Sugar-activated ion transport in canine lingual epithelium. Implications for sugar taste transduction.
Sugar-activated ion transport in canine lingual epithelium. Implications for sugar taste transduction.
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糖激活的离子转运在犬舌上皮中。对糖味转移的影响。
DOI：
10.1085/jgp.92.1.87
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发表时间：
1988-07
影响因子：
3.8
通讯作者：
DeSimone, J A
中科院分区：
文献类型：
--
作者：
Mierson, S;DeSimone, S K;Heck, G L;DeSimone, J A
有充分的证据表明，包括味蕾细胞在内的舌上皮细胞顶端区域的离子传输途径可能在盐味接收中发挥作用。在本文中，我们提供的证据表明，就狗而言，还存在与糖味觉转导相关的糖激活离子传输途径。证据来自两条平行的实验：（a）对分离的犬舌上皮的离子传输研究，以及（b）来自犬鼓索的记录。体外结果表明，粘膜浴中的单糖和二糖在与哺乳动物糖味反应一致的浓度范围内刺激短路电流呈剂量依赖性增加。由葡萄糖、果糖或蔗糖在 30 mM NaCl 或 Krebs-Henseleit 缓冲液 (K-H) 中引起的跨上皮电流被阿米洛利部分阻断。在糖类激活的电流载体中，Na 的电流响应比 K 的电流响应更大。用 3-O-甲基葡萄糖刺激期间 K-H 中的离子通量测量表明，糖诱发的电流是由于 Na 流入的增加所致。根据氚化 3-O-甲基葡萄糖的测量，哇巴因或阿米洛利减少了糖引起的 Na 内流，而不影响糖转运。阿米洛利抑制犬鼓索对 0.5 M NaCl 的反应达 70-80%，对 0.5 M KCl 的反应抑制约 40%。这与阿米洛利对 NaCl 和 KCl 体外支持的短路电流的抑制百分比一致。阿米洛利还部分抑制鼓索对蔗糖和果糖的反应。结果表明，在狗中：（a）促进Na味觉的离子转运蛋白也促进了对K的部分反应，并且（b）糖激活的、偏好Na的离子转运系统是介导糖味传导的一种机制。文献中的结果表明人类也有类似的甜味机制。
There is good evidence indicating that ion-transport pathways in the apical regions of lingual epithelial cells, including taste bud cells, may play a role in salt taste reception. In this article, we present evidence that, in the case of the dog, there also exists a sugar- activated ion-transport pathway that is linked to sugar taste transduction. Evidence was drawn from two parallel lines of experiments: (a) ion-transport studies on the isolated canine lingual epithelium, and (b) recordings from the canine chorda tympani. The results in vitro showed that both mono- and disaccharides in the mucosal bath stimulate a dose-dependent increase in the short-circuit current over the concentration range coincident with mammalian sugar taste responses. Transepithelial current evoked by glucose, fructose, or sucrose in either 30 mM NaCl or in Krebs-Henseleit buffer (K-H) was partially blocked by amiloride. Among current carriers activated by saccharides, the current response was greater with Na than with K. Ion flux measurements in K-H during stimulation with 3-O-methylglucose showed that the sugar-evoked current was due to an increase in the Na influx. Ouabain or amiloride reduced the sugar-evoked Na influx without effect on sugar transport as measured with tritiated 3-O-methylglucose. Amiloride inhibited the canine chorda tympani response to 0.5 M NaCl by 70-80% and the response to 0.5 M KCl by approximately 40%. This agreed with the percent inhibition by amiloride of the short-circuit current supported in vitro by NaCl and KCl. Amiloride also partially inhibited the chorda tympani responses to sucrose and to fructose. The results indicate that in the dog: (a) the ion transporter subserving Na taste also subserves part of the response to K, and (b) a sugar-activated, Na- preferring ion-transport system is one mechanism mediating sugar taste transduction. Results in the literature indicate a similar sweet taste mechanism for humans.