The role of the gut sweet taste receptor in regulating GLP-1, PYY, and CCK release in humans
The role of the gut sweet taste receptor in regulating GLP-1, PYY, and CCK release in humans
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肠道甜味受体在调节人体 GLP-1、PYY 和 CCK 释放中的作用
DOI：
10.1152/ajpendo.00077.2011
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发表时间：
2011-08-01
影响因子：
5.1
通讯作者：
Beglinger, C.
中科院分区：
文献类型：
--
作者：
Gerspach, A. C.;Steinert, R. E.;Beglinger, C.
胃肠甜味感受器在调节人类GLP-1、PYY和CCK释放中的作用。AM J生理学内分泌代谢酶301：E317-E325,2011。2011年5月3日首次出版；DOI：10.1152/ajpendo.00077.2011。-最近发现的胃肠道甜味受体对控制食物摄入量和葡萄糖动态平衡具有重要意义。乳糖醇对甜味受体T1R2/T1R3有抑制作用。本研究的目的是以乳酸为探针，观察阻断T1R2/T1R3对GLP-1、PYY和CCK释放的影响，以探讨T1R2/T1R3的生理作用。这项研究是一项随机、双盲、安慰剂对照的交叉研究，包括35名健康受试者。在第一部分中，受试者在300毫升水或500毫升混合液体餐中加入或不加入乳糖醇，灌胃给予75克葡萄糖。在第二部分中，受试者接受十二指肠内灌流葡萄糖(29.3克葡萄糖/100毫升；速度：2.5毫升/分钟，180分钟)或混合液体餐(相同速度)加或不加乳糖醇。结果表明：1)乳糖醇可显着降低胃内和十二指肠葡萄糖刺激部分GLP-1和PYY的分泌，但不影响CCK的分泌(P
Gerspach AC, Steinert RE, Schonenberger L, Graber-Maier A, Beglinger C. The role of the gut sweet taste receptor in regulating GLP-1, PYY, and CCK release in humans. Am J Physiol Endocrinol Metab 301: E317-E325, 2011. First published May 3, 2011; doi:10.1152/ajpendo.00077.2011.-The recent identification of sweet taste receptors in the gastrointestinal tract has important implications in the control of food intake and glucose homeostasis. Lactisole can inhibit the sweet taste receptor T1R2/T1R3. The objective was to use lactisole as a probe to investigate the physiological role of T1R2/T1R3 by assessing the effect of T1R2/T1R3 blockade on GLP-1, PYY, and CCK release in response to 1) intragastric administration of nutrients or 2) intraduodenal perfusion of nutrients. The study was performed as a randomized, double-blind, placebo-controlled crossover study that included 35 healthy subjects. In part I, subjects received intragastrically 75 g of glucose in 300 ml of water or 500 ml of a mixed liquid meal with or without lactisole. In part II, subjects received an intraduodenal perfusion of glucose (29.3 g glucose/100 ml; rate: 2.5 ml/min for 180 min) or a mixed liquid meal (same rate) with or without lactisole. The results were that 1) lactisole induced a significant reduction in GLP-1 and PYY but not CCK secretion in both the intragastric and the intraduodenal glucose-stimulated parts (P