The control of meal size is the best studied aspect of the control of energy balance, and manipulation of this system constitutes a promising target to treat obesity. A major part of this control system is based on gastrointestinal hormones such as glucagon-like peptide-1 (GLP-1) or amylin, which are released in response to a meal and which limit the size of an ongoing meal. Both amylin and GLP-1 have also been shown to increase energy expenditure in experimental rodents, but mechanistically we know much less how this effect may be mediated, which brain sites may be involved, and what the physiological relevance of these findings may be. Most studies indicate that the effect of peripheral amylin is centrally mediated via the area postrema, but other brain areas, such as the ventral tegmental area, may also be involved. GLP-1’s effect on eating seems to be mainly mediated by vagal afferents projecting to the caudal hindbrain. Chronic exposure to amylin, GLP-1 or their analogs decrease food intake and body weight gain. Next to the induction of satiation, amylin may also constitute an adiposity signal and in fact interact with the adiposity signal leptin. Amylin analogs are under clinical consideration for their effect to reduce food intake and body weight in humans, and similar to rodents, amylin analogs seem to be particularly active when combined with leptin analogs.

进餐量的控制是控制能量平衡的最佳研究方法，对该系统的操纵构成了治疗肥胖症的有希望的目标。该控制系统的主要部分是基于胃肠激素，例如胰高血糖素样肽1（GLP-1）或胰岛淀粉样多肽，它们会随着进餐而释放，并限制了进餐量。胰岛淀粉样多肽和GLP-1均已被证明会增加实验啮齿动物的能量消耗，但从机理上讲，我们对这种作用是如何介导的，可能涉及的大脑部位以及这些发现的生理相关性知之甚少。大多数研究表明，周围胰岛淀粉样多肽的作用是通过视网膜后区域集中介导的，但其他大脑区域，例如腹侧被盖区域也可能参与其中。GLP-1对进食的影响似乎主要由投射到尾后脑的迷走神经传入介导。长期暴露于胰岛淀粉样多肽，GLP-1或其类似物会减少食物摄入和体重增加。在引起饱食感之后，胰岛淀粉样多肽还可以构成肥胖信号并且实际上与肥胖信号瘦素相互作用。胰岛淀粉样多肽类似物由于其减少人类食物摄入和减轻体重的作用而在临床上正在考虑之中，并且与啮齿动物相似，胰岛淀粉样多肽类似物与瘦素类似物结合时似乎特别有效。胰岛淀粉样多肽还可以构成肥胖信号，并且实际上与肥胖信号瘦素相互作用。胰岛淀粉样多肽类似物由于其减少人类食物摄入和减轻体重的作用而在临床上正在考虑之中，并且与啮齿动物相似，胰岛淀粉样多肽类似物与瘦素类似物结合时似乎特别有效。胰岛淀粉样多肽还可以构成肥胖信号，并且实际上与肥胖信号瘦素相互作用。胰岛淀粉样多肽类似物由于其减少人类食物摄入和减轻体重的作用而在临床上正在考虑之中，并且与啮齿动物相似，胰岛淀粉样多肽类似物与瘦素类似物结合时似乎特别有效。