Berthoud H R, Bereiter D A, Trimble E R, Siegel E G, Jeanrenaud B
Diabetologia. 1981 Mar;20 Suppl:393-401.
Using chronically catheterized, freely moving male Wistar rats, we have shown that the sweet taste of a saccharin solution reliably triggers a rapid cephalic phase insulin response (CPIR), in the absence of any significant change of glycemia. To establish the neural mediation of this reflex response we used rats that were cured from streptozotocin diabetes by intrahepatic islet-transplantation as a denervated B-cell preparation. The complete lack of any saccharin-induced CPIR in these rats suggests that it is indeed mediated by the peripheral autonomic nervous system, and that the insulin-stimulating gastrointestinal hormones are not involved in this response. It was further found that this reflex insulin secretion is not easily extinguishable and thus might have an unconditioned component. To investigate the central neural pathways involved in this reflex response we used both electrophysiological methods in anesthetized and semi-micro CNS manipulations in freely moving rats. On the basis of our preliminary results, and several reports, using the decerebrate rat preparation for measuring behavioral or saliva secretory oral taste reactivity, it appears that the CPIR might be organized at the brain stem/midbrain level, receiving strong modulatory influences from the diencephalon. But much further work has to be done to establish the central nervous circuitry. Finally, in two experiments, aiming at the question of how important and physiologically relevant the CPIR might be, we found that, on one hand, its lack can result in pathological oral glucose tolerance and on the other hand its exaggeration might contribute to the behavioral reaction to highly palatable sweet food and the resulting development of dietary obesity.
利用长期插管、自由活动的雄性Wistar大鼠，我们已经表明，在血糖无任何显著变化的情况下，糖精溶液的甜味可靠地触发快速头期胰岛素反应（CPIR）。为了确定这种反射反应的神经介导机制，我们使用通过肝内胰岛移植治愈链脲佐菌素糖尿病的大鼠作为去神经支配的B细胞制剂。这些大鼠完全缺乏任何糖精诱导的CPIR，这表明它确实是由外周自主神经系统介导的，并且胰岛素刺激的胃肠激素不参与这种反应。进一步发现，这种反射性胰岛素分泌不容易消退，因此可能有非条件性成分。为了研究参与这种反射反应的中枢神经通路，我们在麻醉大鼠中使用了电生理方法，并在自由活动的大鼠中进行了半微中枢神经系统操作。根据我们的初步结果以及几份报告，使用去大脑大鼠制剂来测量行为或唾液分泌性口腔味觉反应性，似乎CPIR可能在脑干/中脑水平组织起来，接受来自间脑的强烈调节影响。但要建立中枢神经回路还需要做更多的工作。最后，在两个实验中，针对CPIR可能有多重要以及在生理上有多大相关性的问题，我们发现，一方面，其缺乏会导致病理性口服葡萄糖耐量，另一方面，其过度可能会导致对高度可口甜食的行为反应以及由此产生的饮食性肥胖。
