潜力。
