Tonosaki Kazuyuki, Hori Yasunori, Shimizu Yasutake, Tonosaki Keiichi
Department of Oral Physiology, School of Dentistry, Meikai University, Saitama 350-0283, Japan.
Biomed Res. 2007 Apr;28(2):79-83. doi: 10.2220/biomedres.28.79.
Tasting sweet food elicits insulin release prior to increasing plasma glucose levels, known as cephalic phase insulin release (CPIR). The characteristic of CPIR is that plasma insulin secretion occurs before the rise of the plasma glucose level. In this experiment, we examined whether taste stimuli placed on the tongue could induce CPIR. We used female Wistar rats and five basic taste stimuli: sucrose (sweet), sodium chloride (salty), HCl (sour), quinine (bitter) or monosodium glutamate (umami). Rats reliably exhibited CPIR to sucrose. Sodium chloride, HCl, quinine, or monosodium glutamate did not elicit CPIR. The non-nutritive sweetener saccharine elicited CPIR. However, starch, which is nutritive but non-sweet, did not elicit CPIR although rats showed a strong preference for starch which is a source of glucose. In addition, we studied whether CPIR was related to taste receptor cell activity. We carried out the experiment in rats with bilaterally cut chorda tympani nerves, one of the gustatory nerves. After sectioning, CPIR was not observed for sweet stimulation. From these results, we conclude that sweetness information conducted by thistaste nerve provides essential information for eliciting CPIR.
品尝甜味食物会在血浆葡萄糖水平升高之前引发胰岛素释放，这被称为头期胰岛素释放（CPIR）。CPIR的特点是血浆胰岛素分泌在血浆葡萄糖水平升高之前发生。在本实验中，我们研究了置于舌上的味觉刺激是否能诱导CPIR。我们使用雌性Wistar大鼠和五种基本味觉刺激：蔗糖（甜）、氯化钠（咸）、盐酸（酸）、奎宁（苦）或味精（鲜味）。大鼠对蔗糖可靠地表现出CPIR。氯化钠（盐）、盐酸、奎宁或味精不会引发CPIR。非营养性甜味剂糖精能引发CPIR。然而，淀粉虽然有营养但不甜，尽管大鼠对作为葡萄糖来源的淀粉表现出强烈偏好，但它不会引发CPIR。此外，我们研究了CPIR是否与味觉受体细胞活性有关。我们在双侧切断鼓索神经（味觉神经之一）的大鼠中进行了实验。切断后，甜味刺激未观察到CPIR。从这些结果中，我们得出结论，由这条味觉神经传导的甜味信息为引发CPIR提供了必要信息。
