Institute of Veterinary Physiology and Zurich Center for Integrative Human Physiology, University of Zurich, 8057 Zurich, Switzerland.
Physiol Behav. 2011 Apr 18;103(1):25-30. doi: 10.1016/j.physbeh.2010.10.016. Epub 2010 Oct 28.
Amylin is secreted by pancreatic beta-cells and seems to function as a physiological signal of satiation and possibly also as an adiposity signal. Amylin's satiating effect is mediated via a direct action at area postrema (AP) neurons. The central pathways mediating amylin's effects rely on connections from the AP to the nucleus of the solitary tract and lateral parabrachial nucleus. Amylin was shown to interact, probably at the brainstem, with other satiating signals, namely cholecystokinin, glucagon-like peptide 1 and peptide YY, and other adiposity signals, namely leptin and insulin. The interaction with leptin, which is thought to involve the hypothalamus, may have important implications for the development of new and improved hormonal anti-obesity treatments. Steve Woods has contributed to the recent literature on amylin's eating inhibitory effect by some frequently cited publications. Steve's work concentrated more on the central administration of amylin and on amylin's potential role as an adiposity signal. His work will be reviewed here and discussed in the context of other important findings on amylin's role in the control of energy homeostasis.
胰岛淀粉样多肽由胰岛β细胞分泌，似乎作为饱腹感的生理信号发挥作用，也可能作为肥胖信号发挥作用。胰岛淀粉样多肽的饱腹感作用是通过对后区（AP）神经元的直接作用介导的。介导胰岛淀粉样多肽作用的中枢途径依赖于从 AP 到孤束核和外侧臂旁核的连接。已经表明，胰岛淀粉样多肽与其他饱腹感信号（即胆囊收缩素、胰高血糖素样肽 1 和肽 YY）以及其他肥胖信号（即瘦素和胰岛素）相互作用，可能在脑干。与瘦素的相互作用被认为涉及下丘脑，这可能对开发新的和改进的激素抗肥胖治疗具有重要意义。Steve Woods 通过一些经常被引用的出版物为胰岛淀粉样多肽的抑制进食作用的最新文献做出了贡献。Steve 的工作更多地集中在胰岛淀粉样多肽的中枢给药以及胰岛淀粉样多肽作为肥胖信号的潜在作用上。将在这里回顾他的工作，并结合其他关于胰岛淀粉样多肽在能量平衡控制中的作用的重要发现进行讨论。
